adenine and Viremia
adenine has been researched along with Viremia in 87 studies
Viremia: The presence of viruses in the blood.
Research Excerpts
Excerpt | Relevance | Reference |
---|---|---|
"Adefovir dipivoxil (ADV) is a nucleotide analogue with proven efficacy in chronic hepatitis B (CHB)." | 9.16 | Five years of treatment with adefovir dipivoxil in Chinese patients with HBeAg-positive chronic hepatitis B. ( Barker, K; Daozhen, X; Dixon, J; Guangbi, Y; Hao, W; Hong, R; JinLin, H; Junqi, N; Minde, Z; Xiaqiu, Z; Yagang, C; Yaozong, W; Yimin, M; Youming, C; Yuming, W, 2012) |
"Low-dose TDF monotherapy can control HBV viremia for an extended period of time without the emergence of resistance and is more potent than adefovir at the standard dosage." | 9.12 | Low-dose tenofovir is more potent than adefovir and is effective in controlling HBV viremia in chronic HBeAg-negative hepatitis B. ( Colombo, S; Del Poggio, P; Jamoletti, C; Oggionni, M; Puhalo, V; Zaccanelli, M, 2007) |
"Adefovir dipivoxil is safe for the treatment of chronic hepatitis B in patients with varying degrees of renal dysfunction and lamivudine-resistant HBV and results in biochemical and virological efficacy similar to that reported in the general population." | 9.11 | Efficacy and safety of adefovir dipivoxil in kidney recipients, hemodialysis patients, and patients with renal insufficiency. ( Brosgart, C; Chaix, ML; Currie, G; Fontaine, H; Morales, E; Nalpas, B; Pol, S; Serpaggi, J; Vallet-Pichard, A; Varaut, A; Verkarre, V, 2005) |
"There are few data on the utility of tenofovir diphosphate (TFV-DP) in dried blood spots (DBSs) to predict future viral load (VL) in postpartum women with HIV on antiretroviral therapy (ART)." | 8.12 | Use of Tenofovir Diphosphate Levels to Predict Viremia During the Postpartum Period in Women Living With Human Immunodeficiency Virus (HIV): A Nested Case-Control Study. ( Allerton, J; Castillo-Mancilla, J; Hsiao, NY; Hu, NC; Kabanda, S; Lesosky, M; Malaba, TR; Myer, L; Odayar, J; Orrell, C; Phillips, TK; Wiesner, L, 2022) |
"HBV DNA was extracted from blood samples of two patients with HBeAg-positive chronic HBV infection and persistent viremia despite tenofovir treatment, and subsequently amplified by PCR before full-length HBV genomes were assembled by deep sequencing." | 8.12 | Novel hepatitis B virus reverse transcriptase mutations in patients with sustained viremia despite long-term tenofovir treatment. ( Bajpai, PS; Bukh, J; Dalegaard, MI; Fahnøe, U; Lundh, A; Ryom, L; Weis, N; Winckelmann, A, 2022) |
"Tenofovir diphosphate (TFV-DP) in dried blood spots (DBS) is associated with viral suppression in persons living with HIV (PLWH) taking tenofovir disoproxil fumarate (TDF)." | 7.91 | Predictive Value of Tenofovir Diphosphate in Dried Blood Spots for Future Viremia in Persons Living With HIV. ( Anderson, PL; Bushman, LR; Castillo-Mancilla, JR; Coleman, SS; Coyle, RP; Ellison, L; Gardner, EM; Kiser, JJ; MaWhinney, S; Morrow, M; Zheng, JH, 2019) |
"We determined the cumulative virological, serological and biochemical outcomes of 165 lamivudine-resistant chronic hepatitis B patients on lamivudine and adefovir for up to 5 years." | 7.78 | Outcome of lamivudine-resistant chronic hepatitis B after up to 5 years of combination therapy with adefovir. ( Fung, J; Hung, IF; Lai, CL; Liu, K; Seto, WK; Wong, DK; Yuen, JC; Yuen, MF, 2012) |
" His HBV is unresponsive to tenofovir/emtricitabine treatment demonstrated by persistent viremia despite lacking known resistance mutations and while having an undetectable HIV-1 viral load." | 7.77 | HIV-HBV vaccine escape mutant infection with loss of HBV surface antibody and persistent HBV viremia on tenofovir/emtricitabine without antiviral resistance. ( Holodniy, M; Schirmer, P; Winters, M, 2011) |
