carbamates and HIV Infections studies

HIV Infections: Includes the spectrum of human immunodeficiency virus infections that range from asymptomatic seropositivity, thru AIDS-related complex (ARC), to acquired immunodeficiency syndrome (AIDS).

Research Excerpts

Excerpt	Relevance	Reference
" In a phase 2 study we aimed to assess the efficacy and safety of grazoprevir (MK-5172; HCV NS3/4A protease inhibitor) and two doses of elbasvir (MK-8742; HCV NS5A inhibitor) in patients with HCV mono-infection and HIV/HCV co-infection."	9.20	Efficacy and safety of 8 weeks versus 12 weeks of treatment with grazoprevir (MK-5172) and elbasvir (MK-8742) with or without ribavirin in patients with hepatitis C virus genotype 1 mono-infection and HIV/hepatitis C virus co-infection (C-WORTHY): a rando ( Barr, E; Bourliere, M; DeJesus, E; Dutko, F; Gerstoft, J; Haber, B; Hezode, C; Howe, AY; Hwang, P; Kugelmas, M; Mallolas, J; Murillo, A; Nahass, R; Pol, S; Robertson, M; Serfaty, L; Shaughnessy, M; Shibolet, O; Sulkowski, M; Vierling, JM; Wahl, J; Weis, N; Zuckerman, E, 2015)
" The C-EDGE CO-INFECTION study assessed the efficacy, safety, and tolerability of grazoprevir (MK-5172) plus elbasvir (MK-8742) in patients with HCV and HIV co-infection."	9.20	Efficacy and safety of grazoprevir (MK-5172) and elbasvir (MK-8742) in patients with hepatitis C virus and HIV co-infection (C-EDGE CO-INFECTION): a non-randomised, open-label trial. ( Barr, E; Bloch, M; Gress, J; Katlama, C; Klopfer, S; Lalezari, J; Mallolas, J; Matthews, GV; Nelson, M; Nguyen, BY; Orkin, C; Platt, HL; Robertson, MN; Rockstroh, JK; Saag, MS; Shaughnessy, M; Sulkowski, M; Wahl, J; Zamor, PJ, 2015)
"STRATEGY-PI is a 96 week, international, multicentre, randomised, open-label, phase 3b trial in which HIV-infected adults with a plasma HIV-1 RNA viral load of less than 50 copies per mL for at least 6 months who were taking a ritonavir-boosted protease inhibitor with emtricitabine plus tenofovir were randomly assigned (2:1) either to switch to coformulated elvitegravir, cobicistat, emtricitabine, and tenofovir or to continue on their existing regimen."	9.19	Simplification to coformulated elvitegravir, cobicistat, emtricitabine, and tenofovir versus continuation of ritonavir-boosted protease inhibitor with emtricitabine and tenofovir in adults with virologically suppressed HIV (STRATEGY-PI): 48 week results o ( Arribas, JR; Di Perri, G; Ebrahimi, R; Gathe, J; Nguyen, T; Pialoux, G; Piontkowsky, D; Reynes, J; Tebas, P; White, K, 2014)
"Coformulated elvitegravir, cobicistat, emtricitabine, and tenofovir disoproxil fumarate (tenofovir) might be a safe and efficacious switch option for virologically suppressed patients with HIV who have neuropsychiatric side-effects on a non-nucleoside reverse transcriptase inhibitor (NNRTI) or who are on a multitablet NNRTI-containing regimen and want a regimen simplification."	9.19	Switching to coformulated elvitegravir, cobicistat, emtricitabine, and tenofovir versus continuation of non-nucleoside reverse transcriptase inhibitor with emtricitabine and tenofovir in virologically suppressed adults with HIV (STRATEGY-NNRTI): 48 week r ( Antela, A; Domingo, P; Garner, W; Girard, PM; Guyer, B; Henry, K; Markowitz, M; Mills, A; Nguyen, T; Piontkowsky, D; Pozniak, A; Stellbrink, HJ; White, K, 2014)
"Steady-state pharmacokinetics in pregnant women prescribed ritonavir-boosted fosamprenavir (FPV) to prevent HIV transmission were assessed in the second trimester, third trimester, and postpartum."	9.17	Steady-state pharmacokinetics, cord blood concentrations, and safety of ritonavir-boosted fosamprenavir in pregnancy. ( Aberg, JA; Castor, D; Cespedes, MS; Ford, SL; Lee, D; Lou, Y; Pakes, GE, 2013)
"Abstract Our objective was to evaluate the liver toxicity of antiretroviral regimens including fosamprenavir plus ritonavir (FPV/r) 1400/100 mg once daily (QD) in HIV/hepatitis C virus (HCV)-coinfected patients."	9.15	Liver toxicity of antiretroviral combinations including fosamprenavir plus ritonavir 1400/100 mg once daily in HIV/hepatitis C virus-coinfected patients. ( Delgado-Fernández, M; García-Figueras, C; López-Cortés, LF; Macías, J; Márquez-Solero, M; Martínez-Pérez, MA; Mata, R; Merchante, N; Merino, D; Omar, M; Pasquau, J; Pineda, JA; Ríos-Villegas, MJ; Rivero, A, 2011)
"A systematic literature review of Phase III clinical trials identified 2 trials of SOF+R-PHOTON-1 (A Phase 3, Open-Label Study to Investigate the Efficacy and Safety of GS-7977 Plus Ribavirin in Chronic Genotype 1, 2 and 3 Hepatitis C Virus [HCV] and Human Immunodeficiency Virus [HIV] Co-Infected Subjects) and PHOTON-2 (A Phase 3, Open-Label Study to Investigate the Efficacy and Safety of Sofosbuvir Plus Ribavirin in Chronic Genotype 1, 2, 3 and 4 Hepatitis C Virus [HCV] and Human Immunodeficiency Virus [HIV] Co-Infected Subjects) suitable for comparison with the trial of DCV+SOF in patients coinfected with HIV and HCV-ALLY-2 (A Phase 3 Evaluation of Daclatasvir Plus Sofosbuvir in Treatment-naïve and Treatment-experienced Chronic Hepatitis C [Genotype 1, 2, 3, 4, 5, or 6] Subjects Coinfected With Human Immunodeficiency Virus [HIV])."	8.93	Daclatasvir and Sofosbuvir Versus Sofosbuvir and Ribavirin in Patients with Chronic Hepatitis C Coinfected with HIV: A Matching-adjusted Indirect Comparison. ( Ackerman, P; Kalsekar, A; Kelley, C; Mu, F; Peeples, M; Signorovitch, J; Song, J; Swallow, E; Yuan, Y, 2016)
"Report the real-world experience of the efficacy and safety of sofosbuvir/velpatasvir/voxilaprevir (SOF/VEL/VOX) in chronic hepatitis C virus (HCV) infected patients who have previously experienced a direct-acting antiviral (DAA) containing regimen."	8.02	Efficacy of sofosbuvir/velpatasvir/voxilaprevir in direct-acting antiviral experienced patients with hepatitis C virus. ( Da, BL; Dieterich, D; Kushner, T; Lourdusamy, V; Saberi, B, 2021)
"Among 41 patients treated, 35 (85%) patients had genotype 1b HCV infection, 6 (15%) had co-infection with human immunodeficiency virus, 35 (85%) failed previous peginterferon and ribavirin therapy, 25 (61%) had compensated liver cirrhosis, and 3 (7%) had liver transplantation."	7.85	Real-life efficacy and safety of paritaprevir/ritonavir, ombitasvir, and dasabuvir in chronic hepatitis C patients in Hong Kong. ( But, DY; Chan, CK; Chan, HL; Chan, KH; Fung, J; Hui, YT; Lai, CL; Lai, MS; Lam, YS; Lao, WC; Li, C; Lui, GC; Seto, WK; Tsang, OT; Wong, GL; Wong, VW; Yuen, MF, 2017)
"Safety and tolerability evaluation of adapted dose regimens containing fosamprenavir/ritonavir (FPV/r) in HIV-infected subjects with viral hepatitis co-infection."	7.83	Fosamprenavir/ritonavir in patients with viral hepatitis coinfection: an observational multicohort study. ( Cerini, C; Cozzi-Lepri, A; d'Arminio Monforte, A; Giralda, M; Nasta, P; Pimenta, JM; Salmon, D; Winnock, M, 2016)
" During the first year of treatment, exenatide, in combination with metformin and repaglinide, led to a weight loss of 14 kg and fat mass and waist circumference were respectively reduced from 31 to 25."	7.77	Exenatide improves weight loss insulin sensitivity and β-cell function following administration to a type 2 diabetic HIV patient on antiretroviral therapy. ( Buysschaert, M; de la Tribonnière, X; Hermans, MP; Oriot, P; Selvais, P, 2011)
"The aim of this study was to compare amprenavir pharmacokinetics in HIV/hepatitis C virus (HCV)-co-infected cirrhotic patients receiving non-boosted fosamprenavir 700 mg twice daily with HCV/HIV-co-infected non-cirrhotic subjects and HIV-mono-infected subjects receiving fosamprenavir/ritonavir 700/100 mg twice daily."	7.75	Unboosted fosamprenavir is associated with low drug exposure in HIV-infected patients with mild-moderate liver impairment resulting from HCV-related cirrhosis. ( Bonora, S; Carosi, G; de Requena, DG; Gatti, F; Loregian, A; Matti, A; Nasta, P; Pagni, S; Palù, G; Parisi, SG; Prestini, K; Puoti, M, 2009)
"To report successful desensitization to amprenavir after the occurrence of a maculopapular exanthem in an HIV-infected patient with late-stage disease and limited antiretroviral treatment options."	7.73	Amprenavir-induced maculopapular exanthem followed by desensitization in a patient with late-stage human immunodeficiency virus. ( Huynh, P; Kohli-Pamnani, A; Lobo, F, 2006)
"To examine the clinical significance of HIV protease mutations detected before and after therapy with amprenavir."	7.72	HIV protease mutations associated with amprenavir resistance during salvage therapy: importance of I54M. ( Chou, S; Marousek, GI; Murphy, MD, 2004)
" However, evening atazanavir plus ritonavir and lopinavir/ritonavir regimens are not recommended in combination with the 3D regimen."	6.82	Evaluation of Drug-Drug Interactions Between Hepatitis C Antiviral Agents Ombitasvir, Paritaprevir/Ritonavir, and Dasabuvir and HIV-1 Protease Inhibitors. ( Awni, W; Dutta, S; Khatri, A; Menon, R; Podsadecki, T; Trinh, R; Wang, H, 2016)
" Healthy volunteer studies have demonstrated a decrease in glucose disposal associated with dosing with specific antiretrovirals."	6.75	Effect of boosted fosamprenavir or lopinavir-based combinations on whole-body insulin sensitivity and lipids in treatment-naive HIV-type-1-positive men. ( Back, DJ; Boffito, M; Jackson, AG; Mandalia, S; Moyle, GJ; Randell, PA; Taylor, J; Tjia, JF, 2010)
" The secondary outcome measures were SVR12 stratified by the presence of decompensated cirrhosis, prior treatment, HCC, and HIV/hepatitis C virus coinfection and the occurrence rate of serious adverse events requiring treatment cessation or hospitalization."	5.62	Efficacy and safety of sofosbuvir/velpatasvir in a real-world chronic hepatitis C genotype 3 cohort. ( Ang, TL; Fock, KM; Koh, J; Kumar, LS; Kumar, R; Kwek, A; Law, NM; Lee, ZC; Li, W; Tan, J; Tan, YB; Teo, EK; Thurairajah, PH; Wong, YJ, 2021)
" No discontinuations were attributed to treatment-related adverse events."	5.43	12 Weeks of Daclatasvir in Combination With Sofosbuvir for HIV-HCV Coinfection (ALLY-2 Study): Efficacy and Safety by HIV Combination Antiretroviral Regimens. ( Ackerman, P; Bhore, R; Luetkemeyer, AF; McDonald, C; Noviello, S; Ramgopal, M, 2016)
"DCV was dosed at week 4 and at week 8 of treatment, and RBV at week 8."	5.43	Daclatasvir plasma level and resistance selection in HIV patients with hepatitis C virus cirrhosis treated with daclatasvir, sofosbuvir, and ribavirin. ( Andreis, S; Basso, M; Cattelan, AM; Cavinato, S; Dal Bello, F; Loregian, A; Messa, L; Nannetti, G; Palù, G; Parisi, SG; Scaggiante, R, 2016)
"We conducted a nonrandomized clinical trial of 12 or 24 weeks of paritaprevir-ritonavir-ombitasvir plus dasabuvir (PrOD) with or without ribavirin in persons with HCV-1/HIV coinfection suppressed with antiretroviral therapy."	5.34	Hepatitis C Virus (HCV) Direct-Acting Antiviral Therapy in Persons With Human Immunodeficiency Virus-HCV Genotype 1 Coinfection Resulting in High Rate of Sustained Virologic Response and Variable in Normalization of Soluble Markers of Immune Activation. ( Alston-Smith, BL; Anthony, DD; Balagopal, A; Bhattacharya, D; Cohen, DE; Damjanovska, S; Kowal, CM; Shive, CL; Smeaton, LM; Sulkowski, MS; Wyles, DL, 2020)
"Elbasvir/grazoprevir is a once-daily fixed-dose combination therapy for the treatment of chronic HCV infection, including HCV/HIV coinfection."	5.30	Assessment of drug interaction potential between the HCV direct-acting antiviral agents elbasvir/grazoprevir and the HIV integrase inhibitors raltegravir and dolutegravir. ( Butterton, JR; Caro, L; Fandozzi, C; Feng, HP; Fraser, I; Guo, Z; Huang, X; Iwamoto, M; Jumes, P; Ma, J; Mangin, E; Marshall, WL; Panebianco, D; Ross, LL; Talaty, J; Yeh, WW, 2019)
"To evaluate the efficacy and safety of pegylated interferon-lambda-1a (Lambda)/ribavirin (RBV)/daclatasvir (DCV) for treatment of patients coinfected with chronic hepatitis C virus (HCV) and human immunodeficiency virus (HIV)."	5.24	Safety and Efficacy of Pegylated Interferon Lambda, Ribavirin, and Daclatasvir in HCV and HIV-Coinfected Patients. ( Conway, B; Lazzarin, A; Luetkemeyer, A; Molina, JM; Nelson, M; Portsmouth, S; Romanova, S; Rubio, R; Srinivasan, S; Xu, D, 2017)
" In a phase 2 study we aimed to assess the efficacy and safety of grazoprevir (MK-5172; HCV NS3/4A protease inhibitor) and two doses of elbasvir (MK-8742; HCV NS5A inhibitor) in patients with HCV mono-infection and HIV/HCV co-infection."	5.20	Efficacy and safety of 8 weeks versus 12 weeks of treatment with grazoprevir (MK-5172) and elbasvir (MK-8742) with or without ribavirin in patients with hepatitis C virus genotype 1 mono-infection and HIV/hepatitis C virus co-infection (C-WORTHY): a rando ( Barr, E; Bourliere, M; DeJesus, E; Dutko, F; Gerstoft, J; Haber, B; Hezode, C; Howe, AY; Hwang, P; Kugelmas, M; Mallolas, J; Murillo, A; Nahass, R; Pol, S; Robertson, M; Serfaty, L; Shaughnessy, M; Shibolet, O; Sulkowski, M; Vierling, JM; Wahl, J; Weis, N; Zuckerman, E, 2015)
" The C-EDGE CO-INFECTION study assessed the efficacy, safety, and tolerability of grazoprevir (MK-5172) plus elbasvir (MK-8742) in patients with HCV and HIV co-infection."	5.20	Efficacy and safety of grazoprevir (MK-5172) and elbasvir (MK-8742) in patients with hepatitis C virus and HIV co-infection (C-EDGE CO-INFECTION): a non-randomised, open-label trial. ( Barr, E; Bloch, M; Gress, J; Katlama, C; Klopfer, S; Lalezari, J; Mallolas, J; Matthews, GV; Nelson, M; Nguyen, BY; Orkin, C; Platt, HL; Robertson, MN; Rockstroh, JK; Saag, MS; Shaughnessy, M; Sulkowski, M; Wahl, J; Zamor, PJ, 2015)
"STRATEGY-PI is a 96 week, international, multicentre, randomised, open-label, phase 3b trial in which HIV-infected adults with a plasma HIV-1 RNA viral load of less than 50 copies per mL for at least 6 months who were taking a ritonavir-boosted protease inhibitor with emtricitabine plus tenofovir were randomly assigned (2:1) either to switch to coformulated elvitegravir, cobicistat, emtricitabine, and tenofovir or to continue on their existing regimen."	5.19	Simplification to coformulated elvitegravir, cobicistat, emtricitabine, and tenofovir versus continuation of ritonavir-boosted protease inhibitor with emtricitabine and tenofovir in adults with virologically suppressed HIV (STRATEGY-PI): 48 week results o ( Arribas, JR; Di Perri, G; Ebrahimi, R; Gathe, J; Nguyen, T; Pialoux, G; Piontkowsky, D; Reynes, J; Tebas, P; White, K, 2014)
"Coformulated elvitegravir, cobicistat, emtricitabine, and tenofovir disoproxil fumarate (tenofovir) might be a safe and efficacious switch option for virologically suppressed patients with HIV who have neuropsychiatric side-effects on a non-nucleoside reverse transcriptase inhibitor (NNRTI) or who are on a multitablet NNRTI-containing regimen and want a regimen simplification."	5.19	Switching to coformulated elvitegravir, cobicistat, emtricitabine, and tenofovir versus continuation of non-nucleoside reverse transcriptase inhibitor with emtricitabine and tenofovir in virologically suppressed adults with HIV (STRATEGY-NNRTI): 48 week r ( Antela, A; Domingo, P; Garner, W; Girard, PM; Guyer, B; Henry, K; Markowitz, M; Mills, A; Nguyen, T; Piontkowsky, D; Pozniak, A; Stellbrink, HJ; White, K, 2014)
"Steady-state pharmacokinetics in pregnant women prescribed ritonavir-boosted fosamprenavir (FPV) to prevent HIV transmission were assessed in the second trimester, third trimester, and postpartum."	5.17	Steady-state pharmacokinetics, cord blood concentrations, and safety of ritonavir-boosted fosamprenavir in pregnancy. ( Aberg, JA; Castor, D; Cespedes, MS; Ford, SL; Lee, D; Lou, Y; Pakes, GE, 2013)
"Abstract Our objective was to evaluate the liver toxicity of antiretroviral regimens including fosamprenavir plus ritonavir (FPV/r) 1400/100 mg once daily (QD) in HIV/hepatitis C virus (HCV)-coinfected patients."	5.15	Liver toxicity of antiretroviral combinations including fosamprenavir plus ritonavir 1400/100 mg once daily in HIV/hepatitis C virus-coinfected patients. ( Delgado-Fernández, M; García-Figueras, C; López-Cortés, LF; Macías, J; Márquez-Solero, M; Martínez-Pérez, MA; Mata, R; Merchante, N; Merino, D; Omar, M; Pasquau, J; Pineda, JA; Ríos-Villegas, MJ; Rivero, A, 2011)
"To evaluate the pharmacokinetic compatibility of a ritonavir-boosted indinavir-fosamprenavir combination among patients with human immunodeficiency virus (HIV)."	5.13	Pharmacokinetics of an indinavir-ritonavir-fosamprenavir regimen in patients with human immunodeficiency virus. ( Acosta, EP; Easley, KA; Lennox, JL; Ofotokun, I; Pan, Y, 2008)
"AbbVie's 3 direct-acting antiviral (3D) regimen containing ombitasvir, paritaprevir, ritonavir, and dasabuvir with and without ribavirin is approved for the treatment of chronic hepatitis C virus (HCV) genotype 1 infection."	4.95	Ombitasvir/Paritaprevir/Ritonavir and Dasabuvir: Drug Interactions With Antiretroviral Agents and Drugs forSubstance Abuse. ( King, JR; Menon, RM, 2017)
"A systematic literature review of Phase III clinical trials identified 2 trials of SOF+R-PHOTON-1 (A Phase 3, Open-Label Study to Investigate the Efficacy and Safety of GS-7977 Plus Ribavirin in Chronic Genotype 1, 2 and 3 Hepatitis C Virus [HCV] and Human Immunodeficiency Virus [HIV] Co-Infected Subjects) and PHOTON-2 (A Phase 3, Open-Label Study to Investigate the Efficacy and Safety of Sofosbuvir Plus Ribavirin in Chronic Genotype 1, 2, 3 and 4 Hepatitis C Virus [HCV] and Human Immunodeficiency Virus [HIV] Co-Infected Subjects) suitable for comparison with the trial of DCV+SOF in patients coinfected with HIV and HCV-ALLY-2 (A Phase 3 Evaluation of Daclatasvir Plus Sofosbuvir in Treatment-naïve and Treatment-experienced Chronic Hepatitis C [Genotype 1, 2, 3, 4, 5, or 6] Subjects Coinfected With Human Immunodeficiency Virus [HIV])."	4.93	Daclatasvir and Sofosbuvir Versus Sofosbuvir and Ribavirin in Patients with Chronic Hepatitis C Coinfected with HIV: A Matching-adjusted Indirect Comparison. ( Ackerman, P; Kalsekar, A; Kelley, C; Mu, F; Peeples, M; Signorovitch, J; Song, J; Swallow, E; Yuan, Y, 2016)
"A fixed-dose tablet comprising ombitasvir (an NS5A replication complex inhibitor), paritaprevir (an NS3/4A protease inhibitor) and ritonavir (a cytochrome P450 inhibitor) taken in combination with dasabuvir (an NS5B polymerase inhibitor) is indicated for the treatment of chronic hepatitis C virus (HCV) genotype 1 infection in several countries, including the USA (copackaged as Viekira Pak(™)) and those of the EU (Viekirax(®) and Exviera(®))."	4.91	Ombitasvir/Paritaprevir/Ritonavir Plus Dasabuvir: A Review in Chronic HCV Genotype 1 Infection. ( Deeks, ED, 2015)
"Darunavir is the result of wide and in-depth investigation into HIV protease inhibitors (PIs)."	4.84	[Chemical characteristics, mechanism of action and antiviral activity of darunavir]. ( Hidalgo Tenorio, C; Pasquau Liaño, J, 2008)
" We report the occurrence of spontaneous intracranial bleeding in an human immunodeficiency virus (HIV)-infected adolescent with hemophilia A who was receiving amprenavir (APV)."	4.81	Possible linkage of amprenavir with intracranial bleeding in an HIV-infected hemophiliac. ( Bakshi, S; Black, K; Kodoth, S; Pahwa, S; Scimeca, P, 2001)
"Report the real-world experience of the efficacy and safety of sofosbuvir/velpatasvir/voxilaprevir (SOF/VEL/VOX) in chronic hepatitis C virus (HCV) infected patients who have previously experienced a direct-acting antiviral (DAA) containing regimen."	4.02	Efficacy of sofosbuvir/velpatasvir/voxilaprevir in direct-acting antiviral experienced patients with hepatitis C virus. ( Da, BL; Dieterich, D; Kushner, T; Lourdusamy, V; Saberi, B, 2021)
"The current recommendation for treating hepatitis C virus (HCV) in HIV patients includes the combination of sofosbuvir (SOF) and daclatasvir (DCV)."	4.02	Single-pill sofosbuvir and daclatasvir for treating hepatis C in patients co-infected with human immunodeficiency virus. ( Dehghan Manshadi, SA; Kalantari, S; Karimi, J; Malekzadeh, R; Malekzadeh, Z; Mardani, M; Merat, D; Merat, S; Mirminachi, B; Mohraz, M; Nikbin, M; Norouzi, A; Poustchi, H; Rasoolinejad, M; Sali, S; Sedghi, R; Sharifi, AH; Somi, MH; Tabarsi, P; Tayeri, K, 2021)
"Grazoprevir/elbasvir (GZR/EBR) was approved for the treatment of chronic hepatitis C virus (HCV) genotype 1 and 4 infected patients with or without compensated liver cirrhosis."	3.96	Real-world experience with Grazoprevir/Elbasvir in the treatment of previously "difficult to treat" patients infected with hepatitis C virus genotype 1 and 4. ( Belica-Wdowik, T; Berak, H; Białkowska-Warzecha, J; Blaszkowska, M; Buczyńska, I; Czauż-Andrzejuk, A; Deroń, Z; Dobracka, B; Dybowska, D; Flisiak, R; Garlicki, A; Halota, W; Horban, A; Janczewska, E; Jaroszewicz, J; Klapaczyński, J; Laurans, Ł; Lorenc, B; Mazur, W; Pabjan, P; Pawłowska, M; Piekarska, A; Simon, K; Sitko, M; Socha, Ł; Tomasiewicz, K; Tronina, O; Tudrujek-Zdunek, M; Zarębska-Michaluk, D, 2020)
"Our study demonstrated that liver transplant patients with a recurrence of hepatitis C who are initiating ribavirin combined with a sofosbuvir-daclatasvir direct-acting antiviral regimen may be at risk of lower tacrolimus concentrations because of probable ribavirin-induced anaemia and higher fibrosis score, although there are no effects on cyclosporine levels."	3.91	Comparison of the effect of direct-acting antiviral with and without ribavirin on cyclosporine and tacrolimus clearance values: results from the ANRS CO23 CUPILT cohort. ( Barrail-Tran, A; Botta-Fridlund, D; Cagnot, C; Canva, V; Coilly, A; Conti, F; D'Alteroche, L; Danjou, H; De Ledinghen, V; Duclos-Vallée, JC; Durand, F; Duvoux, C; Fougerou-Leurent, C; Gelé, T; Goldwirt, L; Houssel-Debry, P; Kamar, N; Laforest, C; Lavenu, A; Leroy, V; Moreno, C; Pageaux, GP; Radenne, S; Samuel, D; Taburet, AM, 2019)