"We report a case of an immunocompromised patient affected by chronic hepatitis B virus (HBV) with high basal HBV viremia (>8 log(10) IU/ml) who failed an entecavir regimen, despite the absence of primary or secondary drug resistance mutations." | 7.77 | Successful switch to tenofovir after suboptimal response to entecavir in an immunocompromised patient with chronic hepatitis B and without genotypic hepatitis B virus resistance. ( Andreoni, M; Bertoli, A; Ceccarelli, L; Perno, CF; Salpini, R; Sarrecchia, C; Sordillo, P; Svicher, V; Volpi, A, 2011) |
"The aim of the study was to identify and characterize hepatitis B virus (HBV) polymerase gene mutations associated with ongoing HBV replication in HIV/HBV-coinfected individuals receiving tenofovir (TDF)." | 7.75 | Prolonged use of tenofovir in HIV/hepatitis B virus (HBV)-coinfected individuals does not lead to HBV polymerase mutations and is associated with persistence of lamivudine HBV polymerase mutations. ( Arrifin, N; Audsley, J; Ayres, A; Bartholomeusz, A; Crowe, SM; Lewin, SR; Locarnini, SA; Mijch, A; Sasadeusz, J; Yuen, LK, 2009) |
"Despite the failure of tenofovir DF/FTC as prophylaxis, selection for drug-resistant transmission did not occur and the blunting of postinfection levels of viremia likely reduced the probability of subsequent forward transmissions during the acute phase." | 7.74 | Drug-susceptible HIV-1 infection despite intermittent fixed-dose combination tenofovir/emtricitabine as prophylaxis is associated with low-level viremia, delayed seroconversion, and an attenuated clinical course. ( Carrington, M; Davis, B; Duh, FM; Jean-Pierre, P; La Roche, M; Markowitz, M; Mehandru, S; Mohri, H; Poles, M; Prada, N, 2008) |
"We studied the impact of hepatitis B virus (HBV) polymerase/reverse transcriptase (Pol/Rt) heterogeneity on adefovir rescue therapy in 34 consecutive chronic hepatitis B patients with viral breakthrough during lamivudine monotherapy." | 7.74 | Emergence of hepatitis B virus quasispecies with lower susceptibility to nucleos(t)ide analogues during lamivudine treatment. ( Bonino, F; Brunetto, MR; Ciccorossi, P; Coco, B; Colombatto, P; Flichman, D; Maina, AM; Moriconi, F; Oliveri, F; Sacco, R, 2007) |
" To understand predictors of residual viremia, we measured HIV RNA levels <50 copies/mL in patients after 1 year of treatment with efavirenz and lamivudine plus either tenofovir disoproxil fumarate (n=55) or stavudine (n=45), by use of an HIV RNA assay with a limit of detection of 2." | 7.73 | Predictors of residual viremia in HIV-infected patients successfully treated with efavirenz and lamivudine plus either tenofovir or stavudine. ( Havlir, DV; Ignacio, CC; Koelsch, KK; Lu, B; Margot, N; Miller, MD; Strain, MC; Wong, JK, 2005) |
"We studied the impact of tenofovir disoproxil fumarate, given as an antiretroviral medication, on patients with chronic hepatitis B virus (HBV) co-infection." | 7.73 | Impact of tenofovir-containing antiretroviral therapy on chronic hepatitis B in a cohort co-infected with human immunodeficiency virus. ( Berger, A; Bickel, M; Carlebach, A; Klauke, S; Lutz, T; Staszewski, S; Stephan, C; Stuermer, M, 2005) |
"Treatment for chronic hepatitis B as a once-daily oral dose was well tolerated and associated with significant and sustained reductions in serum HBV DNA levels during treatment." | 6.69 | A placebo-controlled phase I/II study of adefovir dipivoxil in patients with chronic hepatitis B virus infection. ( Chopra, KB; Gilson, RJ; Jaffe, HS; Murray-Lyon, IM; Nelson, MR; Newell, AM; Rice, SJ; Tedder, RS; Toole, J; Weller, IV, 1999) |
"Current therapies for the treatment of chronic hepatitis B virus (HBV) infection do not eliminate viral replication once therapy is stopped, resulting in a rapid rebound of viremia in a majority of patients." | 5.32 | Use of adefovir in the treatment of the chronic hepatitis B virus infection with resistance to lamivudine. ( Barcena Marugan, R; Cid Gomez, L; Lopez Serrano, P, 2003) |
"Adefovir dipivoxil (ADV) is a nucleotide analogue with proven efficacy in chronic hepatitis B (CHB)." | 5.16 | Five years of treatment with adefovir dipivoxil in Chinese patients with HBeAg-positive chronic hepatitis B. ( Barker, K; Daozhen, X; Dixon, J; Guangbi, Y; Hao, W; Hong, R; JinLin, H; Junqi, N; Minde, Z; Xiaqiu, Z; Yagang, C; Yaozong, W; Yimin, M; Youming, C; Yuming, W, 2012) |
"We investigated the impact of early viral load decline on virus-specific T-cell reactivity in 30 hepatitis B e antigen (HBeAg)-positive patients with chronic hepatitis B randomized to monotherapy with adefovir dipivoxil (ADV) or in combination with emtricitabine (ADV/FTC)." | 5.12 | Impact of early viral kinetics on T-cell reactivity during antiviral therapy in chronic hepatitis B. ( Anderson, J; Bowden, S; Cooksley, H; Hui, CK; Lau, GK; Lewin, S; Locornini, S; Mondou, E; Naoumov, NV; Perelson, AS; Powers, KA; Ribeiro, RM; Rousseau, F; Shudo, E; Sorbel, J, 2007) |
"Low-dose TDF monotherapy can control HBV viremia for an extended period of time without the emergence of resistance and is more potent than adefovir at the standard dosage." | 5.12 | Low-dose tenofovir is more potent than adefovir and is effective in controlling HBV viremia in chronic HBeAg-negative hepatitis B. ( Colombo, S; Del Poggio, P; Jamoletti, C; Oggionni, M; Puhalo, V; Zaccanelli, M, 2007) |
"Adefovir dipivoxil is safe for the treatment of chronic hepatitis B in patients with varying degrees of renal dysfunction and lamivudine-resistant HBV and results in biochemical and virological efficacy similar to that reported in the general population." | 5.11 | Efficacy and safety of adefovir dipivoxil in kidney recipients, hemodialysis patients, and patients with renal insufficiency. ( Brosgart, C; Chaix, ML; Currie, G; Fontaine, H; Morales, E; Nalpas, B; Pol, S; Serpaggi, J; Vallet-Pichard, A; Varaut, A; Verkarre, V, 2005) |
"There are few data on the utility of tenofovir diphosphate (TFV-DP) in dried blood spots (DBSs) to predict future viral load (VL) in postpartum women with HIV on antiretroviral therapy (ART)." | 4.12 | Use of Tenofovir Diphosphate Levels to Predict Viremia During the Postpartum Period in Women Living With Human Immunodeficiency Virus (HIV): A Nested Case-Control Study. ( Allerton, J; Castillo-Mancilla, J; Hsiao, NY; Hu, NC; Kabanda, S; Lesosky, M; Malaba, TR; Myer, L; Odayar, J; Orrell, C; Phillips, TK; Wiesner, L, 2022) |
"HBV DNA was extracted from blood samples of two patients with HBeAg-positive chronic HBV infection and persistent viremia despite tenofovir treatment, and subsequently amplified by PCR before full-length HBV genomes were assembled by deep sequencing." | 4.12 | Novel hepatitis B virus reverse transcriptase mutations in patients with sustained viremia despite long-term tenofovir treatment. ( Bajpai, PS; Bukh, J; Dalegaard, MI; Fahnøe, U; Lundh, A; Ryom, L; Weis, N; Winckelmann, A, 2022) |
"Tenofovir diphosphate (TFV-DP) in dried blood spots (DBS) is associated with viral suppression in persons living with HIV (PLWH) taking tenofovir disoproxil fumarate (TDF)." | 3.91 | Predictive Value of Tenofovir Diphosphate in Dried Blood Spots for Future Viremia in Persons Living With HIV. ( Anderson, PL; Bushman, LR; Castillo-Mancilla, JR; Coleman, SS; Coyle, RP; Ellison, L; Gardner, EM; Kiser, JJ; MaWhinney, S; Morrow, M; Zheng, JH, 2019) |