"Among 41 patients treated, 35 (85%) patients had genotype 1b HCV infection, 6 (15%) had co-infection with human immunodeficiency virus, 35 (85%) failed previous peginterferon and ribavirin therapy, 25 (61%) had compensated liver cirrhosis, and 3 (7%) had liver transplantation."	3.85	Real-life efficacy and safety of paritaprevir/ritonavir, ombitasvir, and dasabuvir in chronic hepatitis C patients in Hong Kong. ( But, DY; Chan, CK; Chan, HL; Chan, KH; Fung, J; Hui, YT; Lai, CL; Lai, MS; Lam, YS; Lao, WC; Li, C; Lui, GC; Seto, WK; Tsang, OT; Wong, GL; Wong, VW; Yuen, MF, 2017)
"The combination of ombitasvir, dasabuvir, and paritaprevir/ritonavir (considered as the 3D regimen) has proven to be associated with high sustained virologic response and optimal tolerability in hepatitis C virus-infected patients."	3.83	Severe Hyperbilirubinemia in an HIV-HCV-Coinfected Patient Starting the 3D Regimen That Resolved After TDM-Guided Atazanavir Dose Reduction. ( Cattaneo, D; Clementi, E; Gervasoni, C; Milazzo, L; Riva, A, 2016)
"Safety and tolerability evaluation of adapted dose regimens containing fosamprenavir/ritonavir (FPV/r) in HIV-infected subjects with viral hepatitis co-infection."	3.83	Fosamprenavir/ritonavir in patients with viral hepatitis coinfection: an observational multicohort study. ( Cerini, C; Cozzi-Lepri, A; d'Arminio Monforte, A; Giralda, M; Nasta, P; Pimenta, JM; Salmon, D; Winnock, M, 2016)
" Two distinct FAAH inhibitory compounds, URB597 and PF-3845 were tested, and contrasted with standard antinociceptive gabapentin or vehicle treatment, for attenuation of tactile allodynia, cold allodynia, and mechanical hyperalgesia."	3.81	Attenuation of persistent pain-related behavior by fatty acid amide hydrolase (FAAH) inhibitors in a rat model of HIV sensory neuropathy. ( Jergova, S; Nasirinezhad, F; Pearson, JP; Sagen, J, 2015)
" During the first year of treatment, exenatide, in combination with metformin and repaglinide, led to a weight loss of 14 kg and fat mass and waist circumference were respectively reduced from 31 to 25."	3.77	Exenatide improves weight loss insulin sensitivity and β-cell function following administration to a type 2 diabetic HIV patient on antiretroviral therapy. ( Buysschaert, M; de la Tribonnière, X; Hermans, MP; Oriot, P; Selvais, P, 2011)
"Fosamprenavir (FPV) efficacy in human immunodeficiency virus (HIV)-infected pediatric patients is still being evaluated in ongoing clinical trials."	3.76	Long-term efficacy and safety of fosamprenavir in human immunodeficiency virus-infected pediatric patients. ( Briz, V; de José, MI; de Ory, SJ; González-Tomé, MI; León Leal, JA; Mellado, MJ; Moreno, D; Muñoz-Fernández, MA; Palladino, C; Policarpo, SN; Ramos, JT; Silveira, LF, 2010)
"To assess whether we confirmed the association between exposure to abacavir and risk of myocardial infarction (MI) and to estimate the impact of exposure to other nucleoside reverse transcriptase inhibitors (NRTIs), protease inhibitors (PIs), and non-NRTIs on risk of MI, we conducted a case-control study nested within the French Hospital Database on HIV."	3.76	Impact of individual antiretroviral drugs on the risk of myocardial infarction in human immunodeficiency virus-infected patients: a case-control study nested within the French Hospital Database on HIV ANRS cohort CO4. ( Boccara, F; Costagliola, D; Cotte, L; Gilquin, J; Lang, S; Mary-Krause, M; Partisani, M; Simon, A, 2010)
"The aim of this study was to compare amprenavir pharmacokinetics in HIV/hepatitis C virus (HCV)-co-infected cirrhotic patients receiving non-boosted fosamprenavir 700 mg twice daily with HCV/HIV-co-infected non-cirrhotic subjects and HIV-mono-infected subjects receiving fosamprenavir/ritonavir 700/100 mg twice daily."	3.75	Unboosted fosamprenavir is associated with low drug exposure in HIV-infected patients with mild-moderate liver impairment resulting from HCV-related cirrhosis. ( Bonora, S; Carosi, G; de Requena, DG; Gatti, F; Loregian, A; Matti, A; Nasta, P; Pagni, S; Palù, G; Parisi, SG; Prestini, K; Puoti, M, 2009)
"To report successful desensitization to amprenavir after the occurrence of a maculopapular exanthem in an HIV-infected patient with late-stage disease and limited antiretroviral treatment options."	3.73	Amprenavir-induced maculopapular exanthem followed by desensitization in a patient with late-stage human immunodeficiency virus. ( Huynh, P; Kohli-Pamnani, A; Lobo, F, 2006)
" We describe the effect of the coadministration of Amprenavir/Ritonavir (APV/r) and FosAmprenavir (FosAPV) on cyclosporine (CsA) concentrations in two patients receiving OLT for end-stage liver disease due to hepatitis C Virus."	3.73	Pharmacokinetic interaction between Amprenavir/Ritonavir and FosAmprenavir on cyclosporine in two patients with human immunodeficiency virus infection undergoing orthotopic liver transplantation. ( Bonora, S; Cocchi, S; Codeluppi, M; Di Benedetto, F; Esposito, R; Gennari, W; Gerunda, GE; Guaraldi, G; Luzi, K; Masetti, M; Motta, A; Pecorari, M, 2006)
"To examine the clinical significance of HIV protease mutations detected before and after therapy with amprenavir."	3.72	HIV protease mutations associated with amprenavir resistance during salvage therapy: importance of I54M. ( Chou, S; Marousek, GI; Murphy, MD, 2004)
"Amprenavir (APV) is an HIV protease inhibitor (PI) used for the treatment of either naive or PI-experienced HIV-infected patients."	3.72	Resistance profiles observed in virological failures after 24 weeks of amprenavir/ritonavir containing regimen in protease inhibitor experienced patients. ( Affolabi, D; Bossi, P; Bricaire, F; Calvez, V; Costagliola, D; Delaugerre, C; Katlama, C; Ktorza, N; Lamotte, C; Marcelin, AG; Mohand, HA; Peytavin, G; Voujon, D; Wirden, M, 2004)
"The efficacy of an amprenavir (APV)-containing therapy without (group A) or with (group B) ritonavir was assessed in patients with failure of previous protease inhibitor therapy for human immunodeficiency virus (HIV) infection."	3.71	Amprenavir inhibitory quotient and virological response in human immunodeficiency virus-infected patients on an amprenavir-containing salvage regimen without or with ritonavir. ( Clavel, F; Damond, F; Descamps, D; Duval, X; Lamotte, C; Leport, C; Peytavin, G; Race, E; Vilde, JL, 2002)
" Efficacy was defined as HCV RNA below the lower limit of detection 12 weeks after the end of treatment (SVR12), while safety endpoints included the incidence of grade 3 and 4 adverse events (AEs) following treatment, and the proportion of patients who stopped treatment prematurely due to AEs."	2.90	A pilot study of safety and efficacy of HCV retreatment with sofosbuvir/velpatasvir/voxilaprevir in patients with or without HIV (RESOLVE STUDY). ( Chua, J; Comstock, E; Covert, E; Emmanuel, B; Hoffmann, J; Husson, J; Kattakuzhy, S; Kottilil, S; Masur, H; Mathur, P; Price, A; Rosenthal, E; Tang, L; Wilson, E, 2019)
" When combined with the CYP3A4 substrate daclatasvir, the daclatasvir dosage should be reduced from 60 to 30 mg once daily."	2.84	Daclatasvir 30 mg/day is the correct dose for patients taking atazanavir/cobicistat. ( Burger, DM; Colbers, EP; de Kanter, CT; Drenth, JP; Smolders, EJ; Velthoven-Graafland, K, 2017)
" Most common adverse events (AEs) were fatigue, neutropenia, anemia, asthenia and headache."	2.84	Efficacy and safety of daclatasvir plus pegylated-interferon alfa 2a and ribavirin in previously untreated HCV subjects coinfected with HIV and HCV genotype-1: a Phase III, open-label study. ( Ackerman, P; Berenguer, J; Cheinquer, H; Côté, P; Dieterich, D; Eley, T; Fessel, WJ; Gadano, A; Hernandez, D; Hughes, E; Lazzarin, A; Liu, Z; Matthews, G; McPhee, F; Mendez, P; Molina, JM; Moreno, C; Noviello, S; Pineda, JA; Pulido, F; Rivero, A; Rockstroh, J; Sulkowski, MS; Zakharova, N, 2017)
" However, evening atazanavir plus ritonavir and lopinavir/ritonavir regimens are not recommended in combination with the 3D regimen."	2.82	Evaluation of Drug-Drug Interactions Between Hepatitis C Antiviral Agents Ombitasvir, Paritaprevir/Ritonavir, and Dasabuvir and HIV-1 Protease Inhibitors. ( Awni, W; Dutta, S; Khatri, A; Menon, R; Podsadecki, T; Trinh, R; Wang, H, 2016)
" These data indicate that the 3-direct-acting-antiviral regimen can be administered with dolutegravir or abacavir plus lamivudine without dose adjustment."	2.82	Drug-Drug Interaction between the Direct-Acting Antiviral Regimen of Ombitasvir-Paritaprevir-Ritonavir plus Dasabuvir and the HIV Antiretroviral Agent Dolutegravir or Abacavir plus Lamivudine. ( Khatri, A; Menon, R; Podsadecki, T; Trinh, R; Zhao, W, 2016)
"Cobicistat (COBI) is a pharmacoenhancer with no antiretroviral activity."	2.80	Brief Report: Cobicistat Compared With Ritonavir as a Pharmacoenhancer for Atazanavir in Combination With Emtricitabine/Tenofovir Disoproxil Fumarate: Week 144 Results. ( Abram, ME; Andrade-Villanueva, JF; Antunes, F; Arastéh, K; Cao, H; Chetchotisakd, P; DeJesus, E; Fehr, J; Gallant, JE; Koenig, E; Liu, HC; Rizzardini, G; Szwarcberg, J, 2015)
" The most common adverse events were diarrhea, upper respiratory tract infection, gastroenteritis and otitis media."	2.79	Pharmacokinetics, safety and antiviral activity of fosamprenavir/ritonavir-containing regimens in HIV-infected children aged 4 weeks to 2 years-48-week study data. ( Cassim, H; Cheng, K; Cotton, M; Ford, SL; Garges, HP; Givens, N; Lou, Y; Pavía-Ruz, N; Perger, T; Ross, LL; Sievers, J; Wire, MB, 2014)
" The most common adverse events were vomiting, cough, and diarrhea; 18 subjects experienced serious adverse events, including 9 with suspected abacavir hypersensitivity."	2.79	Pharmacokinetics and 48-week safety and antiviral activity of fosamprenavir-containing regimens in HIV-infected 2- to 18-year-old children. ( Cheng, K; Cotton, M; Duiculescu, D; Ford, SL; Fortuny, C; Garges, HP; Givens, N; Lou, Y; Perger, T; Ross, LL; Sievers, J; Tamarirt, DP; Wire, MB, 2014)
" A pediatric population pharmacokinetic model for APV was developed and simulation was used to identify dosing regimens for pediatric patients receiving FPV in combination with ritonavir (RTV) which resulted in concentrations similar to those in adults receiving FPV/RTV 700/100 mg BID."	2.79	Population pharmacokinetic modeling and simulation of amprenavir following fosamprenavir/ritonavir administration for dose optimization in HIV infected pediatric patients. ( Barbour, AM; Gibiansky, L; Wire, MB, 2014)
" Cobicistat (COBI) is a pharmacoenhancer with no antiretroviral activity in vitro."	2.78	Cobicistat versus ritonavir as a pharmacoenhancer of atazanavir plus emtricitabine/tenofovir disoproxil fumarate in treatment-naive HIV type 1-infected patients: week 48 results. ( Andrade-Villanueva, J; Antunes, F; Arastéh, K; Callebaut, C; Cheng, AK; Chetchotisakd, P; DeJesus, E; Fehr, J; Gallant, JE; Koenig, E; Liu, Y; Moyle, G; Rhee, MS; Rizzardini, G; Szwarcberg, J; Zhong, L, 2013)
"The pharmacokinetic data support coadministration of daclatasvir with atazanavir/ritonavir, efavirenz and/or tenofovir."	2.78	Assessment of pharmacokinetic interactions of the HCV NS5A replication complex inhibitor daclatasvir with antiretroviral agents: ritonavir-boosted atazanavir, efavirenz and tenofovir. ( Bertz, R; Bifano, M; Grasela, D; Hartstra, J; Hwang, C; Kandoussi, H; Oosterhuis, B; Sevinsky, H; Tiessen, R; Velinova-Donga, M, 2013)
" Decreases in estimated glomerular filtration rate occurred within the first few weeks of dosing in participants receiving EVG/COBI/FTC/TDF, remained within the normal range and did not progress at week 24 or 48; no participant experienced a clinical adverse event or discontinued study drug due to changes in serum creatinine or renal function."	2.76	Randomized, phase 2 evaluation of two single-tablet regimens elvitegravir/cobicistat/emtricitabine/tenofovir disoproxil fumarate versus efavirenz/emtricitabine/tenofovir disoproxil fumarate for the initial treatment of HIV infection. ( Chuck, SL; Cohen, C; DeJesus, E; Elion, R; Kearney, BP; Liu, HC; Ramanathan, S; Rashbaum, B; Ruane, P; Shamblaw, D; Warren, DR; Yale, K, 2011)
"Objective An open-label, three-period pharmacokinetic study was conducted to investigate the drug interaction potential between fosamprenavir (FPV) and tenofovir disoproxil fumarate (TDF)."	2.75	Steady-state amprenavir and tenofovir pharmacokinetics after coadministration of unboosted or ritonavir-boosted fosamprenavir with tenofovir disoproxil fumarate in healthy volunteers. ( Andrews, M; Condoluci, DV; Luber, AD; Olson, K; Pakes, GE; Pappa, KA; Peloquin, CA; Slowinski, PD, 2010)
" Healthy volunteer studies have demonstrated a decrease in glucose disposal associated with dosing with specific antiretrovirals."	2.75	Effect of boosted fosamprenavir or lopinavir-based combinations on whole-body insulin sensitivity and lipids in treatment-naive HIV-type-1-positive men. ( Back, DJ; Boffito, M; Jackson, AG; Mandalia, S; Moyle, GJ; Randell, PA; Taylor, J; Tjia, JF, 2010)
" Adverse events (AEs) associated with the study medication occurred in 21% of patients."	2.74	Fosamprenavir (GW433908)/ritonavir in HIV-infected patients: efficacy and safety results from the Spanish Expanded Access Program. ( Luque, I; Mallolas, J; Pérez-Elias, MJ; Rodríguez-Alcántara, F; Sánchez-Conde, M; Soriano, V, 2009)
" Four patients discontinued treatment for adverse events, all before week 4."	2.74	Efficacy and safety of ritonavir-boosted dual protease inhibitor therapy in antiretroviral-naive HIV-1-infected patients: the 2IP ANRS 127 study. ( Aboulker, JP; Bentata, M; Brun-Vézinet, F; Capitant, C; Chazallon, C; Descamps, D; Katlama, C; Landman, R; Peytavin, G; Pialoux, G; Yéni, P, 2009)
" For subjects with mild hepatic impairment, the studied regimen of fosamprenavir 700 mg twice daily plus ritonavir 100 mg once daily delivered 17% higher values for the maximum plasma amprenavir concentration at the steady state (C(max)), 22% higher values for the area under the plasma concentration versus time curve over the dosing interval at the steady state [AUC(0-tau)], similar values for the concentration at the end of the dosing interval (C(tau)), and 114% higher unbound C(tau) values."	2.74	Pharmacokinetics of fosamprenavir plus ritonavir in human immunodeficiency virus type 1-infected adult subjects with hepatic impairment. ( Clotet, B; Felizarta, F; Gutiérrez, F; Hernández-Quero, J; Lou, Y; Morellon, ML; Nichols, G; Ortega, E; Pérez-Elías, MJ; Pineda, JA; Rodríguez-Torres, M; Wire, MB, 2009)
" This randomized, two 14-day-period, crossover pharmacokinetic study compared the steady-state plasma APV concentrations, safety, and tolerability of FPV at 1,400 mg QD boosted with either 100 mg or 200 mg of RTV QD in 36 healthy volunteers."	2.73	Plasma amprenavir pharmacokinetics and tolerability following administration of 1,400 milligrams of fosamprenavir once daily in combination with either 100 or 200 milligrams of ritonavir in healthy volunteers. ( Lancaster, CT; Lou, Y; Luber, AD; Pappa, KA; Ruane, PJ; Shelton, MJ; Wire, MB, 2007)
"Brecanavir (BCV) is a novel, potent protease inhibitor in development for the treatment of human immunodeficiency virus (HIV-1) infection with low nM in vitro 50% inhibitory concentrations (IC50s) against many multiprotease inhibitor resistant viruses."	2.73	Safety and pharmacokinetics of brecanavir, a novel human immunodeficiency virus type 1 protease inhibitor, following repeat administration with and without ritonavir in healthy adult subjects. ( Anderson, MT; Ford, SL; Johnson, MA; Murray, SC; Ng-Cashin, J; Reddy, YS, 2007)
"Brecanavir/ritonavir was well tolerated with no serious adverse events or clinically concerning changes in laboratory parameters."	2.73	Preliminary safety and efficacy data of brecanavir, a novel HIV-1 protease inhibitor: 24 week data from study HPR10006. ( Garges, HP; Lalezari, JP; Tomkins, SA; Ward, DJ, 2007)
" Coadministration of these drugs might result in complex pharmacokinetic drug-drug interactions."	2.73	Amprenavir and lopinavir pharmacokinetics following coadministration of amprenavir or fosamprenavir with lopinavir/ritonavir, with or without efavirenz. ( Barditch-Crovo, P; Carson, KA; Flexner, C; Hendrix, CW; Khan, W; Pakes, GE; Parish, M; Parsons, T; Pham, PA; Qaqish, R; Radebaugh, C, 2007)
"Lopinavir-ritonavir is a preferred protease inhibitor co-formulation for initial HIV-1 treatment."	2.72	The KLEAN study of fosamprenavir-ritonavir versus lopinavir-ritonavir, each in combination with abacavir-lamivudine, for initial treatment of HIV infection over 48 weeks: a randomised non-inferiority trial. ( DeJesus, E; Eron, J; Estrada, V; Gathe, J; Katlama, C; Lackey, P; Patel, L; Shaefer, M; Staszewski, S; Sutherland-Phillips, D; Vavro, C; Wannamaker, P; Yau, L; Yeni, P; Yeo, J; Young, B, 2006)
"When amprenavir-ritonavir was coadministered with efavirenz, amprenavir-ritonavir maintained a mean amprenavir C(min,ss) above the mean 50% inhibitory concentration of amprenavir previously determined for both wild-type HIV-1 isolates and HIV-1 strains isolated from PI-experienced patients."	2.71	Steady-state pharmacokinetics of amprenavir coadministered with ritonavir in human immunodeficiency virus type 1-infected patients. ( Bidault, R; Bollens, D; Choudet, N; Demarles, D; Gillotin, C; Goujard, C; Meynard, JL; Rousseau, C; Taburet, AM; Vincent, I, 2003)
"ESS40011 was a 24-week, multicenter, open-label, clinical trial in which antiretroviral therapy-naïve and -experienced HIV-1-infected adults were randomized 3:1 to receive either APV600/RTV BID or APV1200 BID, in combination with > or = 2 non-protease inhibitor antiretroviral drugs."	2.71	Twice-daily amprenavir 1200 mg versus amprenavir 600 mg/ritonavir 100 mg, in combination with at least 2 other antiretroviral drugs, in HIV-1-infected patients. ( Gathe, JC; Griffith, S; Hernandez, JE; Lancaster, CT; Liao, Q; Nadler, JP; Pappa, KA; Pollard, RB; Richmond, GJ, 2003)
"Enfuvirtide is a novel antiretroviral that blocks HIV-1 cell fusion and viral entry."	2.71	A controlled Phase II trial assessing three doses of enfuvirtide (T-20) in combination with abacavir, amprenavir, ritonavir and efavirenz in non-nucleoside reverse transcriptase inhibitor-naive HIV-infected adults. ( Becker, S; Carlson, M; DeJesus, E; Delehanty, J; DeMasi, R; Haas, FF; Haubrich, R; Henry, D; Lalezari, JP; Northfelt, DW; Powderly, W; Richmond, G; Riddler, S; Salgo, M; Sista, PR; Thompson, M; Valentine, F; Wolfe, P; Wright, D, 2003)
" Compared with amprenavir 1,200 mg BID, both GW433908 1,395 mg BID and GW433908 1,860 mg BID delivered equivalent steady-state (ss) values for area under the plasma amprenavir concentration-time curve (AUC) at the end of a dosing interval (tau), lower maximum plasma amprenavir concentrations (30% lower), and higher plasma amprenavir concentrations at the end of a dosing interval (28% higher for GW433908 1,395 mg BID and 46% higher for GW433908 1,860 mg BID)."	2.71	Six-week randomized controlled trial to compare the tolerabilities, pharmacokinetics, and antiviral activities of GW433908 and amprenavir in human immunodeficiency virus type 1-infected patients. ( Arasteh, K; Eron, J; Millard, J; Naderer, OJ; Pollard, RB; Raffi, F; Stellbrink, HJ; Teofilo, E; Wire, MB; Wood, R; Yeo, J, 2004)
" 5%), was the only drug-related grade 2-4 adverse event with a significant difference (P = 0."	2.71	The NEAT study: a 48-week open-label study to compare the antiviral efficacy and safety of GW433908 versus nelfinavir in antiretroviral therapy-naive HIV-1-infected patients. ( Boghossian, J; Gray, GE; Millard, JM; Nadler, JP; Quinones, AR; Rodriguez-French, A; Sepulveda, GE; Wannamaker, PG, 2004)
" Patients receiving the same doses of lopinavir/ritonavir (n = 10) or amprenavir with ritonavir (n = 8) were chosen as controls for pharmacokinetic analyses."	2.71	Deep salvage with amprenavir and lopinavir/ritonavir: correlation of pharmacokinetics and drug resistance with pharmacodynamics. ( Baldini, F; Cauda, R; Cingolani, A; De Luca, A; Di Giambenedetto, S; Hoetelmans, RM, 2004)
" After 12-hour pharmacokinetic sampling, the third protease inhibitor (PI) was added, and pharmacokinetics sampling was repeated 14 days later."	2.71	The pharmacokinetics, safety, and initial virologic response of a triple-protease inhibitor salvage regimen containing amprenavir, saquinavir, and ritonavir. ( Corbett, AH; Eron, JJ; Fiscus, SA; Kashuba, AD; Rezk, NL, 2004)
"Amprenavir (APV) has been shown to be effective in naive or treatment-experienced HIV-1 infected patients."	2.71	Efficacy, safety and predictive factors of virological success of a boosted amprenavir-based salvage regimen in heavily antiretroviral-experienced HIV-1-infected patients. ( Boulmé, R; Clevenbergh, P; Dellamonica, P; Kirstetter, M, 2004)
"No methadone dosage was changed in any subject."	2.71	Pharmacokinetics and pharmacodynamics of methadone enantiomers after coadministration with amprenavir in opioid-dependent subjects. ( Bigelow, GE; Christopher, J; Fuchs, EJ; Hendrix, CW; Lou, Y; Martinez, E; Snidow, JW; Wakeford, J; Wire, MB, 2004)
" In this pharmacokinetic and pharmacodynamic analysis, the relationship of drug exposure, demographics, and cotherapy measures to antiviral response in a cohort of largely treatment-experienced children treated with amprenavir and nucleoside reverse transcriptase inhibitors was examined."	2.71	Pharmacokinetic and pharmacodynamic analysis of amprenavir-containing combination therapy in HIV-1-infected children. ( Blanche, S; Johnson, M; Lou, Y; Randall, S; Stein, DS, 2004)
"Amprenavir was rapidly absorbed, with a mean time to maximum concentration (T(max)) occurring 0."	2.71	Single-dose safety and pharmacokinetics of amprenavir (141W94), a human immunodeficiency virus type 1 (HIV-1) protease inhibitor, in HIV-infected children. ( Chadwick, EG; Homans, JD; Kovacs, A; Lou, Y; Symonds, WT; Yogev, R, 2005)