"We determined the cumulative virological, serological and biochemical outcomes of 165 lamivudine-resistant chronic hepatitis B patients on lamivudine and adefovir for up to 5 years." | 3.78 | Outcome of lamivudine-resistant chronic hepatitis B after up to 5 years of combination therapy with adefovir. ( Fung, J; Hung, IF; Lai, CL; Liu, K; Seto, WK; Wong, DK; Yuen, JC; Yuen, MF, 2012) |
"Although one animal had a gradual increase in viremia from 3 years onwards, the other 4 tenofovir-treated animals maintained undetectable viremia with occasional viral blips (≤ 300 RNA copies/ml plasma)." | 3.78 | Prolonged tenofovir treatment of macaques infected with K65R reverse transcriptase mutants of SIV results in the development of antiviral immune responses that control virus replication after drug withdrawal. ( Abel, K; Canfield, DR; Forthal, DN; Geng, Y; Heneine, W; Jayashankar, K; Johnson, JA; LaBranche, CC; Landucci, G; Lipscomb, J; Montefiori, D; Tarara, RP; Trott, KA; Van Rompay, KK, 2012) |
" His HBV is unresponsive to tenofovir/emtricitabine treatment demonstrated by persistent viremia despite lacking known resistance mutations and while having an undetectable HIV-1 viral load." | 3.77 | HIV-HBV vaccine escape mutant infection with loss of HBV surface antibody and persistent HBV viremia on tenofovir/emtricitabine without antiviral resistance. ( Holodniy, M; Schirmer, P; Winters, M, 2011) |
"We report a case of an immunocompromised patient affected by chronic hepatitis B virus (HBV) with high basal HBV viremia (>8 log(10) IU/ml) who failed an entecavir regimen, despite the absence of primary or secondary drug resistance mutations." | 3.77 | Successful switch to tenofovir after suboptimal response to entecavir in an immunocompromised patient with chronic hepatitis B and without genotypic hepatitis B virus resistance. ( Andreoni, M; Bertoli, A; Ceccarelli, L; Perno, CF; Salpini, R; Sarrecchia, C; Sordillo, P; Svicher, V; Volpi, A, 2011) |
"To assess the peripheral T lymphocyte subsets in chronic hepatitis B virus (HBV) infection, and their dynamics in response to adefovir dipivoxil monotherapy." | 3.77 | Parallel decline of CD8+CD38+ lymphocytes and viremia in treated hepatitis B patients. ( Cao, W; Li, TS; Qiu, ZF, 2011) |
" Interestingly, one of the previously described patients, who was initially successfully switched from ADF to tenofovir (TDF) and became virologically suppressed subsequently, experienced a moderate but remarkable rebound of HBV viremia after switching from TDF to entecavir, due to the emergence of renal toxicity." | 3.76 | Selection and counterselection of the rtI233V adefovir resistance mutation during antiviral therapy. ( Funk, A; Helm, M; Olotu, C; Rockstroh, JK; Schildgen, O; Sirma, H; Zöllner, B, 2010) |
"The aim of the study was to identify and characterize hepatitis B virus (HBV) polymerase gene mutations associated with ongoing HBV replication in HIV/HBV-coinfected individuals receiving tenofovir (TDF)." | 3.75 | Prolonged use of tenofovir in HIV/hepatitis B virus (HBV)-coinfected individuals does not lead to HBV polymerase mutations and is associated with persistence of lamivudine HBV polymerase mutations. ( Arrifin, N; Audsley, J; Ayres, A; Bartholomeusz, A; Crowe, SM; Lewin, SR; Locarnini, SA; Mijch, A; Sasadeusz, J; Yuen, LK, 2009) |
"Despite the failure of tenofovir DF/FTC as prophylaxis, selection for drug-resistant transmission did not occur and the blunting of postinfection levels of viremia likely reduced the probability of subsequent forward transmissions during the acute phase." | 3.74 | Drug-susceptible HIV-1 infection despite intermittent fixed-dose combination tenofovir/emtricitabine as prophylaxis is associated with low-level viremia, delayed seroconversion, and an attenuated clinical course. ( Carrington, M; Davis, B; Duh, FM; Jean-Pierre, P; La Roche, M; Markowitz, M; Mehandru, S; Mohri, H; Poles, M; Prada, N, 2008) |