"Ritonavir exposure was not significantly different between arms."	2.71	Combining fosamprenavir with lopinavir/ritonavir substantially reduces amprenavir and lopinavir exposure: ACTG protocol A5143 results. ( Acosta, EP; Collier, AC; Downey, GF; Eshleman, SH; Kashuba, AD; Klingman, K; Mellors, JW; Scott, TR; Tierney, C; Vergis, EN, 2005)
" APV SP concentrations were consistently lower than BP concentrations, ZDV SP concentrations approximated BP concentrations early but became greater later in the dosing interval, and 3TC SP concentrations were substantially greater than BP concentrations throughout."	2.70	The pharmacokinetics of amprenavir, zidovudine, and lamivudine in the genital tracts of men infected with human immunodeficiency virus type 1 (AIDS clinical trials group study 850). ( Acosta, EP; Eron, JJ; Fiscus, SA; Gerber, JG; Gulick, RM; Murphy, RL; Pereira, AS; Smeaton, LM; Snyder, S; Tidwell, RR, 2002)
" Drug-related treatment-emergent adverse events reported in >3% of patients in the safety population were nausea in 279 patients (12."	2.70	Safety profile and tolerability of amprenavir in patients enrolled in an early access program. ( Garrett, L; Garris, C; Graham, N; Pedneault, L; Rogers, M; Scott, T, 2001)
" Patients were randomized to 800-mg APV combined with 800-mg indinavir (IDV), 750-mg nelfinavir (NFV), or 800-mg saquinavir-soft gel capsule (SGV-SGC), all three times daily without nucleoside reverse transcriptase inhibitors, or APV given alone for 3 weeks and then with 150-mg lamivudine (3TC) and 300-mg zidovudine (ZDV), twice daily."	2.70	A phase II trial of dual protease inhibitor therapy: amprenavir in combination with indinavir, nelfinavir, or saquinavir. ( Eron, JJ; Haubrich, R; Lang, W; Millard, J; Pagano, G; Pedneault, L; Snowden, W; Tisdale, M; Wolfram, J, 2001)
"Amprenavir was reasonably well tolerated with few treatment-limiting adverse events."	2.70	A dose-ranging study to evaluate the antiretroviral activity and safety of amprenavir alone and in combination with abacavir in HIV-infected adults with limited antiretroviral experience. ( Antunes, F; Blake, D; Clumeck, N; Danner, SA; Haubrich, R; Millard, J; Mustafa, N; Myers, RE; Nacci, P; Schooley, RT; Sereni, D; Thompson, M; Tisdale, M; van Der Ende, ME, 2001)
"Treatment with amprenavir, zidovudine, and lamivudine together reduced the levels of HIV RNA significantly more than did amprenavir monotherapy."	2.69	Treatment with amprenavir alone or amprenavir with zidovudine and lamivudine in adults with human immunodeficiency virus infection. AIDS Clinical Trials Group 347 Study Team. ( Caliendo, AM; Currier, JS; D'Aquila, RT; DeGruttola, V; Eron, JJ; Frank, I; Gerber, JG; Gulick, RM; Kuritzkes, DR; Murphy, RL; Smeaton, L; Sommadossi, JP; Tung, R, 1999)
"Amprenavir was rapidly absorbed, with the time to maximum concentration occurring within 1 to 2 h after dosing."	2.69	Safety and pharmacokinetics of amprenavir (141W94), a human immunodeficiency virus (HIV) type 1 protease inhibitor, following oral administration of single doses to HIV-infected adults. ( Chittick, GE; Hanson, CD; Roskell, NS; Sadler, BM; Symonds, WT, 1999)
" The most common adverse events considered to be possibly drug related were nausea, rash, oral paresthesia, diarrhea, and fatigue."	2.69	A phase II safety and efficacy study of amprenavir in combination with zidovudine and lamivudine in HIV-infected patients with limited antiretroviral experience. Amprenavir PROAB2002 Study Team. ( Antunes, F; Brown, DJ; Clumeck, N; Fetter, A; Haubrich, R; Kahl, L; Lang, W; Pagano, G; Richman, D; Schooley, R; Sereni, D; Stein, A; Thompson, M; van der Ende, ME, 1999)
"Amprenavir levels were measured before and after adding efavirenz."	2.69	Combination therapy with amprenavir, abacavir, and efavirenz in human immunodeficiency virus (HIV)-infected patients failing a protease-inhibitor regimen: pharmacokinetic drug interactions and antiviral activity. ( Falloon, J; Kavlick, MF; LaFon, S; Lane, HC; Manion, DJ; Masur, H; Mitsuya, H; Piscitelli, S; Rogers, M; Sadler, B; Vogel, S; Yoshimura, K, 2000)
"Amprenavir was safe and generally well tolerated."	2.69	Amprenavir in combination with lamivudine and zidovudine versus lamivudine and zidovudine alone in HIV-1-infected antiretroviral-naive adults. Amprenavir PROAB3001 International Study Team. ( Brothers, CH; Feinberg, J; Fischl, M; Goodgame, JC; Hardy, WD; Jablonowski, H; Morrow, P; Nacci, P; Pedneault, L; Pottage, JC; Stein, A; Vafidis, I; Yeo, J, 2000)
"Amprenavir (APV) is a new HIV-I protease inhibitor used in combination with other antiretroviral agents for the treatment of HIV-1 infection."	2.69	Safety profile and tolerability of amprenavir in the treatment of adult and pediatric patients with HIV infection. ( Brothers, C; Fetter, A; Millard, J; Pagano, G; Pedneault, L; Tymkewycz, P; Yeo, J, 2000)
" All the studies that reported the sustained virologic response (SVR) and adverse events of DAAs in HIV/HCV co-infected patients were included."	2.66	Efficacy and safety of direct acting antiviral regimens for hepatitis C virus and human immunodeficiency virus co-infection: systematic review and network meta-analysis. ( Fan, XG; Ma, SJ; Xiong, YH; Zheng, YX, 2020)
" The safety data available for LDV/SOF±RBV and OBV/PTV/r±DSV±RBV show that discontinuation due to adverse events was necessary in no more than 3% of patients and the frequency of serious adverse events was between 0 and 11%, in particular in real-world studies."	2.55	Hepatitis C: efficacy and safety in real life. ( Flisiak, R; Flisiak-Jackiewicz, M; Pogorzelska, J, 2017)
" As a fixed-dose combination tablet given once daily, EFV/FTC/TDF was the first available STR combining efficacy, tolerability and convenience, with the simplest dosing schedule and smallest numbers of pills of any ART combination therapy."	2.50	Single-tablet regimens in HIV: does it really make a difference? ( Aldir, I; Horta, A; Serrado, M, 2014)
"Cobicistat has a lower potential for off-target drug interactions than the standard boosting agent ritonavir, due to its more selective inhibition of CYP3A and lower likelihood for enzymatic induction, and is devoid of anti-HIV activity."	2.50	Cobicistat: a review of its use as a pharmacokinetic enhancer of atazanavir and darunavir in patients with HIV-1 infection. ( Deeks, ED, 2014)
" Finally, observed/predicted drug-drug interactions between antiretrovirals and antifungals are summarized along with clinical recommendations."	2.50	Clinically relevant drug-drug interactions between antiretrovirals and antifungals. ( Mitra, AK; Pal, D; Patel, M; Paturi, DK; Vadlapatla, RK, 2014)
"Cobicistat is a new pharmacokinetic booster that is a selective inhibitor of cytochrome P450 3A, the main metabolizing pathway of several antiretrovirals."	2.49	Cobicistat: a new boost for the treatment of human immunodeficiency virus infection. ( Priano, J; Schafer, JJ; Shah, BM; Squires, KE, 2013)
" This therapeutic principle called 'boosting' helped to overcome the obstacles of this class of drugs concerning unfavorable pharmacokinetics, resulting in either a high frequency of dosing or subtherapeutic plasma concentrations."	2.48	Safety of pharmacoenhancers for HIV therapy. ( Haberl, A; von Hentig, N, 2012)
"Fosamprenavir is a protease inhibitor (PI) approved for the treatment of HIV-1 infection."	2.44	Fosamprenavir calcium plus ritonavir for HIV infection. ( Arduino, RC; Torres, HA, 2007)
"Amprenavir is an HIV-1 protease inhibitor, the first in vitro activity studies of which were published in 1995."	2.43	Amprenavir or fosamprenavir plus ritonavir in HIV infection: pharmacology, efficacy and tolerability profile. ( Arvieux, C; Tribut, O, 2005)
"Amprenavir has a large volume of distribution, is 90% bound to plasma proteins and is a substrate of P-glycoprotein."	2.43	Fosamprenavir : clinical pharmacokinetics and drug interactions of the amprenavir prodrug. ( Shelton, MJ; Studenberg, S; Wire, MB, 2006)
" However, early HAART often consisted of drugs with complex dosing schedules, strict food requirements, treatment-limiting adverse effects, and the need to take 16-20 pills/day."	2.43	An update and review of antiretroviral therapy. ( Piacenti, FJ, 2006)
" This agent combines the pharmacological profile of amprenavir with a low pill burden and flexible dosing schedule."	2.42	Fosamprenavir: advancing HIV protease inhibitor treatment options. ( Becker, S; Thornton, L, 2004)
"Fosamprenavir was generally well tolerated in clinical trials."	2.42	Fosamprenavir: a review of its use in the management of antiretroviral therapy-naive patients with HIV infection. ( Chapman, TM; Perry, CM; Plosker, GL, 2004)
"Fosamprenavir is a recently licensed protease inhibitor (PI) for the treatment of patients with HIV."	2.42	Pharmacokinetics of Telzir (fosamprenavir). ( Wilkins, E, 2004)
" Trial designs include comparisons between the various licensed protease inhibitors, comparisons of protease inhibitors to other classes of potent antiretroviral drugs, investigations with new protease inhibitors, investigations of protease inhibitor-related toxicities and attempts at simplifying current dosing regimens."	2.41	Ongoing trials in HIV protease inhibitors. ( Tavel, JA, 2000)
"Amprenavir was as effective as other protease inhibitors when given with abacavir in a small nonblind trial."	2.41	Amprenavir: a review of its clinical potential in patients with HIV infection. ( Goa, KL; Noble, S, 2000)
"Amprenavir is a novel protease inhibitor with antiviral activity, and was approved in the U."	2.41	[Pharmacological study and clinical effect of HIV protease inhibitor amprenavir]. ( Ishizawa, M; Komatsu, H, 2001)
"Amprenavir has an enzyme inhibition constant (Ki = 0."	2.41	Clinical pharmacology and pharmacokinetics of amprenavir. ( Sadler, BM; Stein, DS, 2002)
"Amprenavir is a viral protease inhibitor with specificity for the HIV protease enzyme."	2.40	Amprenavir. ( Adkins, JC; Faulds, D, 1998)
"Amprenavir is a new peptidomimetic inhibitor of the HIV protease enzyme."	2.40	Coming therapies: amprenavir. ( Gatell, J, 1999)
" The secondary outcome measures were SVR12 stratified by the presence of decompensated cirrhosis, prior treatment, HCC, and HIV/hepatitis C virus coinfection and the occurrence rate of serious adverse events requiring treatment cessation or hospitalization."	1.62	Efficacy and safety of sofosbuvir/velpatasvir in a real-world chronic hepatitis C genotype 3 cohort. ( Ang, TL; Fock, KM; Koh, J; Kumar, LS; Kumar, R; Kwek, A; Law, NM; Lee, ZC; Li, W; Tan, J; Tan, YB; Teo, EK; Thurairajah, PH; Wong, YJ, 2021)
" Incidence rates of liver adverse events (LAE) were calculated; Poisson regression model was used to identify factors associated with LAE."	1.56	Safety and efficacy of daclatasvir at doses other than 60 mg daily in HIV/HCV co-infected subjects: Data from the ICONA/HepaICONA foundation cohorts. ( Bonora, S; Cingolani, A; d'Arminio Monforte, A; Lo Caputo, S; Marinaro, L; Mussini, C; Puoti, M; Rossotti, R; Saracino, A; Soria, A; Tavelli, A; Uberti-Foppa, C, 2020)
"7%): 4 due to severe adverse events (including 3 deaths) and 1 patient´s decision."	1.51	Effectiveness, safety/tolerability of OBV/PTV/r ± DSV in patients with HCV genotype 1 or 4 with/without HIV-1 co-infection, chronic kidney disease (CKD) stage IIIb-V and dialysis in Spanish clinical practice - Vie-KinD study. ( Ahumada, A; Aldamiz-Echevarría, T; Baliellas, C; Barril, G; Benlloch, S; Bonet, L; Carmona, I; Castaño, MA; Castro, Á; de Álvaro, C; de Los Santos, I; Delgado, M; Devesa-Medina, MJ; García-Buey, L; García-Samaniego, J; Gea-Rodríguez, F; González-Parra, E; Gutiérrez, ML; Jiménez-Pérez, M; Laguno, M; Londoño, MC; Losa, JE; Mallolas, J; Manzanares, A; Martín-Granizo, I; Montero-Alonso, M; Montes, ML; Morán-Sánchez, S; Morano, L; Muñoz-Gómez, R; Navascués, CA; Polo-Lorduy, B; Riveiro-Barciela, M; Rivero, A; Roget, M; Serra, MÁ, 2019)
" Serious adverse events occurred in 3."	1.48	The safety and efficacy of elbasvir and grazoprevir in participants with hepatitis C virus genotype 1b infection. ( Barr, E; Cheng, W; George, J; Hwang, P; Kumada, H; Platt, H; Robertson, M; Serfaty, L; Sperl, J; Strasser, S; Talwani, R; Vierling, J; Wahl, J; Zeuzem, S, 2018)
"Local delivery of anti-HIV drugs to the colorectal mucosa, a major site of HIV replication, and their retention within mucosal tissue would allow for a reduction in dose administered, reduced dosing frequency and minimal systemic exposure."	1.43	Colorectal delivery and retention of PEG-Amprenavir-Bac7 nanoconjugates--proof of concept for HIV mucosal pre-exposure prophylaxis. ( Ganapathi, U; Gunaseelan, S; Myers, DR; Nelson, AG; Palombo, MS; Samizadeh, M; Singh, Y; Sinko, PJ; Szekely, Z; Zhang, X, 2016)
" No discontinuations were attributed to treatment-related adverse events."	1.43	12 Weeks of Daclatasvir in Combination With Sofosbuvir for HIV-HCV Coinfection (ALLY-2 Study): Efficacy and Safety by HIV Combination Antiretroviral Regimens. ( Ackerman, P; Bhore, R; Luetkemeyer, AF; McDonald, C; Noviello, S; Ramgopal, M, 2016)
"DCV was dosed at week 4 and at week 8 of treatment, and RBV at week 8."	1.43	Daclatasvir plasma level and resistance selection in HIV patients with hepatitis C virus cirrhosis treated with daclatasvir, sofosbuvir, and ribavirin. ( Andreis, S; Basso, M; Cattelan, AM; Cavinato, S; Dal Bello, F; Loregian, A; Messa, L; Nannetti, G; Palù, G; Parisi, SG; Scaggiante, R, 2016)
"HRQoL/fatigue was evaluated at baseline (BL), midway, and 12 weeks after the end of treatment (FU)."	1.43	Interferon-free regimens improve health-related quality of life and fatigue in HIV/HCV-coinfected patients with advanced liver disease: A retrospective study. ( Aichelburg, MC; Bucsics, T; Chromy, D; Grabmeier-Pfistershammer, K; Mandorfer, M; Peck-Radosavljevic, M; Reiberger, T; Scheiner, B; Schwabl, P; Steiner, S; Trauner, M, 2016)
" Raltegravir pharmacokinetic parameters remained unchanged whether administered on or off anti-HCV therapy."	1.42	Raltegravir Pharmacokinetics in Patients on Asunaprevir-Daclatasvir. ( Barrail-Tran, A; Cheret, A; Furlan, V; Molina, JM; Piroth, L; Rosa, I; Rosenthal, E; Taburet, AM; Vincent, C, 2015)
" Adverse events (clinical events and absolute neutrophil counts, total cholesterol and triglycerides, and alanine transaminase) were summarised and DAIDS gradings characterised severity."	1.40	Post-licensing safety of fosamprenavir in HIV-infected children in Europe. ( Duong, T; Ene, L; Galli, L; Giaquinto, C; Goetghebuer, T; Judd, A; Noguera Julian, A; Pimenta, JM; Ramos Amador, JT; Thorne, C, 2014)
"We performed a within-subject open-labeled pharmacokinetic and pharmacodynamic study in 17 HIV-seronegative subjects stabilized on at least 2 weeks of buprenorphine/naloxone therapy."	1.39	The pharmacokinetic and pharmacodynamic interactions between buprenorphine/naloxone and elvitegravir/cobicistat in subjects receiving chronic buprenorphine/naloxone treatment. ( Bruce, RD; Custodio, JM; Friedland, GH; Kearney, BP; Ramanathan, S; Rhee, MS; Wei, LX; Winkle, P, 2013)
"Cobicistat is a novel cytochrome P450 3A4 (CYP3A4) inhibitor in advanced clinical evaluation for use as a pharmacoenhancer of antiretroviral drugs."	1.39	Cobicistat, a pharmacoenhancer for HIV treatments. ( Temesgen, Z, 2013)
" After adjusting for age, gender, HIV risk factor, current CD4 count, pill burden and dosing interval, adherence was higher in patients with undetectable HIV RNA (P < 0."	1.39	Number of daily pills, dosing schedule, self-reported adherence and health status in 2010: a large cross-sectional study of HIV-infected patients on antiretroviral therapy. ( Bocchiola, B; Cahua, T; Castagna, A; Danise, A; Galli, L; Gianotti, N; Lazzarin, A; Maillard, M; Panzini, P; Pazzi, A; Salpietro, S; Zandonà, D, 2013)
"Amprenavir (APV) is a high affinity (0."	1.38	Energetic basis for drug resistance of HIV-1 protease mutants against amprenavir. ( Kar, P; Knecht, V, 2012)
"During the study no serious adverse events were reported."	1.38	Efficacy and safety of a dual boosted protease inhibitor-based regimen, atazanavir and fosamprenavir/ritonavir, against HIV: experience in a pediatric population. ( Adorni, F; Galli, M; Giacomet, V; Mameli, C; Rusconi, S; Viganò, A; Viganò, O; Zuccotti, GV, 2012)
"Treatment with lopinavir and ritonavir, but not amprenavir, induced ER stress, as indicated by a decrease in secreted alkaline phosphatase activities and an increase in the unfolded protein response."	1.36	HIV protease inhibitors induce endoplasmic reticulum stress and disrupt barrier integrity in intestinal epithelial cells. ( Chen, J; Chen, L; Gurley, E; Hylemon, PB; Pandak, WM; Sanyal, AJ; Studer, E; Sun, L; Wang, G; Wang, JY; Wang, X; Wu, X; Zha, W; Zhang, L; Zhou, H, 2010)
"01), so that a marked dosage increase was needed (0."	1.35	Drop in trough blood concentrations of tacrolimus after switching from nelfinavir to fosamprenavir in four HIV-infected liver transplant patients. ( Adani, GL; Bresadola, V; Furlanut, M; Londero, A; Pavan, F; Pea, F; Tavio, M; Viale, P, 2008)
"The influence of nevirapine or efavirenz co-administration on ritonavir-boosted amprenavir pharmacokinetics was investigated in HIV-infected patients with a population pharmacokinetic approach."	1.35	Impact of nevirapine or efavirenz co-administration on ritonavir-boosted amprenavir pharmacokinetics in HIV-infected patients. ( Allavena, C; Biron, C; Dailly, E; Jolliet, P; Raffi, F, 2008)
" The impact of baseline HIV type 1 (HIV-1) mutations, pharmacokinetic (PK) parameters, and genotype inhibitory quotient (GIQ) on the virological response at week 12 (W12) was assessed."	1.34	Interpretation of genotype and pharmacokinetics for resistance to fosamprenavir-ritonavir-based regimens in antiretroviral-experienced patients. ( Boucher, S; Breilh, D; Coureau, G; Dabis, F; Fleury, H; Lacoste, D; Lazaro, E; Merel, P; Neau, D; Pellegrin, I; Pellegrin, JL; Saux, MC; Thiébaut, R, 2007)
"A prospective, open-label, single-site, two-period, crossover pharmacokinetic study was carried out in healthy volunteers."	1.34	Steady-state pharmacokinetics of once-daily fosamprenavir/ritonavir and atazanavir/ritonavir alone and in combination with 20 mg omeprazole in healthy volunteers. ( Brower, R; Frank, I; Kim, D; Luber, AD; Peloquin, CA; Silverman, R, 2007)
"The aim of this pilot study was to examine the pharmacokinetics of atazanavir (ATV) when given in combination with amprenavir (APV) or saquinavir hard-gel capsules (SQV) to human immunodeficiency virus (HIV)-positive patients."	1.33	Steady-state pharmacokinetics of atazanavir given alone or in combination with saquinavir hard-gel capsules or amprenavir in HIV-1-infected patients. ( Castagna, A; Cusato, M; Fusetti, G; Galli, A; Gianotti, N; Guffanti, M; Lazzarin, A; Regazzi, M; Seminari, E; Villani, P, 2005)
" We describe a 65-year-old man with HIV who underwent a 12-hour intensive pharmacokinetic study while receiving esomeprazole with atazanavir-ritonavir and subsequently, an 8-hour study while receiving esomeprazole with fosamprenavir-ritonavir."	1.33	Effects of esomeprazole on the pharmacokinetics of atazanavir and fosamprenavir in a patient with human immunodeficiency virus infection. ( Anderson, PL; Fletcher, CV; Kiser, JJ; Lichtenstein, KA, 2006)
"Fosamprenavir 700 mg bid was then added to the regimen, and pharmacokinetic sampling was repeated for all 3 agents at day 11."	1.32	Steady-State pharmacokinetics of saquinavir hard-gel/ritonavir/fosamprenavir in HIV-1-infected patients. ( Back, D; Boffito, M; Dickinson, L; Fletcher, C; Gazzard, B; Higgs, C; Hill, A; Moyle, G; Nelson, M; Pozniak, A, 2004)
"Amprenavir-based therapy was associated with increases in serum lipid levels but no short-term decrease in insulin sensitivity."	1.31	Prospective, intensive study of metabolic changes associated with 48 weeks of amprenavir-based antiretroviral therapy. ( Buchanan, TA; Dubé, MP; Edmondson-Melançon, H; Goodwin, D; Johnson, D; Martinez, C; Qian, D; Sattler, FR; Williams, V, 2002)
"Amprenavir thus appears to be an interesting alternative for PI salvage therapy."	1.31	Low level of cross-resistance to amprenavir (141W94) in samples from patients pretreated with other protease inhibitors. ( Korn, K; Moschik, B; Paatz, C; Schmidt, B; Uberla, K; Walter, H, 2000)
"Lipodystrophy is the term given to describe a series of changes in body composition [loss of fat in the legs, arms, or face, breast enlargement, central obesity (sometimes called protease paunch), dorsal fat pads (known as buffalo hump, etc."	1.31	Lipodystrophy update. ( , 2002)
"Fosamprenavir was first synthesized at Vertex as part of a collaboration with Glaxo Wellcome and by 1999, it was being developed by Glaxo Wellcome as part of an ongoing agreement between the two companies."	1.31	Fosamprenavir. Vertex Pharmaceuticals/GlaxoSmithKline. ( Corbett, AH; Kashuba, AD, 2002)
" Ziagen appears to have significant antiviral activity, and its dosage is one pill twice a day."	1.30	Glaxo Wellcome's two new drugs. ( , 1998)
" A clinical trial of the protease inhibitor Nelfinavir (Viracept) has shown that dosing twice a day may be as effective as the currently prescribed three times a day."	1.30	Antimicrobial agents and chemotherapy: highlights of the 38th Interscience Conference. ( Prescott, LM, 1998)
" Several studies of regimens that include protease inhibitors compare dosing twice daily to three times a day."	1.30	Antivirals update. ( , 1998)
"Amprenavir has been given "fast track" status by the U."	1.30	Amprenavir: a new protease inhibitor nears approval. ( Highleyman, L, 1999)
" Each drug trial demonstrates the relationship between dosing and resistance; patients are advised to adhere completely to dosing instructions."	1.29	Protease inhibitors and prevention of cross resistance. ( Levin, J, 1995)