"We reported previously on the emergence and clinical implications of simian immunodeficiency virus (SIVmac251) mutants with a K65R mutation in reverse transcriptase (RT), and the role of CD8+ cell-mediated immune responses in suppressing viremia during tenofovir therapy." | 3.74 | Sequential emergence and clinical implications of viral mutants with K70E and K65R mutation in reverse transcriptase during prolonged tenofovir monotherapy in rhesus macaques with chronic RT-SHIV infection. ( Bischofberger, N; Blackwood, EJ; Heneine, W; Johnson, JA; Lipscomb, J; Marthas, ML; Matthews, TB; North, TW; Pedersen, NC; Singh, RP; Van Rompay, KK, 2007) |
"We studied the impact of hepatitis B virus (HBV) polymerase/reverse transcriptase (Pol/Rt) heterogeneity on adefovir rescue therapy in 34 consecutive chronic hepatitis B patients with viral breakthrough during lamivudine monotherapy." | 3.74 | Emergence of hepatitis B virus quasispecies with lower susceptibility to nucleos(t)ide analogues during lamivudine treatment. ( Bonino, F; Brunetto, MR; Ciccorossi, P; Coco, B; Colombatto, P; Flichman, D; Maina, AM; Moriconi, F; Oliveri, F; Sacco, R, 2007) |
" To explore this possibility, we studied whether CD8(+) cells suppress viremia in four rhesus macaques apparently protected by daily or intermittent Truvada (FTC and tenofovir) during 14 low-dose, rectal SHIV(SF162P3) challenges and during a subsequent drug washout period." | 3.74 | Short communication: no evidence of occult SHIV infection as demonstrated by CD8+ cell depletion after chemoprophylaxis-induced protection from mucosal infection in rhesus macaques. ( Adams, DR; Butera, S; Folks, TM; Garcia-Lerma, JG; Heneine, W; Kersh, EN; Luo, W; Mitchell, J; Otten, RA, 2008) |
" To understand predictors of residual viremia, we measured HIV RNA levels <50 copies/mL in patients after 1 year of treatment with efavirenz and lamivudine plus either tenofovir disoproxil fumarate (n=55) or stavudine (n=45), by use of an HIV RNA assay with a limit of detection of 2." | 3.73 | Predictors of residual viremia in HIV-infected patients successfully treated with efavirenz and lamivudine plus either tenofovir or stavudine. ( Havlir, DV; Ignacio, CC; Koelsch, KK; Lu, B; Margot, N; Miller, MD; Strain, MC; Wong, JK, 2005) |
"We studied the impact of tenofovir disoproxil fumarate, given as an antiretroviral medication, on patients with chronic hepatitis B virus (HBV) co-infection." | 3.73 | Impact of tenofovir-containing antiretroviral therapy on chronic hepatitis B in a cohort co-infected with human immunodeficiency virus. ( Berger, A; Bickel, M; Carlebach, A; Klauke, S; Lutz, T; Staszewski, S; Stephan, C; Stuermer, M, 2005) |
"The ability of tenofovir to suppress viremia in simian immunodeficiency virus (SIV)-infected macaques for years despite the presence of virulent viral mutants with reduced in vitro susceptibility is unprecedented in this animal model." | 3.72 | CD8+-cell-mediated suppression of virulent simian immunodeficiency virus during tenofovir treatment. ( Bischofberger, N; Lawson, JR; Marthas, ML; Pahar, B; Singh, RP; Sodora, DL; Van Rompay, KK; Wingfield, C, 2004) |
"All animals treated with adefovir showed a marked drop in viremia titers during drug administration, followed by a rebound of viral replication after drug withdrawal." | 3.72 | Antiviral effect of adefovir in combination with a DNA vaccine in the duck hepatitis B virus infection model. ( Chevallier, M; Cova, L; Gibbs, CS; Guerret, S; Jamard, C; Le Guerhier, F; Thermet, A; Trépo, C; Zoulim, F, 2003) |