Research

Studies (418)

Authors

Clinical Trials (51)

Trial Overview

Trial Outcomes

Number of Participants Who Experienced HIV-1 Virologic Failure (VF)

Timeframe	Studies, this research(%)	All Research%
pre-1990	0 (0.00)	18.7374
1990's	60 (14.35)	18.2507
2000's	187 (44.74)	29.6817
2010's	157 (37.56)	24.3611
2020's	14 (3.35)	2.80

Authors	Studies
Mastrorosa, I	2
Tempestilli, M	3
Notari, S	3
Lorenzini, P	1
Fabbri, G	3
Grilli, E	1
Bellagamba, R	2
Vergori, A	1
Cicalini, S	1
Ammassari, A	3
Agrati, C	3
Antinori, A	3
Martinec, O	1
Huliciak, M	1
Staud, F	1
Cecka, F	1
Vokral, I	1
Cerveny, L	1
Merli, M	1
Rossotti, R	2
Travi, G	1
Ferla, F	1
Lauterio, A	1
Angelini Zucchetti, T	1
Alcantarini, C	1
Bargiacchi, O	1
De Carlis, L	1
Puoti, M	3
Londoño, MC	1
Riveiro-Barciela, M	1
Ahumada, A	1
Muñoz-Gómez, R	1
Roget, M	1
Devesa-Medina, MJ	1
Serra, MÁ	1
Navascués, CA	1
Baliellas, C	1
Aldamiz-Echevarría, T	2
Gutiérrez, ML	1
Polo-Lorduy, B	2
Carmona, I	1
Benlloch, S	1
Bonet, L	1
García-Samaniego, J	1
Jiménez-Pérez, M	1
Morán-Sánchez, S	2
Castro, Á	1
Delgado, M	3
Gea-Rodríguez, F	1
Martín-Granizo, I	2
Montes, ML	1
Morano, L	2
Castaño, MA	1
de Los Santos, I	2
Laguno, M	2
Losa, JE	1
Montero-Alonso, M	1
Rivero, A	4
de Álvaro, C	1
Manzanares, A	2
Mallolas, J	6
Barril, G	1
González-Parra, E	1
García-Buey, L	2
Mandimika, C	2
Ogbuagu, O	2
Manuel Sousa, J	1
Vergara, M	1
Pulido, F	3
Sánchez Antolín, G	1
Hijona, L	1
Carnicer, F	1
Rincón, D	1
Salmerón, J	1
Mateos-Muñoz, B	1
Jou, A	1
Rubín, Á	1
Escarda, A	1
Aguilar, P	1
Carrión, JA	1
Hernández-Guerra, M	1
Chimeno-Hernández, S	1
Espinosa, N	1
Morillas, RM	1
Andrade, RJ	1
Gallego, A	1
Magaz, M	1
Moreno-Planas, JM	1
Estébanez, Á	1
Rico, M	1
Menéndez, F	1
Sampedro, B	1
Izquierdo, S	1
Zozaya, JM	1
Rodríguez, M	1
Lorente, S	1
Von-Wichmann, MÁ	1
Zarębska-Michaluk, D	1
Jaroszewicz, J	1
Buczyńska, I	1
Simon, K	1
Lorenc, B	1
Tudrujek-Zdunek, M	1
Tomasiewicz, K	1
Sitko, M	1
Garlicki, A	1
Janczewska, E	1
Dybowska, D	1
Halota, W	1
Pawłowska, M	1
Pabjan, P	1
Mazur, W	1
Czauż-Andrzejuk, A	1
Berak, H	1
Horban, A	1
Socha, Ł	1
Klapaczyński, J	1
Piekarska, A	1
Blaszkowska, M	1
Belica-Wdowik, T	1
Dobracka, B	1
Tronina, O	1
Deroń, Z	1
Białkowska-Warzecha, J	1
Laurans, Ł	1
Flisiak, R	2
Cordie, A	1
Elsharkawy, A	1
Abdel Alem, S	1
Meshaal, S	1
El Akel, W	1
Abdellatif, Z	1
Kamal, W	1
Al Askalany, M	1
Kamel, S	1
Abdel Aziz, H	1
Kandeel, A	1
Esmat, G	1
Tavelli, A	1
Bonora, S	3
Cingolani, A	2
Lo Caputo, S	3
Saracino, A	2
Soria, A	1
Marinaro, L	1
Uberti-Foppa, C	3
Mussini, C	1
d'Arminio Monforte, A	2
Patel, SV	1
Jayaweera, DT	2
Althoff, KN	1
Eron, JJ	10
Radtchenko, J	1
Mills, A	5
Moyle, G	3
Santiago, S	1
Sax, PE	6
Gillman, J	1
Mounzer, K	1
Elion, RA	1
Huhn, GD	1
Zheng, YX	1
Ma, SJ	1
Xiong, YH	1
Fan, XG	1
Anthony, DD	1
Sulkowski, MS	4
Smeaton, LM	4
Damjanovska, S	1
Shive, CL	1
Kowal, CM	1
Cohen, DE	1
Bhattacharya, D	2
Alston-Smith, BL	1
Balagopal, A	1
Wyles, DL	2
Da, BL	1
Lourdusamy, V	1
Kushner, T	1
Dieterich, D	3
Saberi, B	1
Chayanupatkul, M	1
Chittmittraprap, S	1
Pratedrat, P	1
Chuaypen, N	1
Avihingsanon, A	1
Tangkijvanich, P	1
Wang, R	1
Zheng, Q	1
Wong, YJ	1
Thurairajah, PH	1
Kumar, R	1
Tan, J	1
Fock, KM	1
Law, NM	1
Li, W	1
Kwek, A	1
Tan, YB	1
Koh, J	1
Lee, ZC	1
Kumar, LS	1
Teo, EK	1
Ang, TL	1
Dehghan Manshadi, SA	1
Merat, S	1
Mohraz, M	1
Rasoolinejad, M	1
Sali, S	1
Mardani, M	1
Tabarsi, P	1
Somi, MH	1
Sedghi, R	1
Tayeri, K	1
Nikbin, M	1
Karimi, J	1
Sharifi, AH	1
Kalantari, S	1
Norouzi, A	1
Merat, D	1
Malekzadeh, Z	1
Mirminachi, B	1
Poustchi, H	1
Malekzadeh, R	1
Yunihastuti, E	1
Amelia, F	1
Hapsari, AI	1
Wicaksana, B	1
Natali, V	1
Widhani, A	1
Sulaiman, AS	1
Karjadi, TH	1
Taton, A	1
Colson, P	2
Dhiver, C	2
Ruiz, JM	1
Bregigeon, S	2
Tomei, C	1
Ressiot, E	1
Menard, A	1
Poizot-Martin, I	2
Ravaux, I	1
Lacarelle, B	2
Solas, C	2
Wyles, D	2
Bräu, N	1
Kottilil, S	3
Daar, ES	1
Ruane, P	2
Workowski, K	1
Luetkemeyer, A	3
Adeyemi, O	1
Kim, AY	1
Doehle, B	1
Huang, KC	1
Mogalian, E	1
Osinusi, A	1
McNally, J	1
Brainard, DM	2
McHutchison, JG	2
Naggie, S	1
Sulkowski, M	4
Younossi, ZM	1
Stepanova, M	1
Hunt, S	1
Smolders, EJ	3
Smit, C	1
T M M de Kanter, C	1
Dofferiiof, ASM	1
Arends, JE	1
Brinkman, K	1
Rijnders, B	1
van der Valk, M	2
Reiss, P	1
Burger, DM	3
Uemura, H	1
Tsukada, K	2
Mizushima, D	1
Aoki, T	1
Watanabe, K	1
Kinai, E	1
Teruya, K	2
Gatanaga, H	2
Kikuchi, Y	2
Sugiyama, M	1
Mizokami, M	1
Oka, S	3
Timelli, L	1
Libertone, R	2
Lupi, F	1
Zaccarelli, M	1
Yoshimura, Y	1
Miyata, N	1
Komatsu, H	2
Tachikawa, N	1
Zeuzem, S	2
Serfaty, L	2
Vierling, J	1
Cheng, W	1
George, J	1
Sperl, J	1
Strasser, S	1
Kumada, H	1
Hwang, P	2
Robertson, M	2
Wahl, J	3
Barr, E	3
Talwani, R	1
Platt, H	1
Ghosh, AK	3
Rao, KV	2
Nyalapatla, PR	1
Kovela, S	1
Brindisi, M	1
Osswald, HL	1
Sekhara Reddy, B	1
Agniswamy, J	3
Wang, YF	2
Aoki, M	2
Hattori, SI	1
Weber, IT	3
Mitsuya, H	3
Pineda, JA	4
Rivero-Juárez, A	1
Collado, A	1
Merino, D	2
Morano-Amado, LE	1
Ríos, MJ	1
Pérez-Pérez, M	1
Téllez, F	1
Palacios, R	1
Pérez, AB	1
Mancebo, M	1
Macías, J	2
Braun, DL	1
Hampel, B	1
Kouyos, R	1
Nguyen, H	1
Shah, C	1
Flepp, M	1
Stöckle, M	1
Conen, A	1
Béguelin, C	1
Künzler-Heule, P	1
Nicca, D	1
Schmid, P	1
Delaloye, J	1
Rougemont, M	1
Bernasconi, E	1
Rauch, A	1
Günthard, HF	1
Böni, J	1
Fehr, JS	1
Bischoff, J	1
Rockstroh, JK	5
Feng, HP	2
Guo, Z	2
Ross, LL	5
Fraser, I	1
Panebianco, D	2
Jumes, P	2
Fandozzi, C	2
Caro, L	2
Talaty, J	2
Ma, J	1
Mangin, E	1
Huang, X	2
Marshall, WL	2
Butterton, JR	2
Iwamoto, M	2
Yeh, WW	2
Begovac, J	1
Krznarić, J	1
Bogdanić, N	1
Močibob, L	1
Zekan, Š	1
Wu, J	1
Huang, P	1
Fan, H	1
Tian, T	1
Xia, X	1
Fu, Z	1
Wang, Y	1
Ye, X	1
Yue, M	1
Zhang, Y	1
Chu, X	1
Dunnington, K	1
Du, L	1
Hanley, WD	1
Fraser, IP	1
Mitselos, A	1
Denef, JF	1
De Lepeleire, I	1
de Hoon, JN	1
Vandermeulen, C	1
Martinho, M	1
Valesky, R	1
Maughan, A	1
Sadigh, K	1
Angulo-Diaz, V	1
Villanueva, M	1
Lim, JK	1
Wilson, E	1
Covert, E	1
Hoffmann, J	1
Comstock, E	1
Emmanuel, B	1
Tang, L	1
Husson, J	1
Chua, J	1
Price, A	1
Mathur, P	1
Rosenthal, E	4
Kattakuzhy, S	1
Masur, H	3
Xiao, H	1
Chen, J	2
Wang, J	1
Li, J	1
Yang, F	1
Lu, H	1
Barrail-Tran, A	3
Goldwirt, L	1
Gelé, T	1
Laforest, C	1
Lavenu, A	1
Danjou, H	1
Radenne, S	1
Leroy, V	2
Houssel-Debry, P	1
Duvoux, C	1
Kamar, N	1
De Ledinghen, V	2
Canva, V	1
Conti, F	1
Durand, F	1
D'Alteroche, L	1
Botta-Fridlund, D	1
Moreno, C	2
Cagnot, C	1
Samuel, D	1
Fougerou-Leurent, C	1
Pageaux, GP	2
Duclos-Vallée, JC	1
Taburet, AM	8
Coilly, A	1
Shah, BM	1
Schafer, JJ	1
Priano, J	1
Squires, KE	1
Ucciferri, C	1
Falasca, K	1
Vignale, F	1
Di Nicola, M	1
Pizzigallo, E	1
Vecchiet, J	1
Cahn, P	1
Sued, O	1
Gallant, JE	5
Koenig, E	3
Andrade-Villanueva, J	2
Chetchotisakd, P	2
DeJesus, E	17
Antunes, F	4
Arastéh, K	4
Rizzardini, G	3
Fehr, J	2
Liu, Y	2
Zhong, L	3
Callebaut, C	2
Szwarcberg, J	7
Rhee, MS	4
Cheng, AK	7
Bruce, RD	1
Winkle, P	1
Custodio, JM	2
Wei, LX	1
Kearney, BP	5
Ramanathan, S	4
Friedland, GH	1
Temesgen, Z	3
Pombo, M	1
Olalla, J	1
Del Arco, A	1
De La Torre, J	1
Urdiales, D	1
Aguilar, A	1
Prada, JL	1
García-Alegría, J	1
Ruiz-Mateas, F	1
Kumar, P	1
Huhn, G	1
Sloan, L	1
Small, CB	1
Edelstein, H	1
Felizarta, F	2
Hao, R	1
Ross, L	3
Stancil, B	1
Pappa, K	1

Trial	Phase	Enrollment	Study Type	Start Date	Status
Interferon-Free Therapy for Chronic Hepatitis C Virus Genotype 1 Infection in Participants With HIV-1 Coinfection Receiving Concurrent Antiretroviral Therapy (C_ASCENT)[NCT02194998]	Phase 2	46 participants (Actual)	Interventional	2015-09-16	Terminated (stopped due to The study closed to accrual before the planned accrual goal was attained due to the availability of newer directly-acting antiviral (DAA) treatments for HCV.)
Efficacy of a Fixed-Dose Combination Pill of Sofosbuvir and Daclatasvir in Treating Hepatitis C in 200 Patients Co-infected With Human Immunodeficiency Virus[NCT03369327]	Phase 3	232 participants (Actual)	Interventional	2017-01-01	Completed
A Phase 3, Open-Label Study to Investigate the Efficacy and Safety of Sofosbuvir/GS-5816 Fixed Dose Combination for 12 Weeks in Subjects With Chronic Hepatitis C Virus (HCV) and Human Immunodeficiency Virus (HIV)-1 Coinfection[NCT02480712]	Phase 3	107 participants (Actual)	Interventional	2015-07-01	Completed
A Phase III, Open-Label Clinical Trial to Study the Efficacy and Safety of the Combination Regimen of MK-5172/MK-8742 Versus Sofosbuvir/Pegylated Interferon/Ribavirin (PR) in Treatment-Naïve and PR Prior Treatment Failure Subjects With Chronic HCV GT1, 4 [NCT02358044]	Phase 3	257 participants (Actual)	Interventional	2015-02-27	Completed
A Phase III, Multi-center, Open-label Trial to Investigate the Impact of a Treat, Counsel and Cure Strategy in Men Who Have Sex With Men With Hepatitis C Infection in the Swiss HIV Cohort Study[NCT02785666]	Phase 3	150 participants (Actual)	Interventional	2016-06-30	Completed
Cohort of Liver Transplanted Patients With Hepatitis C Virus Recurrence and Treated With Direct-acting Antiviral Agents[NCT01944527]		699 participants (Actual)	Observational	2013-10-31	Active, not recruiting
A Phase 3, Randomized, Double-Blind Study to Evaluate the Safety and Efficacy of GS-9350-boosted Atazanavir Versus Ritonavir-boosted Atazanavir Each Administered With Emtricitabine/Tenofovir Disoproxil Fumarate in HIV-1 Infected, Antiretroviral Treatment-[NCT01108510]	Phase 3	698 participants (Actual)	Interventional	2010-04-30	Completed
A Study in Underrepresented Patient Population or Regimen Tolerability: SUPPoRT[NCT00727597]	Phase 3	101 participants (Actual)	Interventional	2008-07-31	Completed
A 48 Week, Phase II, Open-label, 2-cohort, Multicenter Study to Evaluate the Pharmacokinetics, Safety, Tolerability and Antiviral Activity of GW433908 and GW433908/RTV When Administered to HIV-1 Infected Protease Inhibitor (PI) Naive and PI-experienced Pe[NCT00071760]	Phase 2	59 participants (Actual)	Interventional	2003-10-23	Completed
A 48 Week, Phase II, Non-Comparative, Open-label, Multi-Cohort, Multicenter Study to Evaluate the Safety, Tolerability, Pharmacokinetics and Antiviral Activity of GW433908/Ritonavir BID When Administered to HIV-1 Infected, PI-Naïve and Experienced, Pediat[NCT00089583]	Phase 2	110 participants (Actual)	Interventional	2004-07-31	Completed
A Phase 3b Randomized, Open-Label Study to Evaluate Switching From Regimens Consisting of a Ritonavir-boosted Protease Inhibitor (PI + RTV) Plus Emtricitabine/Tenofovir Disoproxil Fumarate (FTC/TDF) to the Elvitegravir/Cobicistat/Emtricitabine/Tenofovir D[NCT01475838]	Phase 3	438 participants (Actual)	Interventional	2011-11-30	Completed
The Incidence and Severity of Drug Interactions Before and After Switching Antiretroviral Therapy to Bictegravir/Emtricitabine/Tenofovir Alafenamide in Treatment Experienced Patients[NCT03789968]		411 participants (Actual)	Observational	2019-09-01	Completed
A Phase 3b Randomized, Open Label Study to Evaluate Switching From Regimens Consisting of a Non-nucleoside Reverse Transcriptase Inhibitor (NNRTI) Plus Emtricitabine (FTC) and Tenofovir DF (TDF) to the Elvitegravir/Cobicistat/ Emtricitabine/Tenofovir Diso[NCT01495702]	Phase 3	439 participants (Actual)	Interventional	2011-12-31	Completed
Open-Labeled Trial Of Direct-Acting Antiviral Treatment Of Hepatitis C-Negative Patients Who Receive Kidney Transplants From Hepatitis C-Positive Donors[NCT02743897]	Phase 1/Phase 2	62 participants (Actual)	Interventional	2016-05-01	Completed
A Phase II Randomized Clinical Trial to Study the Efficacy and Safety of the Combination Regimen MK-5172 and MK-8742 ± Ribavirin (RBV) in Subjects With Chronic Hepatitis C Virus Infection[NCT01717326]	Phase 2	573 participants (Actual)	Interventional	2013-02-07	Completed
Open-Labeled Trial Of Zepatier For Treatment Of Hepatitis C-Negative Patients Who Receive Heart Transplants From Hepatitis C-Positive Donors[NCT03146741]	Phase 1/Phase 2	20 participants (Actual)	Interventional	2017-05-16	Completed
A Phase 3 Open-label Safety Study of Cobicistat-containing Highly Active Antiretroviral Regimens in HIV-1 Infected Patients With Mild to Moderate Renal Impairment[NCT01363011]	Phase 3	106 participants (Actual)	Interventional	2011-05-31	Completed
A Phase 3, Randomized, Double-Blind Study to Evaluate the Safety and Efficacy of Elvitegravir/Cobicistat/Emtricitabine/Tenofovir Alafenamide Versus Elvitegravir/Cobicistat/Emtricitabine/ Tenofovir Disoproxil Fumarate in HIV-1 Positive, Antiretroviral Trea[NCT01780506]	Phase 3	872 participants (Actual)	Interventional	2012-12-26	Completed
A Phase 3, Randomized, Double-Blind Study to Evaluate the Safety and Efficacy of Elvitegravir/Cobicistat/Emtricitabine/Tenofovir Alafenamide Versus Elvitegravir/Cobicistat/Emtricitabine/Tenofovir Disoproxil Fumarate in HIV-1 Positive, Antiretroviral Treat[NCT01797445]	Phase 3	872 participants (Actual)	Interventional	2013-03-12	Completed
Efficacy and Safety of Elvitegravir/Cobicistat/Emtricitabine/Tenofovir Alafenamide (Genvoya) as Maintenance Treatment of HIV-1/Hepatitis B Virus (HBV)-Coinfected Patients: an Observational Study[NCT03425994]		275 participants (Actual)	Observational [Patient Registry]	2018-02-06	Active, not recruiting
Pilot Study to Assess the Efficacy and Tolerance to a QUadruple Therapy With Asunaprevir , Daclatasvir, Ribavirin and Pegylated Interferon Alpha-2a, in HIV-HCV Genotype 1 or 4 Coinfected Patients Previously Null Responders to a Standard Pegylated Interfer[NCT01725542]	Phase 2	75 participants (Actual)	Interventional	2012-12-31	Completed
Determining the Sustained Virologic Response of Declatasvir in Egyptian Patients With Hepatitis C Virus Genotype 4[NCT02772744]		250 participants (Anticipated)	Observational	2017-11-01	Not yet recruiting
Efficacy and Tolerability of Grazoprevir and Elbasvir in Peginterferon Alfa Plus Ribavirin Experienced Patients With Chronic Genotype 1 HCV and HIV Co-infection: a Non-randomised, Open-label Clinical Trial[NCT03098121]	Phase 4	40 participants (Actual)	Interventional	2017-10-20	Completed
A Phase 3 Evaluation of Daclatasvir Plus Sofosbuvir in Treatment-naïve and Treatment-experienced Chronic Hepatitis C (Genotype 1, 2, 3, 4, 5, or 6) Subjects Coinfected With Human Immunodeficiency Virus (HIV)[NCT02032888]	Phase 3	238 participants (Actual)	Interventional	2014-02-28	Completed
Short Duration Therapy of Acute Hepatitis C Genotypes 1 or 4: Efficacy and Tolerability of Grazoprevir 100mg/Elbasvir 50mg During 8 Weeks[NCT02886624]	Phase 2	30 participants (Actual)	Interventional	2017-05-31	Completed
A Phase III Open-Label Clinical Trial to Study the Efficacy and Safety of the Combination Regimen Grazoprevir (GZR) and Elbasvir (EBR) in Treatment-Naïve Subjects With Chronic HCV GT1, GT4, and GT6 Infection Who Are Co-Infected With HIV[NCT02105662]	Phase 3	218 participants (Actual)	Interventional	2014-06-03	Completed
A Drug-drug Interaction Study Between the Novel Anti-HCV Agent Daclatasvir and the Antiretroviral Agents Atazanavir/Ritonavir or Atazanavir/Cobicistat in Healthy Volunteers[NCT02565888]	Phase 1	16 participants (Actual)	Interventional	2015-11-30	Completed
A Multicenter Compassionate Use Program of Daclatasvir (BMS-790052) in Combination With Sofosbuvir With or Without Ribavirin for the Treatment of Subjects With Chronic Hepatitis C[NCT02097966]		0 participants	Expanded Access		No longer available
A Phase 3, Open Label Study of Safety and Efficacy With BMS-790052 Plus Peg-Interferon Alfa 2a and Ribavirin in Previously Untreated HCV Patients Coinfected With Human Immunodeficiency Virus (HIV) and Hepatitis C Virus (HCV)[NCT01471574]	Phase 3	549 participants (Actual)	Interventional	2011-12-31	Completed
Phase 3 Open Label Study Evaluating the Efficacy and Safety of Pegylated Interferon Lambda-1a, in Combination With Ribavirin and Daclatasvir, for Treatment of Chronic HCV Infection With Treatment naïve Genotypes 1, 2, 3 or 4 in Subjects Co-infected With H[NCT01866930]	Phase 3	453 participants (Actual)	Interventional	2013-07-11	Terminated (stopped due to Sponsor decision not based on any new unexpected safety findings or efficacy observations.)
Efficacy and Safety of Regimens Restricted to a Combination of Two Boosted Protease Inhibitors as Potent Antiretroviral Therapy in HIV-1 Infected Patients. ANRS 127 2IP[NCT00122603]	Phase 2	61 participants (Actual)	Interventional	2005-12-31	Completed
STALWART: A Randomized, Open-Label, International Study of Subcutaneous Recombinant Interleukin-2 With and Without Concomitant Antiretroviral Therapy in Patients With HIV-1 Infection and CD4+ Cell Counts of 300 Cells/mm3 or More[NCT00110812]	Phase 2	267 participants (Actual)	Interventional	2005-09-30	Completed
Register of Cardiovascular Complications Among People Living With HIV[NCT02453919]		800 participants (Anticipated)	Observational [Patient Registry]	2010-02-28	Recruiting
A Phase 2, Randomized, Double-Blinded Study of the Safety and Efficacy of Elvitegravir/Emtricitabine/Tenofovir Disoproxil Fumarate/GS-9350 Versus Atripla® (Efavirenz 600 mg/Emtricitabine 200 mg/Tenofovir Disoproxil Fumarate 300 mg) in HIV-1 Infected, Anti[NCT00869557]	Phase 2	71 participants (Actual)	Interventional	2009-04-30	Completed
IGHID 11417 - The Safety and Efficacy of Fixed Dose Combination Dolutegravir/Abacavir/Lamivudine FDC Initiated During Acute HIV Infection: Impact on the Latent HIV Reservoir and Long-Term Immunologic Effect[NCT02384395]		40 participants (Actual)	Interventional	2015-09-30	Completed
A Phase 2, Randomized, Double-Blinded Study of the Safety and Efficacy of GS-9350-boosted Atazanavir (ATV/GS-9350) Compared to Ritonavir-boosted Atazanavir (ATV/r) in Combination With Emtricitabine/Tenofovir Disoproxil Fumarate (FTC/TDF) in HIV-1 Infected[NCT00892437]	Phase 2	85 participants (Actual)	Interventional	2009-05-31	Completed
Adolescent Master Protocol[NCT01418014]		678 participants (Actual)	Observational	2007-03-31	Completed
A Phase 3, Randomized, Double-Blind Study to Evaluate the Safety and Efficacy of Elvitegravir/Emtricitabine/Tenofovir Disoproxil Fumarate/GS-9350 Versus Ritonavir-Boosted Atazanavir Plus Emtricitabine/Tenofovir Disoproxil Fumarate in HIV-1 Infected, Antir[NCT01106586]	Phase 3	708 participants (Actual)	Interventional	2010-04-30	Completed
An Open-Label, Multi-Centre, Randomised Study to Investigate Integrase Inhibitor Versus Boosted Protease Inhibitor Antiretroviral Therapy for Patients With Advanced HIV Disease[NCT03696160]	Phase 3	447 participants (Actual)	Interventional	2019-03-05	Active, not recruiting
A Phase 3, Randomized, Double-Blind Study to Evaluate the Safety and Efficacy of Elvitegravir/Emtricitabine/Tenofovir Disoproxil Fumarate/GS-9350 Versus Efavirenz/Emtricitabine/Tenofovir Disoproxil Fumarate in HIV-1 Infected, Antiretroviral Treatment-Naiv[NCT01095796]	Phase 3	707 participants (Actual)	Interventional	2010-03-31	Completed
Accelerated Aging, HIV Infection, Antiretroviral Therapies[NCT01038999]		200 participants (Anticipated)	Observational	2009-04-30	Completed
"PIQD: The Once a Day Protease Inhibitor Regimens. Ritonavir Boosted Atazanavir vs. Ritonavir Boosted Fosamprenavir Used in Combination With Tenofovir and Emtricitabine in HIV-1 Infected Antiretroviral Treatment-Naïve Patients."[NCT00242216]	Phase 4	76 participants (Actual)	Interventional	2004-05-31	Completed
A Randomized, Prospective Study of the Efficacy, Safety and Tolerability of Two Doses of GW433908Ritonavir Given With Abacavir/Lamivudine Fixed Dose Combination[NCT00335270]	Phase 4	100 participants	Interventional	2006-03-31	Completed
Study on Safety and Efficacy of Salvage Therapy With Amprenavir, Lopinavir and Ritonavir 200 Mg/d or 400 Mg/d in HIV-Infected Patients in Virological Failure.ANRS 104 PUZZLE 1[NCT00196625]	Phase 2	100 participants	Interventional	2000-11-30	Completed
A Randomized, Comparative Study of Lopinavir/Ritonavir Versus GW433908 and Ritonavir Versus Lopinavir/Ritonavir and GW433908 (In Combination With Tenofovir Disoproxil Fumarate and One or Two Nucleoside Reverse Transcriptase Inhibitors) in HIV-1-Infected S[NCT00028366]		56 participants	Interventional		Completed
See Detailed Description[NCT00085943]	Phase 3	866 participants	Interventional	2004-05-31	Completed
A Randomized, Double-Blind, Phase II Study of 141W94 (VX-478) Monotherapy vs. 141W94 (VX-478) Plus ZDV Plus 3TC in HIV Infected Individuals[NCT00001085]	Phase 2	94 participants	Interventional		Completed
A Phase II Study of 1) Amprenavir (141W94/VX478) Plus 3TC Plus ZDV (or d4T) or 2) IDV Plus NVP Plus 3TC Plus d4T in Subjects Previously Treated With Amprenavir and 3) Other Treatment Regimens (Observational ARM) in Subjects Previously Treated With Amprena[NCT00001095]	Phase 2	94 participants	Interventional		Completed
A Phase I/II Screening Trial to Identify Potential Partner Compounds to Use in Combination With 141W94[NCT00002372]	Phase 1	48 participants	Interventional		Completed
A Phase II Trial to Evaluate the Safety and Efficacy of Induction Treatment With Lamivudine Plus Stavudine Plus Abacavir Plus Amprenavir/Ritonavir Followed by Supervised Treatment Interruption in Subjects With Acute HIV Infection or Recent Seroconversion[NCT00000940]	Phase 2	121 participants (Actual)	Interventional	1999-05-31	Completed
A Phase II, Randomized Trial of Amprenavir as Part of Dual Protease Inhibitor Regimens (Placebo-Controlled) in Combination With Abacavir, Efavirenz, and Adefovir Dipivoxil Versus Amprenavir Alone in HIV-Infected Subjects With Prior Exposure to Approved Pr[NCT00000912]	Phase 2	475 participants	Interventional		Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

HIV-1 VF was defined as two consecutive HIV-1 RNA results ≥ 200 copies/mL. (NCT02194998)
Timeframe: From treatment initiation to 4 weeks after last dose of HCV study treatment. HIV-1 RNA was measured at weeks 2, 4, 6, 8, 10, 12, 16, 20, 24, and 28. The durations for HCV study treatment for Cohorts A/C and Cohorts B/D were 24 and 12 weeks, respectively.

Number of Participants Who Prematurely Discontinued HCV Study Treatment for Any Reason Other Than HCV Virologic Failure (VF)

Intervention	Participants (Count of Participants)
Cohort A [INI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	0
Cohort B [INI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	0
Cohort C [PI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	0
Cohort D [PI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	1

HCV VF was defined as follows: confirmed increase from nadir in HCV RNA (defined as two consecutive HCV RNA measurements of >1 log10 IU/mL above nadir) at any time point; failure to achieve HCV RNA NCT02194998)
Timeframe: From treatment initiation to either 24 weeks (for Cohort A and C) or 12 weeks (for Cohort B and D). The duration for HCV study treatment for Cohorts A and C and Cohorts B and D was 24 and 12 weeks, respectively.

Number of Participants With an Occurrence of Diagnoses Leading to Premature HCV Study Treatment or HIV-1 Antiretroviral (ARV) Discontinuation.

Intervention	Participants (Count of Participants)
Cohort A [INI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	1
Cohort B [INI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	1
Cohort C [PI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	0
Cohort D [PI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	0

Participants who had diagnoses leading to premature HCV study treatment or HIV-1 ARV discontinuation post treatment initiation. (NCT02194998)
Timeframe: From treatment initiation to end of study follow-up at 48 weeks.The duration for HCV study treatment for Cohorts A and C and Cohorts B and D was 24 and 12 weeks, respectively. The duration for ARV treatment for all cohorts was 48 weeks.

Number of Participants With an Occurrence of Laboratory Abnormality Grade 3 or Higher.

Intervention	Participants (Count of Participants)
Cohort A [INI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	0
Cohort B [INI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	1
Cohort C [PI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	0
Cohort D [PI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	0

"Participants with an observed laboratory abnormalities grade 3 or higher post treatment initiation.~If entry (pre-treatment) lab result was grade 3, then a grade 4 result was required to meet this outcome.~Severity grading was based on DAIDS AE Grading Table, Version 1.0." (NCT02194998)
Timeframe: From treatment initiation to 30 days post date of last dose of HCV study treatment (whether planned or premature discontinuation). The duration for HCV study treatment for Cohorts A and C and Cohorts B and D was 24 and 12 weeks, respectively.

Number of Participants With an Occurrence of Serious Adverse Events (SAEs) as Defined by International Conference on Harmonisation (ICH) Criteria

Intervention	Participants (Count of Participants)
Cohort A [INI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	5
Cohort B [INI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	3
Cohort C [PI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	3
Cohort D [PI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	0

Participants who experienced at least one observed SAEs as defined by ICH after initiating HCV study treatment through 30 days post date of last dose of HCV study treatment. (NCT02194998)
Timeframe: From treatment initiation to 30 days post date of last dose of HCV study treatment (whether planned or premature discontinuation). The duration for HCV study treatment for Cohorts A and C and Cohorts B and D was 24 and 12 weeks, respectively.

Number of Participants With an Occurrence of Signs/Symptoms Grade 3 or Higher

Intervention	Participants (Count of Participants)
Cohort A [INI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	1
Cohort B [INI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	1
Cohort C [PI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	2
Cohort D [PI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	0

"Participants with signs/symptoms of grade 3 or higher post treatment initiation.~Participants with grade 3 sign/symptom prior to treatment initiation must have had one grade higher than pre-treatment to meet this outcome.~Severity grading was based on DAIDS AE Grading Table, Version 1.0." (NCT02194998)
Timeframe: From treatment initiation to 30 days post date of last dose of HCV study treatment (whether planned or premature discontinuation). The duration for HCV study treatment for Cohorts A and C and Cohorts B and D was 24 and 12 weeks, respectively.

Number of Participants With Selected HIV-1 Resistance Mutations Among Participants Who Experience HIV-1 Virologic Failure (VF)

Intervention	Participants (Count of Participants)
Cohort A [INI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	0
Cohort B [INI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	2
Cohort C [PI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	3
Cohort D [PI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	0

Participants with one or more genotype mutations in protease conferring major resistance to any HIV-1 Protease Inhibitors (PI) antiretroviral drug, from a plasma sample drawn following confirmed HIV-1 VF outcome. (NCT02194998)
Timeframe: At confirmation of HIV-1 virologic failure.

Percentage of Participants With Sustained Virologic Response at 12 Weeks After HCV Treatment Discontinuation (SVR12)

Intervention	Participants (Count of Participants)
Cohort A [INI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	0
Cohort B [INI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	0
Cohort C [PI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	0
Cohort D [PI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	0

"SVR12 was defined as HCV RNA less than the assay LLOQ (<15 IU/mL) at 12 weeks post HCV treatment discontinuation.~A two-sided 90% confidence interval was calculated for the percentage of participants with SVR12 response using Clopper-Pearson method.~For those whose HCV early responses prior to SVR12 evaluation met the guidelines for HCV Virologic Failure (VF), their SVR12 outcome was defined as non-response. Those missing a HCV RNA result from the week 12 post HCV treatment discontinuation visit (and missing all subsequent evaluations) were considered non-responders. However, if HCV RNA evaluations subsequent to week 12 post treatment discontinuation were non-missing, then the first HCV RNA subsequent to week 12 post treatment discontinuation was instead used to define the primary outcome." (NCT02194998)
Timeframe: At 12 weeks after last dose of HCV study treatment. The duration for study treatment for Cohorts A and C and Cohorts B and D was 24 and 12 weeks, respectively.

Percentage of Participants With Sustained Virologic Response at 24 Weeks After HCV Treatment Discontinuation (SVR24)

Intervention	percentage of participants (Number)
Cohort A [INI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	95.2
Cohort B [INI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	60
Cohort C [PI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	100
Cohort D [PI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	100

"SVR24 was defined as HCV RNA less than the assay LLOQ (<15 IU/mL) at 24 weeks post treatment discontinuation.~A two-sided 90% confidence interval was calculated for the percentage of SVR24 response using method of Clopper-Pearson.~For those whose HCV early responses prior to SVR24 evaluation met the guidelines for HCV VF, their SVR24 outcome was defined as non-response. Those missing a HCV RNA result from the week 24 post HCV treatment discontinuation visit (and missing all subsequent evaluations) were considered non-responders. However, if HCV RNA evaluations subsequent to week 24 post treatment discontinuation were non-missing, then the first HCV RNA subsequent to week 24 post treatment discontinuation was instead used to define the primary outcome." (NCT02194998)
Timeframe: At 24 weeks after the date of last dose of HCV study treatment. The duration for study treatment for Cohorts A and C and Cohorts B and D was 24 and 12 weeks, respectively.

Change in IP-10 Concentration.

Intervention	percentage of participants (Number)
Cohort A [INI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	90.5
Cohort B [INI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	60
Cohort C [PI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	93.3
Cohort D [PI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	100

Absolute change from baseline in IP-10 (Interferon gamma-induced protein 10) concentration in plasma, calculated as value at the later time point minus baseline value. Baseline was defined as the date of first treatment dose. (NCT02194998)
Timeframe: At baseline, end of HCV treatment (EOT), and 12 weeks post EOT. The EOT for Cohorts A and C and Cohorts B and D was 24 and 12 weeks, respectively.

Change in Soluble CD14 (sCD14)

Intervention	pg/mL (Median)
	Change from baseline to EOT	Change from baseline to 12 weeks post EOT
Cohort A [INI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	-244.4	-127
Cohort B [INI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	-22.2	-29.1
Cohort C [PI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	-116	-83.1
Cohort D [PI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	-61.1	-114.9

Absolute change from baseline in sCD14 levels in plasma calculated as value at the later time point minus baseline value. Baseline was defined as the date of first treatment dose. (NCT02194998)
Timeframe: At baseline, end of HCV treatment (EOT), and 12 weeks post EOT. The EOT for Cohorts A and C and Cohorts B and D was 24 and 12 weeks, respectively.

Levels of IP-10 Concentration.

Intervention	ng/mL (Median)
	Change from baseline to EOT	Change from baseline to 12 weeks post EOT
Cohort A [INI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	307.6	145.2
Cohort B [INI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	-1,063.2	-894.2
Cohort C [PI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	-380.3	-22.6
Cohort D [PI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	318.2	-987.0

Levels of IP-10 (Interferon gamma-induced protein 10) concentration in plasma. Baseline was defined as the date of first treatment dose. (NCT02194998)
Timeframe: At baseline, end of HCV treatment (EOT), and 12 weeks post EOT. The EOT for Cohorts A and C and Cohorts B and D was 24 and 12 weeks, respectively.

Levels of Soluble CD14 (sCD14)

Intervention	pg/mL (Median)
	IP-10 at baseline	IP-10 at EOT	IP-10 at 12 weeks post EOT
Cohort A [INI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	379	100.9	94.6
Cohort B [INI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	120.2	60.4	85.5
Cohort C [PI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	225.5	76.6	82.5
Cohort D [PI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	196.4	182.6	159.5

Levels of sCD14. Baseline was defined as the date of first treatment dose. (NCT02194998)
Timeframe: At baseline, end of HCV treatment (EOT), and 12 weeks post EOT. The EOT for Cohorts A and C and Cohorts B and D was 24 and 12 weeks, respectively.

Percentage of Participants Who Permanently Discontinued Any Study Drug Due to an Adverse Event

Percentage of Participants With Sustained Virologic Response 12 Weeks After Discontinuation of Therapy (SVR12)

Intervention	ng/mL (Median)
	sCD14 at Baseline	sCD14 at EOT	sCD14 at 12 weeks post EOT
Cohort A [INI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	1,832.0	2,126.5	1,977.3
Cohort B [INI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	2,226.8	1,132.8	1,367.4
Cohort C [PI-based ART + PTV/r/OBT + DSV +/- RBV 24 Weeks]	3,157.0	2,421.1	3,424.5
Cohort D [PI-based ART + PTV/r/OBT + DSV +/- RBV 12 Weeks]	3,092.0	2,801.3	2,608.3

Intervention	percentage of participants (Number)
SOF/VEL 12 Weeks	1.9

SVR12 was defined as HCV RNA < the lower limit of quantitation (LLOQ) 12 weeks following the last dose of study drug. (NCT02480712)
Timeframe: Posttreatment Week 12

Percentage of Participants With Virologic Failure

Intervention	percentage of participants (Number)
SOF/VEL 12 Weeks	95.3

"Virologic failure was defined as:~On-treatment virologic failure:~Breakthrough (confirmed HCV RNA ≥ LLOQ after having previously had HCV RNA < LLOQ while on treatment), or~Rebound (confirmed > 1 log10 IU/mL increase in HCV RNA from nadir while on treatment), or~Non-response (HCV RNA persistently ≥ LLOQ through 8 weeks of treatment)~Virologic relapse:~Confirmed HCV RNA ≥ LLOQ during the posttreatment period having achieved HCV RNA < LLOQ at last on-treatment visit" (NCT02480712)
Timeframe: Up to Posttreatment Week 24

HCV RNA Change From Baseline/Day 1

Percentage of Participants That Maintained HIV-1 RNA < 50 Copies/mL While On HCV Treatment

Percentage of Participants With HCV RNA < LLOQ on Treatment

Percentage of Participants With Sustained Virologic Response 4 and 24 Weeks After Discontinuation of Therapy (SVR4 and SVR24)

Intervention	percentage of participants (Number)
SOF/VEL 12 Weeks	1.9

Intervention	log10 IU/mL (Mean)
	Change at Week 1	Change at Week 2	Change at Week 4	Change at Week 6	Change at Week 8	Change at Week 10	Change at Week 12
SOF/VEL 12 Weeks	-4.47	-4.97	-5.15	-5.18	-5.17	-5.17	-5.17

Intervention	percentage of participants (Number)
	Week 4	Week 8	Week 12
SOF/VEL 12 Weeks (Boosted TDF Containing Regimens)	94.4	96.3	96.2
SOF/VEL 12 Weeks (Non TDF Containing Regimens)	100	100	92.9
SOF/VEL 12 Weeks (Non-Boosted TDF Containing Regimens)	97.1	97.1	100

Intervention	percentage of participants (Number)
	Week 1	Week 2	Week 4	Week 6	Week 8	Week 10	Week 12
SOF/VEL 12 Weeks	25.7	68.0	92.2	99.0	100.0	100.0	100.0

SVR4 and SVR24 were defined as HCV RNA < LLOQ at 4 and 24 weeks following the last dose of study drug, respectively. (NCT02480712)
Timeframe: Posttreatment Weeks 4 and 24

Serum Creatinine Change From Baseline At the End of Treatment and At Posttreatment Week 12

Percentage of Participants Achieving Sustained Virologic Response 24 Weeks After Ending Study Treatment (SVR24)

Intervention	percentage of participants (Number)
	SVR4	SVR24
SOF/VEL 12 Weeks	95.3	95.3

Intervention	mg/dL (Mean)
	Change at Week 12	Change at Posttreatment Week 12
SOF/VEL 12 Weeks (Boosted TDF Containing Regimens)	0.09	0.04
SOF/VEL 12 Weeks (Non TDF Containing Regimens)	0.00	-0.06
SOF/VEL 12 Weeks (Non-Boosted TDF Containing Regimens)	0.04	0.02

HCV-RNA levels in plasma were measured using the Roche COBAS®AmpliPrep/COBAS® TaqMan® HCV Test, v2.0 on blood samples drawn from each participant. SVR24 was defined as HCV RNA NCT02358044)
Timeframe: 24 weeks after end of all therapy (Study Week 36)

Percentage of Participants Achieving Sustained Virologic Response 4 Weeks After Ending Study Treatment (SVR4)

Intervention	percentage of participants (Number)
Grazoprevir + Elbasvir	98.4
SOF + PR	89.7

HCV-RNA levels in plasma were measured using the Roche COBAS®AmpliPrep/COBAS® TaqMan® HCV Test, v2.0 on blood samples drawn from each participant. SVR4 was defined as HCV RNA NCT02358044)
Timeframe: 4 weeks after end of all therapy (Study Week 16)

Percentage of Participants Discontinuing Study Treatment Due to an AE

Intervention	percentage of participants (Number)
Grazoprevir + Elbasvir	99.2
SOF + PR	92.1

"An AE was defined as any untoward medical occurrence in a participant administered a pharmaceutical product and which did not necessarily have a causal relationship with this treatment. An AE could therefore be any unfavourable and unintended sign (including an abnormal laboratory finding, for example), symptom, or disease temporally associated with the use of a medicinal product or protocol-specified procedure, whether or not considered related to the medicinal product or protocol-specified procedure. Any worsening of a preexisting condition that was temporally associated with the use of the Sponsor's product, was also an AE.~The percentage of participants who discontinued study treatment due to an AE was reported for each treatment arm. Participants that discontinued study drug treatment due to an AE may have still continued on trial." (NCT02358044)
Timeframe: Up to Week 12

Percentage of Participants Experiencing at Least One Adverse Event (AE) During the Treatment Period Plus First 14 Follow-up Days

Intervention	percentage of participants (Number)
Grazoprevir + Elbasvir	0.8
SOF + PR	0.8

An AE was defined as any untoward medical occurrence in a participant administered a pharmaceutical product and which did not necessarily have a causal relationship with this treatment. An AE could therefore be any unfavourable and unintended sign (including an abnormal laboratory finding, for example), symptom, or disease temporally associated with the use of a medicinal product or protocol-specified procedure, whether or not considered related to the medicinal product or protocol-specified procedure. Any worsening of a preexisting condition that was temporally associated with the use of the Sponsor's product, was also an AE. The percentage of participants who experienced at least one AE was reported for each treatment arm. (NCT02358044)
Timeframe: Treatment + First 14 days of follow-up (Up to Week 14)

Primary: Percentage of Participants Achieving Sustained Virologic Response at 12 Weeks After the End of All Treatment (SVR12)

Intervention	percentage of participants (Number)
Grazoprevir + Elbasvir	51.9
SOF + PR	93.7

Hepatitis C Virus ribonucleic acid (HCV-RNA) levels in plasma were measured using the Roche COBAS®AmpliPrep/COBAS® TaqMan® HCV Test, v2.0 on blood samples drawn from each participant. SVR12 was defined as HCV RNA below the lower limit of quantification (NCT02358044)
Timeframe: 12 weeks after end of all therapy (Study Week 24)

Percentage of Participants Experiencing at Least One Tier 1 Safety Event (Key Safety Parameter) During the Treatment Period and First 14 Follow-up Days

Intervention	percentage of participants (Number)
Grazoprevir + Elbasvir	99.2
SOF + PR	90.5

Tier 1 safety events were pre-specified by the protocol to evaluate safety and test the safety superiority hypothesis. Tier 1 safety events were chosen to assess broad tolerability, hematological side effects and liver-related laboratory abnormalities. For this study, Tier 1 safety events included: any serious drug-related AE, any drug-related AE leading to permanent discontinuation (DC) of all study drugs, neutrophil count <0.75 x 10^9/L, hemoglobin <10 g/dL, severe depression, hepatic events of clinical interest (defined by abnormal increases in alanine aminotransferase [ALT], aspartate aminotransferase [AST], or alkaline phosphatase [ALP]), or events meeting stopping rule criteria for DC from trial (due to abnormal increases of ALT, AST, or ALP with/without pre-specified related AEs). The percentage of participants who experienced each individual event that was defined as a Tier 1 safety event during the study treatment period was reported for each treatment arm. (NCT02358044)
Timeframe: Treatment + First 14 days of follow-up (Up to Week 14)

Change From Baseline in CD4 Cell Count at Week 144

Change From Baseline in CD4 Cell Count at Week 192

Change From Baseline in CD4 Cell Count at Week 48

Change From Baseline in CD4 Cell Count at Week 96

Percentage of Participants With HIV-1 RNA < 50 Copies/mL at Week 144

Intervention	percentage of participants (Number)
	Total Tier 1 AEs	Tier 1 AE: Serious drug-related AE	Tier 1 AE: DC due to drug-related AE	Tier 1 AE: Neutrophil count <0.75 x 10^9/L	Tier 1 AE: Hemoglobin <10 g/dL	Tier 1 AE: Severe depression	Tier 1 AE: Hepatic event of clinical interest	Tier 1 AE: Trial DC due to stopping rule
Grazoprevir + Elbasvir	0.8	0.0	0.0	0.0	0.8	0.0	0.0	0.0
SOF + PR	27.8	2.4	0.8	12.7	14.3	0.0	0.0	0.0

Intervention	cells/μL (Mean)
ATV+COBI+FTC/TDF	310
ATV+RTV+FTC/TDF	332

Intervention	cells/μL (Mean)
ATV+COBI+FTC/TDF	350
ATV+RTV+FTC/TDF	343

Intervention	cells/μL (Mean)
ATV+COBI+FTC/TDF	213
ATV+RTV+FTC/TDF	219

Intervention	cells/μL (Mean)
ATV+COBI+FTC/TDF	277
ATV+RTV+FTC/TDF	287

The percentage of participants with HIV-1 RNA < 50 copies/mL at Week 144 was analyzed using the snapshot algorithm. (NCT01108510)
Timeframe: Week 144

Percentage of Participants With HIV-1 RNA < 50 Copies/mL at Week 192

Intervention	percentage of participants (Number)
ATV+COBI+FTC/TDF	72.1
ATV+RTV+FTC/TDF	74.1

The percentage of participants with HIV-1 RNA < 50 copies/mL at Week 192 was analyzed using the snapshot algorithm. (NCT01108510)
Timeframe: Week 192

Percentage of Participants With HIV-1 RNA < 50 Copies/mL at Week 48

Intervention	percentage of participants (Number)
ATV+COBI+FTC/TDF	71.6
ATV+RTV+FTC/TDF	79.7

The percentage of participants with HIV-1 RNA < 50 copies/mL at Week 48 was analyzed using the snapshot algorithm, which defines a participant's virologic response status using only the viral load at the prespecified time point within an allowed window of time, along with study drug discontinuation status. (NCT01108510)
Timeframe: Week 48

Percentage of Participants With HIV-1 RNA < 50 Copies/mL at Week 96

Intervention	percentage of participants (Number)
ATV+COBI+FTC/TDF	85.2
ATV+RTV+FTC/TDF	87.4

The percentage of participants with HIV-1 RNA < 50 copies/mL at Week 96 was analyzed using the snapshot algorithm. (NCT01108510)
Timeframe: Week 96

Number of Subjects Developing Any Treatment-related Grade 3-4 Adverse Events

Number of Subjects Needing to Switch Comparator Drugs (FPV/r or EFV)

Intervention	percentage of participants (Number)
ATV+COBI+FTC/TDF	77.9
ATV+RTV+FTC/TDF	79.3

Intervention	participants (Number)
Once Daily (QD) Regimen of Lexiva	2
QD Regimen of Sustiva	3

"Subjects were randomized and initiated treatment on one of the antiretroviral arms(FPV/r or EFV) at study Entry visit. Subjects would be switched for the follwing reasons:~To resolve a Grade 3 or 4 Adverse Event~The subject experienced a virologic failure (as defined in section 3.6.2)~The investigator believes the subject is at a significant risk for failing to comply with the protocol AND the investigator believes a regimen substitution is likely to resolve the compliance issue~The investigator believes there is any other significant safety concern for the subject associated with remaining on the current regimen (e.g., hypersensitivity reaction, increased risk of suicide)" (NCT00727597)
Timeframe: 96 weeks

Number of Participants Who Permanently Discontinued the Treatment Due to Adverse Event

Intervention	participants (Number)
Once Daily (QD) Regimen of Lexiva	1
QD Regimen of Sustiva	2

An AE is any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product and which does not necessarily have a causal relationship with this treatment. An AE can therefore be any unfavorable and unintended sign (that could include a clinically significant abnormal laboratory finding), symptom, or disease temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. (NCT00071760)
Timeframe: Day 1 and up to Week 684

Number of Participants Who Permanently Discontinued the Treatment Due to an AE

Intervention	Participants (Count of Participants)
Cohort 2, Arm A - 4 Weeks to <6 Months	1
Cohort 1, Arm A - 6 Months to <2 Years	1

Number of Participants With the Indicated Treatment-emergent (TE) Grade 3/4 Adverse Events (AE)

Intervention	participants (Number)
Cohort 2, Arm A - 4 Weeks to <6 Months	1
Cohort 1, Arm A - 6 Months to <2 Years	2

An AE is any untoward medical occurrence in a patient or clinical investigation subject, temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. An AE is considered TE if it has an onset date on or after the date of the first dose of study drug, and on or before the date of the final dose of study drug. As per the Division of AIDS Table for Grading the Severity of Adult and Pediatric AEs, Grade 3=severe; Grade 4=potentially life-threatening. (NCT00071760)
Timeframe: Baseline (Day 1) until Week 48

Number of Participants With Treatment Emergent Adverse Events (AEs)

Intervention	participants (Number)
Cohort 2, Arm A - 4 Weeks to <6 Months	11
Cohort 1, Arm A - 6 Months to <2 Years	10

Number of Participants With Treatment Limiting Toxicities

Intervention	Participants (Count of Participants)
Cohort 2, Arm A - 4 Weeks to <6 Months	25
Cohort 1, Arm A - 6 Months to <2 Years	29

Treatment limiting toxicities are defined as those that are related to investigational medicinal products and deemed to be unacceptable, leading to restriction of further dose escalation. (NCT00071760)
Timeframe: Day 1 and up to Week 684

Absolute Values of Alanine Amino Transferase (ALT) and Aspartate Amino Transferase (AST) at Baseline (Day 1), Weeks 4, 12, 24, 36, and 48

Intervention	Participants (Count of Participants)
Cohort 2, Arm A - 4 Weeks to <6 Months	0
Cohort 1, Arm A - 6 Months to <2 Years	0

Blood samples of the participants were collected for the evaluation of ALT and AST. Clinical chemistry analyses were carried out using the observed analysis strategy. (NCT00071760)
Timeframe: Baseline (Day 1) and Weeks 4, 12, 24, 36, and 48

Absolute Values of Cholesterol, Glucose, High Density Lipoprotein (HDL) Cholesterol, Low Density Lipoprotein (LDL) and Triglyceride (TG) at Baseline (Day 1), Weeks 4, 12, 24, 36, and 48

Intervention	International units per liter (IU/L) (Median)
	ALT, Day 1; n=26;30	ALT, Week 4; n=23;28	ALT, Week 12; n=22;27	ALT, Week 24; n=22;26	ALT, Week 36; n=20;25	ALT, Week 48; n=18;24	AST, Day 1; n=26;30	AST, Week 4; n=23;28	AST, Week 12; n=22;27	AST, Week 24; n=22;26	AST, Week 36; n=20;24	AST, Week 48; n=18;23
Cohort 1, Arm A - 6 Months to <2 Years	20.0	15.5	15.0	15.5	16.0	16.0	44.0	35.0	40.0	36.5	34.0	34.0
Cohort 2, Arm A - 4 Weeks to <6 Months	22.0	14.0	15.0	16.0	15.5	15.0	43.5	32.0	35.0	34.0	35.0	34.5

Blood samples of all participants were generally collected under non-fasting conditions (given the age of participants) for the evaluation of cholesterol, serum glucose, HDL cholesterol, LDL cholesterol and triglyceride (TG). Clinical chemistry analyses were carried out using the observed analysis strategy. (NCT00071760)
Timeframe: Baseline (Day 1) and Weeks 4, 12, 24, 36, and 48

Absolute Values of Cholesterol, Glucose, High Density Lipoprotein (HDL) Cholesterol, Low Density Lipoprotein (LDL) and Triglyceride (TG) at Baseline (Day 1), Weeks 4, 12, 24, 36, and 48

Intervention	Millimoles per liter (mmol/L) (Median)
	Cholesterol, Day 1; n=22;29	Cholesterol, Week 4; n=4;2	Cholesterol, Week 24; n=22;26	Cholesterol, Week 36; n=3;2	Cholesterol, Week 48; n=18;24	Glucose, Day 1; n=26;30	Glucose, Week 4; n=23;28	Glucose, Week 12; n=22;27	Glucose, Week 24; n=22;26	Glucose, Week 36; n=20;25	Glucose, Week 48; n=18;24	HDL, Day 1; n=22;29	HDL, Week 4; n=4;2	HDL, Week 24; n=22;26	HDL, Week 36; n=3;2	HDL, Week 48; n=18;24	LDL, Day 1; n=22;28	LDL, Week 4; n=4;2	LDL, Week 24; n=22;26	LDL, Week 36; n=3;2	LDL, Week 48; n=18;24	TG, Day 1; n=22;29	TG, Week 4; n=4;2	TG, Week 24; n=22;26	TG, Week 36; n=3;2	TG, Week 48; n=18;24
Cohort 2, Arm A - 4 Weeks to <6 Months	2.235	3.085	4.175	3.030	3.890	4.80	4.60	4.70	4.55	4.50	4.45	0.655	0.825	0.900	0.640	0.825	0.90	1.25	2.08	1.90	2.33	1.695	2.015	2.155	1.310	1.590

Absolute Values of Cluster of Differentiation 4 (CD4+) Cell Counts by Study Visit

Intervention	Millimoles per liter (mmol/L) (Median)
	Cholesterol, Day 1; n=22;29	Cholesterol, Week 4; n=4;2	Cholesterol, Week 12; n=0;2	Cholesterol, Week 24; n=22;26	Cholesterol, Week 36; n=3;2	Cholesterol, Week 48; n=18;24	Glucose, Day 1; n=26;30	Glucose, Week 4; n=23;28	Glucose, Week 12; n=22;27	Glucose, Week 24; n=22;26	Glucose, Week 36; n=20;25	Glucose, Week 48; n=18;24	HDL, Day 1; n=22;29	HDL, Week 4; n=4;2	HDL, Week 12; n=0;2	HDL, Week 24; n=22;26	HDL, Week 36; n=3;2	HDL, Week 48; n=18;24	LDL, Day 1; n=22;28	LDL, Week 4; n=4;2	LDL, Week 12; n=0;2	LDL, Week 24; n=22;26	LDL, Week 36; n=3;2	LDL, Week 48; n=18;24	TG, Day 1; n=22;29	TG, Week 4; n=4;2	TG, Week 12; n=0;2	TG, Week 24; n=22;26	TG, Week 36; n=3;2	TG, Week 48; n=18;24
Cohort 1, Arm A - 6 Months to <2 Years	2.910	3.885	3.950	4.000	3.150	4.750	4.70	4.80	4.70	4.30	4.60	4.70	0.680	0.690	0.775	0.960	0.805	1.050	1.50	2.45	2.33	2.32	2.08	2.80	1.650	1.645	1.810	1.550	1.700	1.390

Blood samples of participants were collected for the measurement of the CD4+ cells. (NCT00071760)
Timeframe: Baseline (Day 1) and up to week 684

Absolute Values of Cluster of Differentiation 4 (CD4+) Cell Counts by Study Visit

Intervention	Cells/cubic millimeter (Median)
	Baseline (Day 1)	Week 4	Week 12	Week 24	Week 36	Week 48	Week 60	Week 72	Week 84	Week 96	Week 108	Week 120	Week 132	Week 144	Week 156	Week 168	Week 180	Week 192	Week 204	Week 216	Week 228	Week 240	Week 252	Week 264	Week 276	Week 288	Week 300	Week 312	Week 324	Week 336	Week 348	Week 360	Week 372	Week 384	Week 396	Week 408	Week 420	Week 432	Week 444	Week 456	Week 468	Week 480	Week 492	Week 504	Week 516	Week 528	Week 540	Week 552	Week 564	Week 576	Week 588	Week 600	Week 612	Week 624	Week 636	Week 648	Week 660
Cohort 2, Arm A - 4 Weeks to <6 Months	1378	1610	1405	1595	1780	1690	1890	1407	1560	1530	1440	1480	1285	1250	1422	1550	1331.5	1339	1160	1336	1136	1132.5	1379	1109	1180.5	1063	1062	924	980	856	1030	1151	1051	950	971	1005	840	940.5	811	1003	910	1063.5	839	887	776	860	851	756	908	792	873	865.5	720	753	770	720	750

Blood samples of participants were collected for the measurement of the CD4+ cells. (NCT00071760)
Timeframe: Baseline (Day 1) and up to week 684

Absolute Values of Serum Lipase at Baseline (Day 1), Weeks 4, 12, 24, and 48

Blood samples of all participants were collected for the evaluation of serum lipase. Clinical chemistry analyses were carried out using the observed analysis strategy. Change from Baseline in serum lipase was calculated as the value at the indicated time point minus the value at Baseline. (NCT00071760)
Timeframe: Baseline (Day 1) and Weeks 4, 12, 24, and 48

Absolute Values of Serum Lipase at Baseline (Day 1), Weeks 4, 12, 24, and 48

Change From Baseline in Plasma HIV-1 RNA Levels at Each Study Visit

Blood samples of participants were collected to measure plasma HIV-1 RNA copies. Baseline value was defined as the value observed at the day 1 visit or if this value is missing the last value observed before the start of investigational product. Change from baseline value was defined as post-dose value minus baseline value. (NCT00071760)
Timeframe: Baseline (Day 1) and up to Week 684

Change From Baseline in Plasma HIV-1 RNA Levels at Each Study Visit

Median Change From Baseline in Plasma HIV-1 RNA (log10 Copies/mL) at Weeks 4, 12, 24, 36, and 48 (Observed Analysis)

Blood samples of participants were collected to assess the decrease in the number of HIV-1 RNA copies. Change from Baseline in plasma HIV-1 RNA was calculated as the value at the indicated time point minus the value at Baseline. (NCT00071760)
Timeframe: Baseline and Weeks 4, 12, 24, 36, and 48

Median Percent Change From Baseline in CD4+ Cell Count at Weeks 4, 12, 24, 36, and 48

Blood samples of participants were collected for the measurement of the percentage of total lymphocytes that are CD4+ cells. Observed analysis was used for the summary of proportion endpoints using viral load data. Change from Baseline in percentage was calculated as the value at indicated time points minus the value at Baseline. (NCT00071760)
Timeframe: Baseline and Weeks 4, 12, 24, 36, and 48

Median Percent Cluster of Differentiation Antigen 4 (CD4+) Cell Count at Baseline and at Weeks 4, 12, 24, 36, and 48

Blood samples of participants were collected for the measurement of the percentage of total lymphocytes that are CD4+ cells. Observed analysis was used for the summary of proportion endpoints using viral load data. CD4+ cells are white blood cells that are important in fighting infection. HIV infects CD4+ cells, replicates in them, and destroys them. A CD4+ cell count provides a measure of the status of the immune system and to what extent it is affected by HIV. (NCT00071760)
Timeframe: Baseline and Weeks 4, 12, 24, 36, and 48

Median Plasma HIV-1 RNA (log10 Copies/mL) at Baseline and Weeks 4, 12, 24, 36, and 48 (Observed Analysis)

Blood samples of participants were collected to assess the decrease in the number of HIV-1 RNA copies. (NCT00071760)
Timeframe: Baseline and Weeks 4, 12, 24, 36, and 48

Number of Confirmed Virologic Failure Participants (Par.) With Treatment-emergent HIV Genotypic Resistance in Reverse Transcriptase and Protease

A blood sample was drawn for par. failing to respond to therapy, and the mutations present in the virus were identified. For each par., the mutations found at the time of failure were compared with any mutations found in the blood sample at baseline. New International AIDS Society-USA defined resistance mutations that developed at the time of failure were tabulated by drug class. VF, virologic failure; NRTI, nucleoside reverse transcriptase inhibitor; NNRTI, non-nucleoside reverse transcriptase inhibitor; PI, protease inhibitor. Par. are grouped by study arm and prior therapy experience. (NCT00071760)
Timeframe: Baseline through Week 48

Number of Confirmed Virologic Failure Participants (Par.) With Treatment-emergent Reductions in Drug Susceptibility (DS)

A blood sample was drawn for par. failing to respond to therapy, and changes in DS for HIV isolated from the par. for each drug used in the study were assessed. The changes in DS detected by phenotypic assay in virus from the sample collected at the time of failure was compared with DS in the virus from the blood sample at baseline. Par. are grouped by study arm and prior therapy experience. DS is the state of HIV being susceptible to the antiretroviral agent (the virus can be inhibited by the drug). Reduced DS (i.e., HIV is resistant to the antiretroviral agent) can lead to treatment failure. (NCT00071760)
Timeframe: Baseline through Week 48

Number of Participants Reporting Perfect Adherence at Weeks 2, 12, 24, and 48 as Assessed by the Study Coordinator Using the Adherence Questionnaire

A separate questionnaire was administered for FPV and RTV. Items 1-4 of the Adherence Questionnaire measured a participant's adherence with FPV or RTV during the last 3 days and the weekend prior to the indicated study visits. Perfect adherence was defined as not missing any doses of FPV or RTV since the last study visit. (NCT00071760)
Timeframe: Weeks 2, 12, 24, and 48

Number of Participants With at Least a 1.0 log10 HIV-1 RNA Decrease From Baseline at Weeks 4, 12, 24, 36, and 48 (MSD=F Analysis)

Blood samples of participants were collected to assess the decrease in the number of HIV-1 RNA copies. In the MSD=F analysis, participants who had missing data at or had discontinued the study prior to a certain time point or had changed their background antiretroviral regimen are classified as non-responders. (NCT00071760)
Timeframe: Baseline and Weeks 4, 12, 24, 36, and 48

Number of Participants With Clinical Chemistry Toxicities

Blood samples were collected for the analysis of all clinical chemistry parameters. Laboratory toxicities were graded using the Division of AIDS (DAIDS) table for grading the severity of adult and pediatric adverse events, where grade 1=mild, grade 2=moderate, grade 3=severe and grade 4=potentially life-threatening. Results for participants with Grade 1 to 4 clinical chemistry toxicities is presented. (NCT00071760)
Timeframe: Day 1 and up to Week 684

Number of Participants With Hematology Toxicities

Blood samples were collected for the analysis of all hematology parameters. Laboratory toxicities were graded using the DAIDS Table for grading the severity of adult and pediatric adverse events, where grade 1=mild, grade 2=moderate, grade 3=severe and grade 4=potentially life-threatening. Results for participants with Grade 1 to 4 hematology toxicities is presented. (NCT00071760)
Timeframe: Day 1 and up to Week 684

Number of Participants With Plasma HIV-1 Ribonucleic Acid (RNA) <400 Copies Per Milliliter at Baseline and Weeks 4, 12, 24, 36, and 48 (MSD=F)

Blood samples of participants were collected to measure plasma HIV-1 RNA concentrations. Viral load, measured in RNA copies per milliliter of plasma, is an efficacy measure for antiretroviral drugs. In the Missing, Switch, or Discontinuation=Failure (MSD=F) analysis, participants who had missing data at or had discontinued the study prior to a certain time point or had changed their background antiretroviral regimen are classified as non-responders. (NCT00071760)
Timeframe: Baseline and Weeks 4, 12, 24, 36, and 48

Number of Participants With Plasma Human Immuno Virus Type 1 (HIV-1) Ribonucleic Acid (RNA) Levels < 400 Copies/Milliliter at Each Study Visit

Blood samples of participants were collected to measure plasma HIV-1 RNA concentrations. (NCT00071760)
Timeframe: Baseline (Day 1) and up to Week 684

Number of Participants With the Indicated Response Scores for the Parent/Guardian (P/G) Perception of FPV Oral Suspension Questionnaire: Items 1 to 4

P/G perceptions of FPV/RTV BID were assessed using a P/G Perception of Study Medication questionnaire administered during Weeks 2, 24, and 48/premature study discontinuation. Questions 1 to 4 ask directly about the P/G's assessment of 1=color, 2=texture/consistency, 3=odor, and 4=general satisfaction. Questions 5 to 10 ask about the P/G's perception of the child's assessment of the oral suspension. Data are reported as the number of participants with the indicated response by question, response category (1-3=dislike, 4=neutral, 5-7=like), and timing of visit. (NCT00071760)
Timeframe: Weeks 2, 24, and 48/premature study discontinuation

Number of Participants With the Indicated Response Scores for the Parent/Guardian Perception of the Child's Assessment of FPV Oral Suspension Questionnaire: Items (I) 5 to 10

Parent/guardian perceptions of FPV/RTV BID was assessed using a Parent/Guardian Perception of Study Medication questionnaire. Questions 1 to 4 ask directly about the parent/guardian's assessment of the color, texture/consistency, odor, and general satisfaction. Questions 5 to 10 ask about the parent/guardian's perception of the child's assessment of the oral suspension (Items: 5=reaction to new medicine [med.]; 6=taste; 7=acceptance; 8=swallowing; 9=willingness compared to other med.; 10=overall liking. Data for items 6/10 are reported in response categories: 1-3=dislike; 4=neutral; 5-7=like. (NCT00071760)
Timeframe: Weeks (W) 2, 24, and 48/premature study discontinuation

Number of Participants With the Indicated Treatment-emergent (TE) Grade 3/4 Laboratory Abnormalities

TE toxicities were presented for each laboratory parameter. A toxicity was considered TE if it was greater than the Baseline grade, and if it was observed on/after the date of the first dose of study drug (SD), and on/before the date of the last dose of SD. Per the Division of AIDS Table for Grading the Severity of Adult and Pediatric AEs, Grade 3=severe; Grade 4=potentially life-threatening. (NCT00071760)
Timeframe: Baseline (Day 1) until Week 48

Number of Participants With the Indicated Virological Outcome at Week 48

Blood samples of participants were collected to measure plasma HIV-1 RNA concentrations. PI-exp = PI-experienced. Virologic success was defined as plasma HIV-1 RNA <400 copies/mL. Virologic failure: (1) HIV-1 RNA >=400 copies/mL, (2) change of background antiretroviral treatment (ART), (3) discontinued study due to lack of efficacy, (4) discontinued study with last HIV-1 >=400 copies/mL. No virologic data at Week 48 window: (a) discontinued study due to an adverse event or death, (b) discontinued study due to other reasons (withdrew consent, loss to follow-up, moved, etc.). (NCT00071760)
Timeframe: Week 48

Number of Participants With Treatment-Emergent Changes in HIV-1 Phenotypic Drug Susceptibility

A blood sample was drawn from participant failing to respond to therapy, and the mutations present in the virus were identified. Phenotypic resistance was assessed for virologic failure population and evaluated for Protease Inhibitors (PIs), Nucleotide reverse transcriptase inhibitors (NRTIs), and non-NRTIs (NNTRIs) using Monogram PhenoSense Assay. Virologic failure was defined as having failed to achieve a plasma HIV-RNA of <400 copies/mL by Week 24 or having had a confirmed HIV-RNA rebound to ≥400 c/mL at any time after achieving a plasma HIV-RNA of <400 c/mL. (NCT00071760)
Timeframe: Post-Week 48 to Week 684

Number of Participants With Treatment-Emergent Mutations at Virologic Failure Timepoint

A blood sample was drawn from participants failing to respond to therapy, and genotyping was performed to identify the mutations present in the baseline (pre-therapy) and the sample obtained at virologic failure (VF). For each participant, the HIV-1 mutations found at the time of failure were compared with any HIV-1 mutations detected in the blood sample at baseline. New International AIDS Society-USA defined resistance mutations that developed at the time of failure were tabulated by drug class- NRTI, nucleoside reverse transcriptase inhibitor; NNRTI, non-nucleoside reverse transcriptase inhibitor; PI, protease inhibitor. Participants are grouped by study arm (prior therapy experience), results displayed in this table are from participants who met virologic failure criteria from Week 48 through Week 684. (NCT00071760)
Timeframe: Week 48 to Week 684

Plasma Amprenavir (APV) AUC (0-tau[τ])

"Plasma samples were assayed for APV concentrations using a validated assay. The GlaxoSmithKline (GSK) Department of Clinical Pharmacology Modeling and Simulation conducted pharmacokinetic (PK) analysis of the plasma APV concentration-time data using a model-independent approach. As a measure of total drug exposure, the area under the plasma-concentration-versus-time curve over the dosing interval at steady-state (AUC[0-τ]), where τ is the length of the dosing interval, was calculated by the linear up/log down trapezoidal method. hours, hr." (NCT00071760)
Timeframe: Week 48

Plasma Amprenavir (APV) AUC (0-tau[τ])

Plasma APV CL/F Following Dosing Expressed in mL/Min

Apparent clearance of drug from plasma following extravascular administration (CL/F) was calculated as dose/AUC(0-τ). For FPV, doses were expressed in APV molar equivalents (50 mg of FPV = 43.2 mg of APV). (NCT00071760)
Timeframe: Week 48

Plasma APV CL/F Following Dosing Expressed in mL/Min

Plasma APV CL/F Following Dosing Expressed in mL/Min/kg

Apparent clearance of drug from plasma following extravascular administration (CL/F) was calculated using the formulation: APV Dose in mg/kg units divided by AUC(0-τ). For FPV, doses were expressed in APV molar equivalents (50 mg of FPV = 43.2 mg of APV). Normalizing CL/F for bodyweight allows for comparison of CL/F across populations. (NCT00071760)
Timeframe: Week 48

Plasma APV CL/F Following Dosing Expressed in mL/Min/kg

Plasma APV Cmax

The maximum concentration at steady state (Cmax) was measured. (NCT00071760)
Timeframe: Week 48

Plasma APV Cmax

The maximum concentration at steady state (Cmax) was measured. (NCT00071760)
Timeframe: Week 48

Plasma APV Cτ

The plasma concentration at the end of the dosing interval at steady state (Cτ) was measured. (NCT00071760)
Timeframe: Week 48

Plasma APV Cτ

The plasma concentration at the end of the dosing interval at steady state (Cτ) was measured. (NCT00071760)
Timeframe: Week 48

Plasma Ritonavir (RTV) AUC (0-τ)

Plasma samples were assayed for RTV concentrations using a validated assay. The GSK Department of Clinical Pharmacology Modeling and Simulation conducted PK analysis of the plasma RTV concentration-time data using a model-independent approach. As a measure of total drug exposure, the area under the plasma-concentration-versus-time curve over the dosing interval at steady-state (AUC[0-τ]), where τ is the length of the dosing interval, was calculated by the linear up/log down trapezoidal method. (NCT00071760)
Timeframe: Week 48

Plasma RTV CL/F Expressed in mL/Min

Apparent clearance of drug from plasma following extravascular administration (CL/F) was calculated as dose in mg/kg units divided by AUC(0-τ). (NCT00071760)
Timeframe: Week 48

Plasma RTV CL/F Expressed in mL/Min/kg

Apparent clearance of drug from plasma following extravascular administration (CL/F) was calculated as dose in mg/kg units divided by AUC(0-τ). Normalizing CL/F for bodyweight allows for comparison of CL/F across populations. (NCT00071760)
Timeframe: Week 48

Plasma RTV Cmax

The maximum concentration at steady state (Cmax) was measured. (NCT00071760)
Timeframe: Week 48

Plasma RTV Cτ

The plasma concentration at the end of the dosing interval at steady state (Cτ) was measured. (NCT00071760)
Timeframe: Week 48

Plasma Unbound APV Cτ

"Participants who are <2 years old may have reduced protein binding; therefore, plasma unbound APV concentrations were measured to determine dosing recommendations at acceptable dosing volumes. Unbound or free APV is the fraction of drug that is not bound to protein. Cτ is the plasma concentration at the end of the dosing interval at steady state." (NCT00071760)
Timeframe: Week 48

Plasma Unbound APV Cτ

Plasma Unbound APV Percent Protein Binding (%Cτ)

Participants who are <2 years old may have reduced protein binding; therefore, plasma unbound APV concentrations were measured to determine dosing recommendations at acceptable dosing volumes. APV %Cτ unbound is the percentage of the total APV Cτ that is unbound. (NCT00071760)
Timeframe: Week 48

Plasma Unbound APV Percent Protein Binding (%Cτ)

Change From Baseline in Serum Lipase at Week 48

Blood samples of all participants were collected for the evaluation of serum lipase. Clinical chemistry analyses were carried out using the observed analysis strategy. Change from Baseline in serum lipase was calculated as the value at Week 48 minus the value at Baseline. (NCT00089583)
Timeframe: Baseline (Day 1) and Week 48

Number of Participants Who Permanently Discontinued the Treatment Due to Any Adverse Event (AE)

Change From Baseline in Aspartate Aminotransferase (AST) and Alanine Aminotransferase (ALT) at Week 48

Blood samples of the participants were collected for the evaluation of AST and ALT. Clinical chemistry analyses were carried out using the observed analysis strategy. Change from Baseline in AST and ALT was calculated as the value at Week 48 minus the value at Baseline. (NCT00089583)
Timeframe: Baseline (Day 1) and Week 48

Change From Baseline in CD4+ Cell Count at Weeks 2, 12, 24, and 48

Blood samples of participants were collected for the measurement of CD4+ cell count. Observed analysis was used for the summary of proportion endpoints using viral load data. Change from Baseline was calculated as the value at Weeks 2, 12, 24, and 48 minus the value at Baseline. (NCT00089583)
Timeframe: Baseline and Weeks 2, 12, 24, and 48

Change From Baseline in the Percentage of Total Lymphocytes (TLs) That Are CD4+ Cells at Weeks 2, 12, 24, and 48

Blood samples of participants were collected for the measurement of the percentage of total lymphocytes that are CD4+ cells. Observed analysis was used for the summary of proportion endpoints using viral load data. Change from Baseline in percentage was calculated as the value at Weeks 2, 12, 24, and 48 minus the value at Baseline. (NCT00089583)
Timeframe: Baseline and Week 2, 12, 24, 48

Change From Baseline in Triglycerides, Total Cholesterol, Low-density Lipoprotein (LDL) Cholesterol, High-density Lipoprotein (HDL) Cholesterol, and Serum Glucose at Week 48

Blood samples of all participants were collected under fasting conditions for the evaluation of triglycerides, total cholesterol, HDL cholesterol, LDL cholesterol, and serum glucose. Clinical chemistry analyses were carried out using the observed analysis strategy. Change from Baseline in triglycerides, total cholesterol, HDL cholesterol, LDL cholesterol, and serum glucose was calculated as the value at Week 48 minus the value at Baseline. (NCT00089583)
Timeframe: Baseline (Day 1) and Week 48

Cluster of Differentiation Antigen 4 (CD4+) Cell Count at Baseline and at Weeks 2, 12, 24, and 48

Blood samples of participants were collected for the measurement of CD4+ cell count. Observed analysis was used for the summary of proportion endpoints using viral load data. CD4+ cells are white blood cells that are important in fighting infection. HIV infects CD4+ cells, replicates in them, and destroys them. CD4+ cell count provides a measure of the status of the immune system and to what extent it is affected by HIV. (NCT00089583)
Timeframe: Baseline and Weeks 2, 12, 24, and 48

Median Change From Plasma HIV-1 RNA (log10 Copies/mL) at Weeks 2, 12, 24, and 48 (Observed Analysis)

Blood samples of participants were collected to assess the decrease in the number of HIV-1 RNA. Change from Baseline at Weeks 2, 12, 24, and 48 was calculated as value at Week 2, 12, 24, and 48 minus the value at Baseline. (NCT00089583)
Timeframe: Baseline and Weeks 2, 12, 24, and 48

Median Plasma HIV-1 RNA (log10 Copies/mL) at Baseline and Weeks 2, 12, 24, and 48 (Observed Analysis)

Blood samples of participants were collected to assess the decrease in the number of HIV-1 RNA. (NCT00089583)
Timeframe: Baseline and Weeks 2, 12, 24, and 48

Number of Confirmed Virologic Failure Participants (Par.) Since the Week 48 Analysis With Treatment-emergent HIV Genotypic Resistance in Reverse Transcriptase and Protease

A blood sample was drawn for par. remaining in the study after Week 48 and failing to respond to therapy, and the mutations present in the virus were identified. For each par., the mutations found at the time of failure were compared with any mutations found in the blood sample at baseline. New International AIDS Society-USA defined resistance mutations that developed at the time of failure were tabulated by drug class. VF, virologic failure; NRTI, nucleoside reverse transcriptase inhibitor; NNRTI, non-nucleoside reverse transcriptase inhibitor; PI, protease inhibitor. Par. are grouped by study arm and prior therapy experience. (NCT00089583)
Timeframe: After Week 48 through Week 240

Number of Confirmed Virologic Failure Participants (Par.) Since the Week 48 Analysis With Treatment-emergent Reductions in Drug Susceptibility (DS)

A blood sample was drawn for par. remaining in the study after Week 48 and failing to respond to therapy, and changes in DS for HIV isolated from the par. for each drug used in the study were assessed. The changes in DS detected by phenotypic assay in virus from the sample collected at the time of failure was compared with DS in the virus from the blood sample at baseline. Par. are grouped by study arm and prior therapy experience. DS is the state of HIV being susceptible to the antiretroviral agent (the virus can be inhibited by the drug). Reduced DS (i.e., HIV is resistant to the antiretroviral agent) can lead to treatment failure. (NCT00089583)
Timeframe: Week 60 through Week 240

Number of Confirmed Virologic Failure Participants (Par.) With Treatment-emergent HIV Genotypic Resistance in Reverse Transcriptase and Protease

Number of Confirmed Virologic Failure Participants (Par.) With Treatment-emergent Reductions in Drug Susceptibility (DS)

Number of Participants (Par.) With Plasma HIV-1 Ribonucleic Acid (RNA) <400 Copies Per Milliliter at Baseline and Weeks 2,12, 24, and 48 (MSD=F)

Blood samples of participants were collected to measure plasma HIV-1 RNA concentrations. PI-exp = PI-experienced. Viral load, measured in RNA copies per milliliter of plasma, is an efficacy measure for antiretroviral drugs. In the Missing, Switch, or Discontinuation = Failure (MSD=F) analysis, participants who had missing data at or had discontinued the study prior to a certain time point or had changed their background antiretroviral regimen are classified as non-responders. (NCT00089583)
Timeframe: Baseline and Weeks 2, 12, 24, and 48

Number of Participants (Par.) With Virological Outcome (Plasma HIV-1 Ribonucleic Acid [RNA] <400 Copies/mL) at Week 48

Blood samples of participants were collected to measure plasma HIV-1 RNA concentrations. PI-exp = PI-experienced.Virologic success was defined as plasma HIV-1 RNA <400 copies/mL. Virologic failure: (1) HIV-1 RNA >=400 copies/mL, (2) change of background antiretroviral treatment (ART), (3) discontinued study due to lack of efficacy, (4) discontinued study with last HIV-1 >=400 copies/mL. No virologic data at Week 48 window: (a) discontinued study due to an adverse event or death, (b) discontinued study due to other reasons, (c) missing data during window but still on study. (NCT00089583)
Timeframe: Week 48

Number of Participants Reporting Perfect Adherence Over the 3 Days Prior to the Study Visits at Weeks 2, 12, 24, and 48 as Assessed by Study Coordinator Using the Pediatric AIDS Clinical Trials Group (PACTG) Adherence Questionnaire

The PACTG Adherence Questionnaire records individual study drugs, the expected number of doses/24 hour period, and the number of doses missed in the 3 days prior to the study visit. Responses were summarized by age cohort, study drug, treatment regimen, and visit for exploratory analysis only. (NCT00089583)
Timeframe: Weeks 2, 12, 24, and 48

Number of Participants With at Least a 1.0 log10 HIV-1 RNA Decrease From Baseline at Weeks 2, 12, 24, and 48 (Observed Analysis)

Blood samples of participants were collected to assess the decrease in the number of HIV-1 RNA. (NCT00089583)
Timeframe: Baseline and Weeks 2, 12, 24, and 48

Number of Participants With Treatment-emergent (TE) Grade 3/4 Clinical Chemistry Laboratory Abnormalities

"A toxicity was considered TE if it was > than the Baseline grade, and if it was observed on/after the date of the first dose of study drug (SD), and on/before the date of the last dose of SD. Leucopenia is the decrease in the number of leucocytes (white blood cells [WBCs]); neutropenia is the decrease in the number of neutrophils (type of WBCs). Per the Division of AIDS Table for Grading the Severity of Adult and Pediatric AEs: Grade 3 is severe; Grade 4 is potentially life-threatening. ULN, upper limit of normal; LDL, low-density lipoprotein; PC, platelet count." (NCT00089583)
Timeframe: Baseline (Day 1) until Week 48

Percentage of Total Lymphocytes (TLs) That Are CD4+ Cells at Baseline and Weeks 2, 12, 24, and 48

Plasma Amprenavir (APV) AUC (0-tau[τ])

Plasma samples were assayed for APV concentrations using a validated assay. The GlaxoSmithKline (GSK) Department of Clinical Pharmacology Modeling and Simulation conducted pharmacokinetic (PK) analysis of the plasma APV concentration-time data using a model-independent approach. As a measure of total drug exposure, the area under the plasma-concentration-versus-time curve over the dosing interval at steady-state (AUC[0-τ]), where τ is the length of the dosing interval, was calculated by the linear up/log down trapezoidal method. hr, hour; µg, micrograms; mL, milliliter. (NCT00089583)
Timeframe: Week 48

Plasma APV CL/F Following Dosing Expressed in mg

Plasma APV CL/F Following Dosing Expressed in mg/kg

Plasma APV Cmax

The maximum concentration at steady state (Cmax) was measured. (NCT00089583)
Timeframe: Week 48

Plasma APV Cτ

The plasma concentration at the end of the dosing interval at steady-state (Cτ) was measured. (NCT00089583)
Timeframe: Week 48

Plasma APV t1/2

The apparent terminal phase half-life (t1/2) is calculated as loge2/λz. The apparent terminal phase rate constant (λz) is the slope of the terminal portion of the logarithmically transformed concentration-time data as estimated by linear regression. (NCT00089583)
Timeframe: Week 48

Plasma APV Tmax

The time to reach the maximum concentration (Cmax) at steady state is defined as tmax. (NCT00089583)
Timeframe: Week 48

Plasma Ritonavir (RTV) AUC (0-τ)

Plasma samples were assayed for RTV concentrations using a validated assay. The GlaxoSmithKline (GSK) Department of Clinical Pharmacology Modeling and Simulation conducted pharmacokinetic (PK) analysis of the plasma RTV concentration-time data using a model-independent approach. As a measure of total drug exposure, the area under the plasma-concentration-versus-time curve over the dosing interval at steady-state (AUC[0-τ]), where τ is the length of the dosing interval, was calculated by the linear up/log down trapezoidal method. (NCT00089583)
Timeframe: Week 48

Plasma RTV CL/F Following Dosing Expressed in mg

Apparent clearance of drug from plasma following extravascular administration (CL/F) was calculated as dose/AUC(0-τ). (NCT00089583)
Timeframe: Week 48

Plasma RTV CL/F Following Dosing Expressed in mg/kg

Apparent clearance of drug from plasma following extravascular administration (CL/F) was calculated using the formulation: RTV Dose in mg/kg units divided by AUC(0-τ). Normalizing CL/F for bodyweight allows for comparison of CL/F across populations. (NCT00089583)
Timeframe: Week 48

Plasma RTV Cmax

The maximum concentration at steady state (Cmax) was measured. (NCT00089583)
Timeframe: Week 48

Plasma RTV Cτ

The plasma concentration at the end of the dosing interval at steady-state (Cτ) was measured. (NCT00089583)
Timeframe: Week 48

Plasma RTV t1/2

alf-life (t1/2) is calculated as loge2/λz. The apparent terminal phase rate constant (λz) is the slope of the terminal portion of the logarithmically transformed concentration-time data as estimated by linear regression. (NCT00089583)
Timeframe: Week 48

Plasma RTV Tmax

The time to reach the maximum concentration (Cmax) at steady state is defined as (tmax). (NCT00089583)
Timeframe: Week 48

Change From Baseline in CD4+ Cell Count at Week 48

Change From Baseline in CD4+ Cell Count at Week 96

Percentage of Participants With HIV-1 RNA < 50 Copies/mL at Week 48

The FDA-defined Snapshot algorithm was used, which defines a patient's virologic response status using only the viral load at the predefined time point within an allowed window of time. (NCT01475838)
Timeframe: Week 48

Percentage of Participants With HIV-1 RNA < 50 Copies/mL at Week 96

Change From Baseline in CD4+ Cell Count at Week 48

Change From Baseline in CD4+ Cell Count at Week 96

Percentage of Participants With HIV-1 RNA < 50 Copies/mL at Week 48

Percentage of Participants With HIV-1 RNA < 50 Copies/mL at Week 96

Number of Subjects Cured

Subjects with post-treatment sustained virologic response (SVR) = Number of subjects with negative HCV RNA 12 weeks after completing therapy / number of subjects treated post-kidney transplantation (NCT02743897)
Timeframe: Baseline to 24 weeks

Number of Subjects With SAE Attributable to HCV Therapy

Number of subjects with major adverse events attributable to HCV therapy in post-kidney transplant (NCT02743897)
Timeframe: Baseline to 52 weeks

Mean Time to First Achievement of Undetectable Hepatitis C Virus Ribonucleic Acid (HCV RNA)

Blood was drawn from each participant to assess HCV RNA plasma levels using the Roche COBAS™ Taqman™ HCV Test, v2.0 at various time points prior to, during, and after dosing. Kaplan Meier summary statistics were used to characterize the time to first achievement of undetectable HCV RNA. (NCT01717326)
Timeframe: From first dose of study medication until first achievement of undetectable HCV RNA (up to 18 weeks of treatment)

Percentage of Participants Achieving HCV RNA <25 IU/mL at Week 12

HCV-RNA levels in plasma were measured using the Roche COBAS™ Taqman™ HCV Test (v.2.0) on blood samples drawn from each participant during treatment at various time points prior to, during, and after dosing. The Roche COBAS Taqman HCV Test, v2.0 assay (High Pure System) had a LLoQ of 25 IU/mL and a limit of detection of 15.1 IU/mL (in plasma). The percentage of participants achieving HCV RNA levels <25 IU/ml and accompanying 95% CIs were reported at TW12 for each treatment arm of the PP Population (as applicable). 95% confidence intervals provided based on the Clopper-Pearson method. (NCT01717326)
Timeframe: Week 12

Percentage of Participants Achieving HCV RNA <25 IU/mL at Week 2

HCV-RNA levels in plasma were measured using the Roche COBAS™ Taqman™ HCV Test (v.2.0) on blood samples drawn from each participant during treatment at various time points prior to, during, and after dosing. The Roche COBAS Taqman HCV Test, v2.0 assay (High Pure System) had a LLoQ of 25 IU/mL and a limit of detection of 15.1 IU/mL (in plasma). The percentage of participants achieving HCV RNA levels <25 IU/ml and accompanying 95% CIs were reported at TW2 for each treatment arm of the PP Population. 95% confidence intervals provided based on the Clopper-Pearson method. (NCT01717326)
Timeframe: Week 2

Percentage of Participants Achieving HCV RNA <25 IU/mL at Week 4

HCV-RNA levels in plasma were measured using the Roche COBAS™ Taqman™ HCV Test (v.2.0) on blood samples drawn from each participant during treatment at various time points prior to, during, and after dosing. The Roche COBAS Taqman HCV Test, v2.0 assay (High Pure System) had a LLoQ of 25 IU/mL and a limit of detection of 15.1 IU/mL (in plasma). The percentage of participants achieving HCV RNA levels <25 IU/ml and accompanying 95% CIs were reported at TW4 for each treatment arm of the PP Population. 95% confidence intervals provided based on the Clopper-Pearson method. (NCT01717326)
Timeframe: Week 4

Percentage of Participants Achieving Sustained Virologic Response 12 Weeks After the End of All Study Therapy (SVR12)

Blood was drawn from each participant to assess Hepatitis C Virus ribonucleic acid (HCV RNA) plasma levels using the Roche COBAS™ Taqman™ HCV Test, v2.0 at various time points prior to, during, and after dosing. The Roche COBAS Taqman HCV Test, v2.0 assay (High Pure System) had a lower limit of quantification of 25 IU/mL and a limit of detection of 15.1 IU/mL (in plasma). SVR12 was defined as HCV RNA <25 IU/ml at 12 weeks after the end of all study therapy. 95% confidence intervals provided based on the Clopper-Pearson method. (NCT01717326)
Timeframe: 12 weeks after end of therapy (up to 30 weeks)

Percentage of Participants Achieving Sustained Virologic Response 24 Weeks After the End of All Study Therapy (SVR24)

Blood was drawn from each participant to assess Hepatitis C Virus ribonucleic acid (HCV RNA) plasma levels using the Roche COBAS™ Taqman™ HCV Test, v2.0 at various time points prior to, during, and after dosing. The Roche COBAS Taqman HCV Test, v2.0 assay (High Pure System) had a LLoQ of 25 IU/mL and a limit of detection of 15.1 IU/mL (in plasma). SVR24 was defined as HCV RNA <25 IU/ml at 24 weeks after the end of all study therapy. 95% confidence intervals provided based on the Clopper-Pearson method. (NCT01717326)
Timeframe: 24 weeks after end of therapy (up to 42 weeks)

Percentage of Participants Achieving Sustained Virologic Response 4 Weeks After the End of All Therapy (SVR4)

Blood was drawn from each participant to assess Hepatitis C Virus ribonucleic acid (HCV RNA) plasma levels using the Roche COBAS™ Taqman™ HCV Test, v2.0 at various time points prior to, during, and after dosing. The Roche COBAS Taqman HCV Test, v2.0 assay (High Pure System) had a LLoQ of 25 IU/mL and a limit of detection of 15.1 IU/mL (in plasma). SVR4 was defined as HCV RNA <25 IU/ml at 4 weeks after the end of all study therapy. 95% confidence intervals provided based on the Clopper-Pearson method. (NCT01717326)
Timeframe: 4 weeks after end of therapy (up to 22 weeks)

Percentage of Participants Achieving Undetectable HCV RNA at Week 12

HCV-RNA levels in plasma were measured using the Roche COBAS™ Taqman™ HCV Test (v.2.0) on blood samples drawn from each participant during treatment at various time points prior to, during, and after dosing. Undetectable HCV RNA was defined as below the 15.1 IU/ml limit of detection. The percentage of participants achieving undetectable HCV RNA and accompanying 95% CIs were reported at TW12 for each treatment arm of the PP Population (as applicable). 95% confidence intervals provided based on the Clopper-Pearson method. (NCT01717326)
Timeframe: Week 12

Percentage of Participants Achieving Undetectable HCV RNA at Week 2

HCV-RNA levels in plasma were measured using the Roche COBAS™ Taqman™ HCV Test (v.2.0) on blood samples drawn from each participant during treatment at various time points prior to, during, and after dosing. Undetectable HCV RNA was defined as below the 15.1 IU/ml limit of detection. The percentage of participants achieving undetectable HCV RNA and accompanying 95% CIs were reported at TW2 for each treatment arm of the PP Population. 95% confidence intervals provided based on the Clopper-Pearson method. (NCT01717326)
Timeframe: Week 2

Percentage of Participants Achieving Undetectable HCV RNA at Week 4

HCV-RNA levels in plasma were measured using the Roche COBAS™ Taqman™ HCV Test (v.2.0) on blood samples drawn from each participant during treatment at various time points prior to, during, and after dosing. Undetectable HCV RNA was defined as below the 15.1 IU/ml limit of detection. The percentage of participants achieving undetectable HCV RNA and accompanying 95% CIs were reported at TW4 for each treatment arm of the PP Population. 95% confidence intervals provided based on the Clopper-Pearson method. (NCT01717326)
Timeframe: Week 4

Percentage of Participants Discontinuing Study Therapy Due to an AE During the Treatment Period and First 14 Follow-up Days

An AE was defined as any unfavorable and unintended sign (including an abnormal laboratory finding, for example), symptom, or disease temporally associated with the use of a medicinal product or protocol-specified procedure, whether or not considered related to the medicinal product or protocol-specified procedure. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which is temporally associated with the use of the SPONSOR's product, was also an AE. (NCT01717326)
Timeframe: From Day 1 [post-dose] through 14 days following last dose of study drug (up to 20 weeks)

Percentage of Participants Experiencing at Least One Adverse Event (AE) During the Treatment Period and First 14 Follow-up Days

Number of Participants With Post-treatment Sustained Virologic Response (SVR)

The primary analysis will be based on a calculation of SVR rates (number of subjects with SVR; negative HCV RNA after completing Zepatier therapy) / (number of subjects treated with Zepatier post-heart transplantation) (NCT03146741)
Timeframe: Baseline to 24 weeks

Number of Severe Adverse Events (SAE) Attributable to HCV Therapy Post-heart Transplant

Percentage of Participants With HIV-1 RNA < 50 Copies/mL at Week 24 (Cohort 1)

The percentage of participants with HIV-1 RNA < 50 copies/mL at Week 24 was analyzed in Cohort 1 (treatment-naive) using the FDA snapshot analysis algorithm. (NCT01363011)
Timeframe: Week 24

Percentage of Participants With HIV-1 RNA < 50 Copies/mL at Week 24 (Cohort 2)

The percentage of participants with HIV-1 RNA < 50 copies/mL at Week 24 was analyzed in Cohort 2 (treatment-experienced) using the FDA snapshot analysis algorithm. (NCT01363011)
Timeframe: Week 24

Change From Baseline in Actual Glomerular Filtration Rate (aGFR) at Weeks 2, 4, and 24 (Cohort 1)

Change from baseline in aGFR at Weeks 2, 4, and 24 was analyzed in Cohort 1 (treatment-naive). aGFR was calculated using iohexol plasma clearance. (NCT01363011)
Timeframe: Baseline; Weeks 2, 4, and 24

Change From Baseline in aGFR at Weeks 2, 4, and 24 (Cohort 2)

Change from baseline in aGFR at Weeks 2, 4, and 24 was analyzed in Cohort 2 (treatment-experienced). aGFR was calculated using iohexol plasma clearance. (NCT01363011)
Timeframe: Baseline; Weeks 2, 4, and 24

Change From Baseline in eGFR Using the Chronic Kidney Disease, Epidemiology Collaboration (CKD-EPI) Formula Based on Cystatin C Equation at Week 24 (Cohort 1)

Change from baseline in eGFR-CKD-EPI based on cystatin C equation (not adjusted for age, sex, and race) at Week 24 was analyzed in Cohort 1 (treatment-naive). The calculation was normalized to 1.73 m^2 body surface area. (NCT01363011)
Timeframe: Baseline; Week 24

Change From Baseline in eGFR Using the Modification of Diet in Renal (MDRD) Equation at Week 24 (Cohort 1)

Change from baseline in eGFR-MDRD equation at Week 24 was analyzed in Cohort 1 (treatment-naive). The calculation was normalized to 1.73 m^2 body surface area. (NCT01363011)
Timeframe: Baseline; Week 24

Change From Baseline in eGFR-CG at Week 24 (Cohort 2)

Change from baseline in eGFR-CG equation at Week 24 was analyzed in Cohort 2 (treatment-experienced). (NCT01363011)
Timeframe: Baseline; Week 24

Change From Baseline in eGFR-CG at Weeks 48 and 96 (Cohort 1)

Change from baseline in eGFR-CG at Weeks 48 and 96 were analyzed in Cohort 1 (treatment-naive). This outcome is to measure the long-term effect of COBI-containing regimens on renal parameters. (NCT01363011)
Timeframe: Baseline; Weeks 48 and 96

Change From Baseline in eGFR-CG at Weeks 48 and 96 (Cohort 2)

Change from baseline in eGFR-CG at Weeks 48 and 96 were analyzed in Cohort 2 (treatment-experienced). This outcome is to measure the long-term effect of COBI-containing regimens on renal parameters. (NCT01363011)
Timeframe: Baseline; Week 48

Change From Baseline in eGFR-CKD-EPI Based on Cystatin C Equation (Adjusted) at Weeks 48 and 96 (Cohort 1)

Change from baseline in eGFR-CKD-EPI based on cystatin C equation (adjusted for age, sex, and race) at Weeks 48 and 96 were analyzed in Cohort 1 (treatment-naive). The calculation was normalized to 1.73 m^2 body surface area. This outcome is to measure the long-term effect of COBI-containing regimens on renal parameters. (NCT01363011)
Timeframe: Baseline; Weeks 48 and 96

Change From Baseline in eGFR-CKD-EPI Based on Cystatin C Equation (Adjusted) at Weeks 48 and 96 (Cohort 2)

Change from baseline in eGFR-CKD-EPI based on cystatin C equation (adjusted for age, sex, and race) at Weeks 48 and 96 were analyzed in Cohort 2 (treatment-experienced). The calculation was normalized to 1.73 m^2 body surface area. This outcome is to measure the long-term effect of COBI-containing regimens on renal parameters. (NCT01363011)
Timeframe: Baseline; Weeks 48 and 96

Change From Baseline in eGFR-CKD-EPI Based on Cystatin C Equation at Weeks 48 and 96 (Cohort 1)

Change from baseline in eGFR-CKD-EPI based on cystatin C equation (not adjusted for age, sex, and race) at Weeks 48 and 96 were analyzed in Cohort 1 (treatment-naive). The calculation was normalized to 1.73 m^2 body surface area. This outcome is to measure the long-term effect of COBI-containing regimens on renal parameters. (NCT01363011)
Timeframe: Baseline; Weeks 48 and 96

Change From Baseline in eGFR-CKD-EPI Based on Cystatin C Equation at Weeks 48 and 96 (Cohort 2)

Change from baseline in eGFR-CKD-EPI based on cystatin C equation (not adjusted for age, sex, and race) at Weeks 48 and 96 were analyzed in Cohort 2 (treatment-experienced). The calculation was normalized to 1.73 m^2 body surface area. This outcome is to measure the long-term effect of COBI-containing regimens on renal parameters. (NCT01363011)
Timeframe: Baseline; Weeks 48 and 96

Change From Baseline in eGFR-CKD-EPI Based on Cystatin C Equation, Adjusted at Week 24 (Cohort 1)

Change from baseline in eGFR-CKD-EPI based on cystatin C equation (adjusted for age, sex, and race) at Week 24 was analyzed in Cohort 1 (treatment-naive). The calculation was normalized to 1.73 m^2 body surface area. (NCT01363011)
Timeframe: Baseline; Week 24

Change From Baseline in eGFR-CKD-EPI Based on Cystatin C Equation, Adjusted at Week 24 (Cohort 2)

Change from baseline in eGFR-CKD-EPI based on cystatin C equation (adjusted for age, sex, and race) at Week 24 was analyzed in Cohort 2 (treatment-experienced). The calculation was normalized to 1.73 m^2 body surface area. (NCT01363011)
Timeframe: Baseline; Week 24

Change From Baseline in eGFR-CKD-EPI Formula Based on Cystatin C Equation at Week 24 (Cohort 2)

Change from baseline in eGFR-CKD-EPI based on cystatin C equation (not adjusted for age, sex, and race) at Week 24 was analyzed in Cohort 2 (treatment-experienced). The calculation was normalized to 1.73 m^2 body surface area. (NCT01363011)
Timeframe: Baseline; Week 24

Change From Baseline in eGFR-MDRD at Week 24 (Cohort 2)

Change from baseline in eGFR-MDRD equation at Week 24 was analyzed in Cohort 2 (treatment-experienced). The calculation was normalized to 1.73 m^2 body surface area. (NCT01363011)
Timeframe: Baseline; Week 24

Change From Baseline in eGFR-MDRD at Weeks 48 and 96 (Cohort 1)

Change from baseline in eGFR-MDRD at Weeks 48 and 96 were analyzed in Cohort 1 (treatment-naive). The calculation was normalized to 1.73 m^2 body surface area. This outcome is to measure the long-term effect of COBI-containing regimens on renal parameters. (NCT01363011)
Timeframe: Baseline; Weeks 48 and 96

Change From Baseline in eGFR-MDRD at Weeks 48 and 96 (Cohort 2)

Change from baseline in eGFR-MDRD at Weeks 48 and 96 were analyzed in Cohort 2 (treatment-experienced). The calculation was normalized to 1.73 m^2 body surface area. This outcome is to measure the long-term effect of COBI-containing regimens on renal parameters. (NCT01363011)
Timeframe: Baseline; Weeks 48 and 96

Change From Baseline in Estimated Glomerular Filtration Rate (eGFR) Using the Cockcroft-Gault (CG) Equation at Week 24 (Cohort 1)

Change from baseline in eGFR-CG equation at Week 24 was analyzed in Cohort 1 (treatment-naive). (NCT01363011)
Timeframe: Baseline; Week 24

Percentage of Participants Who Experienced Adverse Events (Cohort 1)

Adverse events (AEs) occurring from baseline up to 30 days following the last dose of study drug were summarized for Cohort 1 (treatment-naive). A participant was counted once if they had a qualifying event. (NCT01363011)
Timeframe: Up to 147 weeks plus 30 days

Percentage of Participants Who Experienced Adverse Events (Cohort 2)

Adverse events (AEs) occurring from baseline up to 30 days following the last dose of study drug were summarized for Cohort 2 (treatment-experienced). A participant was counted once if they had a qualifying event. (NCT01363011)
Timeframe: Up to 166 weeks plus 30 days

Percentage of Participants Who Experienced Graded Laboratory Abnormalities (Cohort 1)

Laboratory abnormalities were summarized for Cohort 1 (treatment-naive) and were defined as values that increased at least one toxicity grade from baseline at any time postbaseline up to and including the date of last dose of study drug plus 30 days. A participant was counted once if they had a qualifying event. (NCT01363011)
Timeframe: Up to 147 weeks plus 30 days

Percentage of Participants Who Experienced Graded Laboratory Abnormalities (Cohort 2)

Laboratory abnormalities were summarized for Cohort 2 (treatment-experienced) and were defined as values that increased at least one toxicity grade from baseline at any time postbaseline up to and including the date of last dose of study drug plus 30 days. A participant was counted once if they had a qualifying event. (NCT01363011)
Timeframe: Up to 166 weeks plus 30 days

Percentage of Participants With HIV-1 RNA < 50 Copies/mL at Weeks 48 and 96 (Cohort 1)

The percentage of participants with HIV-1 RNA < 50 copies/mL at Weeks 48 and 96 were analyzed in Cohort 1 (treatment-naive) using the FDA snapshot analysis algorithm. (NCT01363011)
Timeframe: Weeks 48 and 96

Percentage of Participants With HIV-1 RNA < 50 Copies/mL at Weeks 48 and 96 (Cohort 2)

The percentage of participants with HIV-1 RNA < 50 copies/mL at Weeks 48 and 96 were analyzed in Cohort 2 (treatment-experienced) using the FDA snapshot analysis algorithm. (NCT01363011)
Timeframe: Weeks 48 and 96

Plasma Pharmacokinetics of COBI: AUCtau (Cohort 1)

AUCtau was analyzed for Cohort 1 (treatment-naive) and was defined as the concentration of drug over time (area under the plasma concentration versus time curve over the dosing interval). (NCT01363011)
Timeframe: Blood samples were collected at 0 (predose), 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 8.0, 12.0, and 24.0 hours postdose at baseline and Weeks 2, 4, and 24.

Plasma Pharmacokinetics of COBI: AUCtau (Cohort 2)

AUCtau was analyzed for Cohort 2 (treatment-experienced) and was defined as the concentration of drug over time (area under the plasma concentration versus time curve over the dosing interval). (NCT01363011)
Timeframe: Blood samples were collected at 0 (predose), 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 8.0, 12.0, and 24.0 hours postdose at baseline and Weeks 2, 4, and 24.

Plasma Pharmacokinetics of COBI: Cmax (Cohort 1)

Cmax was analyzed for Cohort 1 (treatment-naive) and was defined as the maximum observed concentration of drug in plasma. (NCT01363011)
Timeframe: Blood samples were collected at 0 (predose), 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 8.0, 12.0, and 24.0 hours postdose at baseline and Weeks 2, 4, and 24.

Plasma Pharmacokinetics of COBI: Cmax (Cohort 2)

Cmax was analyzed for Cohort 2 (treatment-experienced) and was defined as the maximum observed concentration of drug in plasma. (NCT01363011)
Timeframe: Blood samples were collected at 0 (predose), 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 8.0, 12.0, and 24.0 hours postdose at baseline and Weeks 2, 4, and 24.

Plasma Pharmacokinetics of COBI: Ctau (Cohort 1)

Ctau was analyzed for Cohort 1 (treatment-naive) and was defined as the observed drug concentration at the end of the dosing interval. (NCT01363011)
Timeframe: Blood samples were collected at 0 (predose), 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 8.0, 12.0, and 24.0 hours postdose at baseline and Weeks 2, 4, and 24.

Plasma Pharmacokinetics of COBI: Ctau (Cohort 2)

Ctau was analyzed for Cohort 2 (treatment-experienced) and was defined as the observed drug concentration at the end of the dosing interval. (NCT01363011)
Timeframe: Blood samples were collected at 0 (predose), 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 8.0, 12.0, and 24.0 hours postdose at baseline and Weeks 2, 4, and 24.

Plasma Pharmacokinetics of COBI: t1/2 (Cohort 1)

t1/2 was analyzed for Cohort 1 (treatment-naive) and was defined as the estimate of the terminal elimination half-life of the drug. (NCT01363011)
Timeframe: Blood samples were collected at 0 (predose), 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 8.0, 12.0, and 24.0 hours postdose at baseline and Weeks 2, 4, and 24.

Plasma Pharmacokinetics of COBI: t1/2 (Cohort 2)

t1/2 was analyzed for Cohort 2 (treatment-experienced) and was defined as the estimate of the terminal elimination half-life of the drug. (NCT01363011)
Timeframe: Blood samples were collected at 0 (predose), 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 8.0, 12.0, and 24.0 hours postdose at baseline and Weeks 2, 4, and 24.

Plasma Pharmacokinetics of COBI: Tmax (Cohort 1)

Tmax was analyzed for Cohort 1 (treatment-naive) and was defined as the time of Cmax. (NCT01363011)
Timeframe: Blood samples were collected at 0 (predose), 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 8.0, 12.0, and 24.0 hours postdose at baseline and Weeks 2, 4, and 24.

Plasma Pharmacokinetics of COBI: Tmax (Cohort 2)

Tmax was analyzed for Cohort 2 (treatment-experienced) and was defined as the time of Cmax. (NCT01363011)
Timeframe: Blood samples were collected at 0 (predose), 0.5, 1.0, 2.0, 3.0, 4.0, 5.0, 8.0, 12.0, and 24.0 hours postdose at baseline and Weeks 2, 4, and 24.

Change From Baseline in CD4+ Cell Count at Week 144

Change From Baseline in CD4+ Cell Count at Week 48

Change From Baseline in CD4+ Cell Count at Week 96

Change From Baseline in Serum Creatinine at Week 144

Change From Baseline in Serum Creatinine at Week 48

Change From Baseline in Serum Creatinine at Week 96

Percent Change From Baseline in Hip BMD at Week 144

Percent Change From Baseline in Hip BMD at Week 96

Percent Change From Baseline in Hip Bone Mineral Density (BMD) at Week 48

Hip BMD was assessed by dual energy x-ray absorptiometry (DXA) scan. (NCT01780506)
Timeframe: Baseline; Week 48

Percent Change From Baseline in Spine BMD at Week 144

Percent Change From Baseline in Spine BMD at Week 48

Percent Change From Baseline in Spine BMD at Week 96

Percent Change From Baseline in Urine Beta-2-microglobulin to Creatinine Ratio at Week 144

Urine Beta-2-microglobulin is a renal biomarker which is used to detect drug-induced kidney injury. (NCT01780506)
Timeframe: Baseline; Week 144

Percent Change From Baseline in Urine Beta-2-microglobulin to Creatinine Ratio at Week 48

Urine Beta-2-microglobulin is a renal biomarker which is used to detect drug-induced kidney injury. (NCT01780506)
Timeframe: Baseline; Week 48

Percent Change From Baseline in Urine Beta-2-microglobulin to Creatinine Ratio at Week 96

Urine Beta-2-microglobulin is a renal biomarker which is used to detect drug-induced kidney injury. (NCT01780506)
Timeframe: Baseline; Week 96

Percent Change From Baseline in Urine RBP to Creatinine Ratio at Week 144

Urine RBP is a renal biomarker which is used to detect drug-induced kidney injury. (NCT01780506)
Timeframe: Baseline; Week 144

Percent Change From Baseline in Urine RBP to Creatinine Ratio at Week 96

Urine RBP is a renal biomarker which is used to detect drug-induced kidney injury. (NCT01780506)
Timeframe: Baseline; Week 96

Percent Change From Baseline in Urine Retinol Binding Protein (RBP) to Creatinine Ratio at Week 48

Urine RBP is a renal biomarker which is used to detect drug-induced kidney injury. (NCT01780506)
Timeframe: Baseline; Week 48

Percentage of Participants With HIV-1 RNA < 50 Copies/mL at Week 48

The percentage of participants achieving HIV-1 RNA < 50 copies/mL at Week 48 was analyzed using the snapshot algorithm, which defines a patient's virologic response status using only the viral load at the predefined time point within an allowed window of time, along with study drug discontinuation status. (NCT01780506)
Timeframe: Week 48

Percentage of Participants Experiencing Treatment-emergent Proteinuria Through Week 144

Grades 1 (mild), 2 (moderate), and 3 (severe) were the highest treatment-emergent postbaseline grades for urine protein using the dipstick method. The worst postbaseline value is presented for each participant. (NCT01780506)
Timeframe: Up to 144 weeks

Percentage of Participants Experiencing Treatment-emergent Proteinuria Through Week 48

Percentage of Participants Experiencing Treatment-emergent Proteinuria Through Week 96

Percentage of Participants With HIV-1 RNA < 20 Copies/mL at Weeks 48, 96, and 144

The percentage of participants achieving HIV-1 RNA < 20 copies/mL at Weeks 48, 96, and 144 were analyzed using the snapshot algorithm, which defines a patient's virologic response status using only the viral load at the predefined time point within an allowed window of time, along with study drug discontinuation status. (NCT01780506)
Timeframe: Weeks 48, 96. and 144

Percentage of Participants With HIV-1 RNA < 50 Copies/mL at Weeks 96 and 144

The percentage of participants achieving HIV-1 RNA < 50 copies/mL at Weeks 96 and 144 were analyzed using the snapshot algorithm, which defines a patient's virologic response status using only the viral load at the predefined time point within an allowed window of time, along with study drug discontinuation status. (NCT01780506)
Timeframe: Weeks 96 and 144

Change From Baseline in CD4+ Cell Count at Week 48

Change From Baseline in CD4+ Cell Count at Week 96

Change From Baseline in Serum Creatinine at Week 48

Change From Baseline in Serum Creatinine at Week 96

Percent Change From Baseline in Hip BMD at Week 96

Percent Change From Baseline in Hip Bone Mineral Density (BMD) at Week 48

Hip BMD was assessed by dual energy x-ray absorptiometry (DXA) scan. (NCT01797445)
Timeframe: Baseline; Week 48

Percent Change From Baseline in Spine BMD at Week 48

Percent Change From Baseline in Spine BMD at Week 96

Percent Change From Baseline in Urine Beta-2-microglobulin to Creatinine Ratio at Week 48

Urine Beta-2-microglobulin is a renal biomarker which is used to detect drug-induced kidney injury. (NCT01797445)
Timeframe: Baseline; Week 48

Percent Change From Baseline in Urine Beta-2-microglobulin to Creatinine Ratio at Week 96

Urine Beta-2-microglobulin is a renal biomarker which is used to detect drug-induced kidney injury. (NCT01797445)
Timeframe: Baseline; Week 96

Percent Change From Baseline in Urine RBP to Creatinine Ratio at Week 96

Urine RBP is a renal biomarker which is used to detect drug-induced kidney injury. (NCT01797445)
Timeframe: Baseline; Week 96

Percent Change From Baseline in Urine Retinol Binding Protein (RBP) to Creatinine Ratio at Week 48

Urine RBP is a renal biomarker which is used to detect drug-induced kidney injury. (NCT01797445)
Timeframe: Baseline; Week 48

Percentage of Participants Achieving HIV-1 RNA < 50 Copies/mL at Week 48

Percentage of Participants With HIV-1 RNA < 50 Copies/mL at Week 96

The percentage of participants achieving HIV-1 RNA < 50 copies/mL at Week 96 was analyzed using the snapshot algorithm, which defines a patient's virologic response status using only the viral load at the predefined time point within an allowed window of time, along with study drug discontinuation status. (NCT01797445)
Timeframe: Week 96

Percentage of Participants With HIV-1 RNA < 20 Copies/mL at Weeks 48 and 96

The percentage of participants achieving HIV-1 RNA < 20 copies/mL at Weeks 48 and 96 was analyzed using the snapshot algorithm, which defines a patient's virologic response status using only the viral load at the predefined time point within an allowed window of time, along with study drug discontinuation status. (NCT01797445)
Timeframe: Weeks 48 and 96

Percentage of Participants With Treatment-emergent Proteinuria Through Week 48

Percentage of Participants With Treatment-emergent Proteinuria Through Week 96

Percentage of Genotype 1 Hepatitis C Virus (HCV)-Infected Treatment-naive Participants With Sustained Virologic Response at Follow-up Week 12 (SVR12)

Percentage of Hepatitis C Virus (HCV)/HIV-coinfected Treatment-experienced Participants With Sustained Virologic Response at Follow-up Week 12 (SVR12)

Percentage of Hepatitis C Virus (HCV)/HIV-coinfected Treatment-naive Participants With Sustained Virologic Response at Follow-up Week 12 (SVR12)

Percentage of Participants of All Genotypes Coinfected With Hepatitis C Virus (HCV)/HIV Who Achieved Sustained Virologic Response Rate at Follow-up Week 12 (SVR12)

SVR12 was defined as HCV RNA levels NCT02032888)
Timeframe: At follow-up Week 12

Number of Participants With Adverse Events (AEs), Serious Adverse Events (SAEs), AEs Leading to Interruption or Discontinuation, Treatment-related AEs/SAEs and Grade 3 to 4 AEs/SAEs and Who Died During Treatment Period

AE was defined as any new unfavorable symptom, sign, or disease or worsening of a preexisting condition that may or may not have a causal relationship with treatment. SAE was defined as a medical event that at any dose resulted in death, persistent or significant disability/incapacity, or drug dependency/abuse; was life-threatening, an important medical event, or a congenital anomaly/birth defect; or required or prolonged hospitalization. AEs were categorized as Grade (Gr) 1=Mild, Gr 2=Moderate, Gr 3=Severe, Gr 4=Life-threatening or disabling, Gr 5=Death. (NCT02032888)
Timeframe: AEs: Day 1 to 7 days after last dose of study treatment (8 weeks or 12 weeks). SAEs: Day 1 to 30 days after last dose of study treatment (8 weeks or 12 weeks)

Number of Participants With Adverse Events (AEs), Serious Adverse Events (SAEs), Treatment-related AEs/SAEs, Grade 3 to 4 AEs/SAEs, and Who Died During Follow-up Period

AE was defined as any new unfavorable symptom, sign, or disease or worsening of a preexisting condition that may or may not have a causal relationship with treatment. SAE was defined as a medical event that at any dose resulted in death, persistent or significant disability/incapacity, or drug dependency/abuse; was life-threatening, an important medical event, or a congenital anomaly/birth defect; or required or prolonged hospitalization. AEs were categorized as Grade (Gr) 1=Mild, Gr 2=Moderate, Gr 3=Severe, Gr 4=Life-threatening or disabling, Gr 5=Death. (NCT02032888)
Timeframe: AEs: Day 1 of follow-up period (Week 9 or Week 13) to 7 days after end of 24 weeks follow-up period. SAEs: Day 1 of follow-up period (Week 9 or Week 13) to 30 days after end of 24 weeks follow-up period.

Number of Participants With Treatment-emergent Grade 3-4 Abnormalities on Laboratory Test Results

Grade 3-4 abnormalities on laboratory test results were defined as: International normalized ratio as 2.1-3.0*upper limit of normal (ULN) for grade 3 and >3.0*ULN for grade 4. Leukocytes as 1.0*10^9-1.5*10^9/L for grade 3 and <1.0*10^9/L for grade 4. Aspartate aminotransferase as 5.1-10.0*ULN for grade 3 and >10.0*ULN for grade 4. Bilirubin (total) as 2.6-5.0*ULN for grade 3 and >5.0*ULN for grade 4. Lipase (total) as 3.1-5.0*ULN for grade 3 and >5.0*ULN for grade 4. Alanine aminotransferase as 5.1-10.0*ULN for grade 3 and >10.0*ULN for grade 4. (NCT02032888)
Timeframe: From screening up to week 24 of post treatment follow--up

Intervention	Units per liter (U/L) (Median)
	Day 1; n=2;11	Week 48; n=1;8
Cohort 2, Arm A - 4 Weeks to <6 Months	20.5	16.0

Intervention	Units per liter (U/L) (Median)
	Day 1; n=2;11	Week 4; n=0;1	Week 12; n=0;1	Week 24; n=0;8	Week 48; n=1;8
Cohort 1, Arm A - 6 Months to <2 Years	22.0	16.0	68.0	19.5	16.0

Intervention	log10 copies/mL (Median)
	Week 4, n=21;28	Week 12, n=22;27	Week 24, n=22;25	Week 36, n=21;25	Week 48, n=18;24
Cohort 1, Arm A - 6 Months to <2 Years	-2.33	-3.14	-3.38	-3.52	-3.56
Cohort 2, Arm A - 4 Weeks to <6 Months	-2.38	-3.11	-3.77	-3.72	-3.90

Intervention	Percentage of cells (Median)
	Week 4, n=20;28	Week 12, n=19;27	Week 24, n=19;26	Week 36, n=18;25	Week 48, n=15;24
Cohort 1, Arm A - 6 Months to <2 Years	3.4	6	6	5	4.7
Cohort 2, Arm A - 4 Weeks to <6 Months	3	2	7	8	5

Intervention	Percentage of cells (Median)
	Baseline, n=23;28	Week 4, n=23;28	Week 12, n=22;27	Week 24, n=22;26	Week 36, n=21;25	Week 48, n=18;24
Cohort 1, Arm A - 6 Months to <2 Years	25	27.5	32	32.8	29.5	31.6
Cohort 2, Arm A - 4 Weeks to <6 Months	27	29	27.5	31.5	32	28

Intervention	log10 copies/mL (Median)
	Baseline, n=26;28	Week 4, n=21;28	Week 12, n=22;27	Week 24, n=22;25	Week 36, n=21;25	Week 48, n=18;24
Cohort 1, Arm A - 6 Months to <2 Years	5.51	2.88	2.07	1.74	1.69	1.69
Cohort 2, Arm A - 4 Weeks to <6 Months	5.80	3.29	2.28	1.69	1.69	1.69

Intervention	participants (Number)
	Any HIV NRTI Mutation	HIV NRTI mutation M184V	Any HIV NNRTI Mutation	HIV NNRTI Mutation K101K/E	Any HIV Major PI Mutations	Any Minor HIV PI Mutations	Minor HIV PI Mutation L10F	Minor HIV PI Mutation L10I	Minor HIV PI Mutation L33L/F	Minor HIV PI Mutation L33F
ART-naïve FPV/RTV Treatment Group	1	1	0	0	0	2	0	1	1	0
PI-experienced, ART-experienced FPV/RTV Treatment Group	0	0	1	1	0	1	1	0	0	1
PI-naïve, ART-experienced FPV/RTV Treatment Group	0	0	0	0	0	0	0	0	0	0

Intervention	participants (Number)
	Any NRTI	Emtricitabine	Lamivudine	Any NNRTI	Any PI	Ritonavir-boosted Fosamprenavir
ART-experienced, PI-naïve FPV/RTV Treatment Group	0	0	0	0	0	0
ART-naïve FPV/RTV Treatment Group	1	1	1	0	0	0
PI-experienced, ART-experienced FPV/RTV Treatment Group	0	0	0	0	1	1

Intervention	Participants (Count of Participants)
	Grade 1	Grade 2	Grade 3	Grade 4
Cohort 1, Arm A - 6 Months to <2 Years	5	14	7	1
Cohort 2, Arm A - 4 Weeks to <6 Months	5	9	3	1

Intervention	participants (Number)
	Baseline	Week 4	Week 12	Week 24	Week 36	Week 48
Cohort 1, Arm A - 6 Months to <2 Years	0	6	18	20	20	22
Cohort 2, Arm A - 4 Weeks to <6 Months	1	5	13	18	19	15

Intervention	participants (Number)
	Week 2, color, dislike, n=23;27	Week 2, color, neutral, n=23;27	Week 2, color, like, n=23;27	Week 24, color, dislike, n=20;24	Week 24, color, neutral, n=20;24	Week 24, color, like, n=20;24	Week 48, color, dislike, n=15;22	Week 48, color, neutral, n=15;22	Week 48, color, like, n=15;22	Week 2, texture, dislike, n=23;27	Week 2, texture, neutral, n=23;27	Week 2, texture, like, n=23;27	Week 24, texture, dislike, n=20;24	Week 24, texture, neutral, n=20;24	Week 24, texture, like, n=20;24	Week 48, texture, dislike, n=15;21	Week 48, texture, neutral, n=15;21	Week 48, texture, like, n=15;21	Week 2, odor, dislike, n=23;27	Week 2, odor, neutral, n=23;27	Week 2, odor, like, n=23;27	Week 24, odor, dislike, n=20;24	Week 24, odor, neutral, n=20;24	Week 24, odor, like, n=20;24	Week 48, odor, dislike, n=15;22	Week 48, odor, neutral, n=15;22	Week 48, odor, like, n=15;22	Week 2, general satisfaction, dislike, n=23;27	Week 2, general satisfaction, neutral, n=23;27	Week 2, general satisfaction, like, n=23;27	Week 24, general satisfaction, dislike, n=20;24	Week 24, general satisfaction, neutral, n=20;24	Week 24, general satisfaction, like, n=20;24	Week 48, general satisfaction, dislike, n=15;22	Week 48, general satisfaction, neutral, n=15;22	Week 48, general satisfaction, like, n=15;22
Cohort 1, Arm A - 6 Months to <2 Years	5	13	9	4	10	10	7	7	8	5	10	12	4	12	8	6	7	8	7	7	13	7	8	9	7	5	10	5	7	15	6	9	9	9	4	9
Cohort 2, Arm A - 4 Weeks to <6 Months	3	7	13	4	2	14	6	1	8	4	7	12	6	4	10	6	1	8	1	3	19	4	2	14	4	1	10	3	4	16	4	0	16	4	1	10

Intervention	participants (Number)
	W2, Item 5, takes all/most med. easily, n=23;27	W2, Item 5, problem taking a few med., n=23;27	W2, Item 5, problem taking most med., n=23;27	W2, Item 5, impossible to take med., n=23;27	W24, Item 5, takes all/most med. easily, n=20;23	W24, Item 5, problem taking a few med., n=20;23	W24, Item 5, problem taking most med., n=20;23	W24, Item 5, impossible to take med., n=20;23	W48, Item 5, takes all/most med. easily, n=14;22	Week 48, Item 5, problem taking a few med., n=14;22	W48, Item 5, problem taking most med., n=14;22	W48, Item 5, impossible to take med., n=14;22	W2, Item 6, dislike, n=23;27	W2, Item 6, neutral, n=23;27	W2, Item 6, like, n=23;27	W24, Item 6, dislike, n=20;23	W24, Item 6, neutral, n=20;23	W24, Item 6, like, n=20;23	W48, Item 6, dislike, n=15;22	W48, Item 6, neutral, n=15;22	W48, Item 6, like, n=15;22	W2, Item 7, no problem taking FPV, n=23;27	W2, Item 7, few problems taking FPV, n=23;27	W2, Item 7, problem taking most of time, n=23;27	W2, Item 7, impossible to take, n=23;27	W24, Item 7, no problem taking FPV, n=20;23	W24, Item 7, few problems taking FPV, n=20;23	W24, Item 7, problem taking most of time, n=20;23	W24, Item 7, impossible to take, n=20;23	W48, Item 7, no problem taking FPV, n=15;22	W48, Item 7, few problems taking FPV, n=15;22	W48, Item 7, problem taking most of time, n=15;22	W48, Item 7, impossible to take, n=15;22	W2, Item 8, swallows with no problem, n=23;27	W2, Item 8, swallows with struggle, n=23;27	W2, Item 8, spits out suspension, n=23;27	W2, Item 8, vomits the suspension, n=23;27	W24, Item 8, swallows with no problem, n=20;23	W24, Item 8, swallows with struggle, n=20;23	W24, Item 8, spits out suspension, n=20;23	W24, Item 8, vomits the suspension, n=20;23	W48, Item 8, swallows with no problem, n=15;22	W48, Item 8, swallows with struggle, n=15;22	W48, Item 8, spits out suspension, n=15;22	W48, Item 8, vomits the suspension, n=15;22	W2, I9, take more willingly than other med., n=23;27	W2, Item 9, about the same, n=23;27	W2, I9, not as willing to take as other med., n=23;27	W24, I9, take more willingly than other med., n=20;22	W24, Item 9, about the same, n=20;22	W24, I9, not as willing to take as other med, n=20;22	W48, I9, take more willingly than other med., n=15;22	W48, Item 9, about the same, n=15;22	W48, I9, not as willing to take as other med, n=15;22	Week 2, Item 10, dislike, n=23;27	Week 2, Item 10, neutral, n=23;27	Week 2, Item 10, like, n=23;27	Week 24, Item 10, dislike, n=20;24	Week 24, Item 10, neutral, n=20;24	Week 24, Item 10, like, n=20;24	Week 48, Item 10, dislike, n=15;22	Week 48, Item 10, neutral, n=15;22	Week 48, Item 10, like, n=15;22
Cohort 1, Arm A - 6 Months to <2 Years	11	10	5	1	10	7	5	1	17	5	0	0	9	10	8	12	5	6	10	6	6	6	9	10	2	10	5	8	0	10	8	2	2	10	10	5	2	12	9	2	0	12	8	1	1	3	15	9	1	20	1	6	14	2	9	9	9	13	7	4	8	7	7
Cohort 2, Arm A - 4 Weeks to <6 Months	10	10	3	0	12	8	0	0	10	4	0	0	12	4	7	11	3	6	9	1	5	7	9	5	2	13	3	4	0	8	4	2	1	9	11	0	3	10	7	3	0	11	3	1	0	3	13	7	3	11	6	5	10	0	11	5	7	7	2	11	7	4	4

Intervention	participants (Number)
	Clinical Chemistry Toxicities - Grade 3	Clinical Chemistry Toxicities - Grade 4	Hematology Toxicities - Grade 3	Hematology Toxicities - Grade 4
Cohort 1, Arm A - 6 Months to <2 Years	4	1	2	1
Cohort 2, Arm A - 4 Weeks to <6 Months	2	0	2	0

Intervention	participants (Number)
	Virological (V) success	V failure (1)	V failure (2)	V failure (3)	V failure (4)	No V data at Week 48 (a)	No V data at Week 48 (b)
Cohort 1, Arm A - 6 Months to <2 Years	20	2	2	1	1	1	1
Cohort 2, Arm A - 4 Weeks to <6 Months	15	3	0	1	2	1	4

Intervention	Participants (Count of Participants)
	Treatment emergent reduced NRTI drug susceptibility	Treatment emergent reduced NNRTI drug susceptibility	Treatment emergent reduced PI drug susceptibility
ART-Naive	0	0	0
PI-Naive	0	0	0

Intervention	Hr per microgram/milliliter (hr*µg/mL) (Geometric Mean)
	45/10 mg/kg BID; n=9, 1	60/10 mg/kg BID; n=2, 2	45/7 mg/kg BID; n=2, 10
FPV/RTV BID: 4 Weeks to <6 Months	26.6	54.2	35.08

Intervention	Micrograms per milliliter (µg/mL) (Geometric Mean)
	45/10 mg/kg BID; n=11, 15	60/10 mg/kg BID; n=3, 5	45/7 mg/kg BID; n=3, 29
FPV/RTV BID: 4 Weeks to <6 Months	0.86	0.60	0.44

Intervention	hr*µg/mL (Geometric Mean)
	7 mg/kg BID; n=2, 22	10 mg/kg BID; n=11, 2
FPV/RTV BID: 4 Weeks to <6 Months	1.921	12.952
FPV/RTV BID: 6 Months to <2 Years	7.363	18.750

Intervention	mL/min (Geometric Mean)
	7 mg/kg BID, n=2, 22	10 mg/kg BID, n=11, 2
FPV/RTV BID: 4 Weeks to <6 Months	335.2	72.1
FPV/RTV BID: 6 Months to <2 Years	134.1	57.9

Intervention	µg/mL (Geometric Mean)
	7 mg/kg BID, n=2, 23	10 mg/kg BID, n=12, 2
FPV/RTV BID: 4 Weeks to <6 Months	0.404	2.388
FPV/RTV BID: 6 Months to <2 Years	1.576	3.823

Intervention	µg/mL (Geometric Mean)
	7 mg/kg BID, n=4, 33	10 mg/kg BID, n=15, 19
FPV/RTV BID: 4 Weeks to <6 Months	0.0795	0.1855
FPV/RTV BID: 6 Months to <2 Years	0.2468	0.4200

Intervention	µg/mL (Mean)
	45/10 mg/kg BID; n=7, 16	60/10 mg/kg BID; n=1, 7	45/7 mg/kg BID; n=1, 16
FPV/RTV BID: 4 Weeks to <6 Months	0.091	0.003	0.027

Intervention	Percentage of total APV Cτ unbound (Mean)
	45/10 mg/kg BID; n=7, 15	60/10 mg/kg BID; n=1, 7	45/7 mg/kg BID; n=1, 16
FPV/RTV BID: 4 Weeks to <6 Months	5.79	5.32	7.55

Intervention	cells/cu mm (Median)
	PI-naïve, Week 2; n=13, 41	PI-naïve, Week 12; n=19, 46	PI-naïve, Week 24; n=18, 44	PI-naïve, Week 48; n=17, 42	PI-exp, Week 2; n=0, 32	PI-exp, Week 12; n=0, 31	PI-exp, Week 24; n=0, 34	PI-exp, Week 48; n=0, 29
FPV Treatment Group	20	170	350	340	NA	NA	NA	NA
FPV/RTV Treatment Group	60	180	184	217	90	200	150	180

Intervention	Millimoles per liter (mmol/L) (Median)
	Triglycerides; n=17, 65	Total cholesterol; n=17, 65	HDL cholesterol; n=17, 65	LDL cholesterol; n=17, 64	Glucose; n=18, 69
FPV Treatment Group	0.1	1.1	0.4	0.6	0.0
FPV/RTV Treatment Group	0.2	0.9	0.3	0.5	0.1

Intervention	Cells per cubic millimeter (cells/cu mm) (Median)
	PI-naïve, Baseline; n= 19, 49	PI-naïve, Week 2; n= 13, 41	PI-naïve, Week 12; n= 19, 46	PI-naïve, Week 24; n= 18, 44	PI-naïve, Week 48; n= 18, 42	PI-exp, Baseline; n= 0, 40	PI-exp, Week 2; n= 0, 32	PI-exp, Week 12; n= 0, 31	PI-exp, Week 24; n= 0, 34	PI-exp, Week 48; n= 0, 29
FPV Treatment Group	810	820	1040	1260	1080	NA	NA	NA	NA	NA
FPV/RTV Treatment Group	370	450	581	609	670	440	605	720	620	540

Intervention	log10/copies (Median)
	PI-naïve, Week 2; n=14, 39	PI-exp, Week 2; n=0, 32	PI-naïve, Week 12; n=19, 46	PI-exp, Week 12; n=0, 33	PI-naïve, Week 24; n=18, 44	PI-exp, Week 24; n=0, 35	PI-naïve, Week 48; n=18, 44	PI-exp, Week 48; n=0, 33
FPV Treatment Group	-1.91	NA	-3.04	NA	-3.16	NA	-3.02	NA
FPV/RTV Treatment Group	-1.84	-1.58	-2.77	-2.23	-2.87	-2.28	-2.83	-2.14

Intervention	log10 copies/mL (Median)
	PI-naïve, Baseline; n=20, 49	PI-exp, Baseline; n=0, 39	PI-naïve, Week 2; n=14, 39	PI-exp, Week 2; n=0, 33	PI-naïve, Week 12; n=19, 46	PI-exp, Week 12; n=0, 34	PI-naïve, Week 24; n=18, 44	PI-exp, Week 24; n=0, 35	PI-naïve, Week 48; n=18, 44	PI-exp, Week 48; n=0, 33
FPV Treatment Group	5.13	NA	3.27	NA	2.03	NA	1.85	NA	1.85	NA
FPV/RTV Treatment Group	4.72	4.53	3.06	3.04	1.94	2.20	1.69	1.80	1.69	1.69

Intervention	Participants (Number)
	Any HIV NRTI Mutation	HIV NRTI mutation M41L	HIV NRTI mutation M184I	HIV NRTI mutation M184V	HIV NRTI mutation T215S/Y	Any Major HIV NNRTI Mutation	HIV NNRTI Mutation K103N	Any Minor HIV NNRTI Mutation	HIV NNRTI Mutation V179D/E	Any HIV Major PI Mutations	HIV Major PI Mutation V32I	HIV Major PI Mutation M46L	HIV Major PI Mutation I47IV	HIV Major PI Mutation T74P	HIV Major PI Mutation I84I/V	Any Minor HIV PI Mutations	Minor HIV PI Mutation L10F	Minor HIV PI Mutation L33F	Minor HIV PI Mutation I62I/V	Minor HIV PI Mutation I85V
ART-Naïve, FPV Treatment Group	1	0	0	1	0	0	0	0	0	1	0	1	0	1	0	1	1	0	0	1
ART-Naïve, FPV/RTV Treatment Group	1	0	1	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0
PI Experienced, ART Experienced, FPV/RTV Treatment Group	2	1	0	2	1	1	1	0	0	1	1	0	1	0	0	2	0	1	1	0

Intervention	Participants (Number)
	Any NRTI	Abacavir	Didanosine	Emtricitabine	Lamivudine	Zidovudine	Any NNRTI	Delaviridine	Efavirenz	Nevirapine	Any PI	Unboosted Fosamprenavir	Ritonavir- boosted Fosamprenavir	Nelfinavir	Tipranavir
ART-Naïve, FPV Treatment Group	1	0	0	1	1	0	0	0	0	0	1	1	NA	0	0
ART-Naïve, FPV/RTV Treatment Group	1	0	1	1	1	0	0	0	0	0	1	NA	0	1	0
PI-experienced, ART-experienced FPV/RTV Treatment Group	3	1	3	3	2	1	1	1	1	1	3	NA	1	0	1

Intervention	participants (Number)
	PI-naïve, Baseline; n=20, 49	PI-exp, Baseline; n=0, 40	PI-naïve, Week 2; n=20, 49	PI-exp, Week 2; n=0, 40	PI-naïve, Week 12; n=20, 49	PI-exp, Week 12; n=0, 40	PI-naïve, Week 24; n=20, 49	PI-exp, Week 24; n=0, 40	PI-naïve, Week 48; n=20, 49	PI-exp, Week 48; n=0, 40
FPV Treatment Group	0	NA	3	NA	13	NA	13	NA	12	NA
FPV/RTV Treatment Group	0	0	9	5	35	19	35	22	36	19

Intervention	participants (Number)
	PI-naïve, virological (V) success; n=20, 49	PI-exp, V success; n=0, 40	PI-naïve, V failure (1); n=20, 49	PI-exp, V failure (1); n=0, 40	PI-naïve, V failure (2); n=20, 49	PI-exp, V failure (2); n=0, 40	PI-naïve, V failure (3); n=20, 49	PI-exp, V failure (3); n=0, 40	PI-naïve;, V failure (4); n=20, 49	PI-exp, V failure (4); n=0, 40	PI-naïve, No V data at Week 48 (a); n=20, 49	PI-exp, No V data at Week 48 (a); n=0, 40	PI-naïve, No V data Week 48 (b); n=20, 49	PI-exp, No V data at Week 48 (b); n=0, 40	PI-naïve, No V data at Week 48 (c); n=20, 49	PI-exp, No V data at Week 48 (c); n=0, 40
FPV Treatment Group	12	NA	4	NA	2	NA	1	NA	1	NA	0	NA	0	NA	0	NA
FPV/RTV Treatment Group	36	19	3	8	4	7	0	0	3	3	1	1	1	0	1	2