"Transgenic Mov-14 mice, which carry the provirus of Moloney murine leukemia virus (Mo-MuLV) in the germ line and begin to produce infectious virus on embryonic day 14, were used to evaluate the ability of 9-(2-phosphonylmethoxyethyl)adenine (PMEA) to cross the placenta and protect embryos from viremia." | 3.68 | Transplacental antiretroviral therapy with 9-(2-phosphonylmethoxyethyl)adenine is embryotoxic in transgenic mice. ( Balzarini, J; Bronson, R; De Clercq, E; Jaenisch, R; Lee, JS; Mullaney, S; Ruprecht, RM; Sharpe, AH, 1991) |
"One major challenge in the treatment of chronic hepatitis B is to maintain long-term viral suppression without promoting the selection of drug-resistant mutations." | 2.79 | No detectable resistance to tenofovir disoproxil fumarate after 6 years of therapy in patients with chronic hepatitis B. ( Borroto-Esoda, K; Corsa, A; Flaherty, J; Kitrinos, KM; Liu, Y; Marcellin, P; Miller, MD; Snow-Lampart, A, 2014) |
"Treatment for chronic hepatitis B as a once-daily oral dose was well tolerated and associated with significant and sustained reductions in serum HBV DNA levels during treatment." | 2.69 | A placebo-controlled phase I/II study of adefovir dipivoxil in patients with chronic hepatitis B virus infection. ( Chopra, KB; Gilson, RJ; Jaffe, HS; Murray-Lyon, IM; Nelson, MR; Newell, AM; Rice, SJ; Tedder, RS; Toole, J; Weller, IV, 1999) |
" Significant improvement in survival was observed after treatment with BCX4430 at 4 mg/kg of body weight per day dosed intraperitoneally (i." | 1.40 | BCX4430, a novel nucleoside analog, effectively treats yellow fever in a Hamster model. ( Babu, YS; Bantia, S; Julander, JG; Kotian, P; Minning, DM; Morrey, JD; Sheridan, WP; Smee, DF; Taubenheim, BR, 2014) |
"A 36 year old man with chronic hepatitis B and cirrhosis was admitted in our Department for the onset of jaundice, ascites and ALT flare (x 35 u." | 1.35 | Salvage therapy with tenofovir followed by adefovir maintenance in a cirrhotic patient with a lamivudine resistant HBV flare. ( Brancaccio, G; Gaeta, GB; Nardiello, S; Precone, V; Sgrò, G; Stornaiuolo, G, 2009) |
"Success in antiviral therapy for chronic hepatitis B is supported by highly sensitive PCR-based assays for hepatitis B virus (HBV) DNA." | 1.34 | COBAS AmpliPrep-COBAS TaqMan hepatitis B virus (HBV) test: a novel automated real-time PCR assay for quantification of HBV DNA in plasma. ( Allice, T; Cerutti, F; Colucci, G; Franchello, A; Gabella, S; Ghisetti, V; Marzano, A; Pittaluga, F; Varetto, S, 2007) |
"Adefovir dipivoxil (ADV) has demonstrated clinical activity against both wild-type and lamivudine-resistant hepatitis B virus (HBV)." | 1.34 | Evolution of viral load and changes of polymerase and precore/core promoter sequences in lamivudine-resistant hepatitis B virus during adefovir therapy. ( Bae, SH; Chang, UI; Choi, JY; Jang, JW; Lee, YC; Sun, HS; Wie, SH; Yang, JM; Yoon, SK, 2007) |
"In the treated animal, viremia was controlled to low or undetectable for the study duration, and virus-specific responses remained low." | 1.33 | SIV-specific T lymphocyte responses in PBMC and lymphoid tissues of SIV-infected pigtailed macaques during suppressive combination antiretroviral therapy. ( Carruth, LM; Clements, JE; Li, M; Mankowski, JL; Miller, MD; Queen, LA; Shen, A; Siliciano, RF; Tarwater, PM; Zink, MC, 2005) |
"Control of off treatment viremia was associated, at least in part, with CD8+ lymphocytes, based on in vivo CD8 depletion studies." | 1.32 | Transient early post-inoculation anti-retroviral treatment facilitates controlled infection with sparing of CD4+ T cells in gut-associated lymphoid tissues in SIVmac239-infected rhesus macaques, but not resistance to rechallenge. ( Bischofberger, N; Blanchard, J; Cline, AN; Lifson, JD; Pandrea, I; Piatak, M; Purcell, J; Rossio, JL; Veazey, RS, 2003) |
"Current therapies for the treatment of chronic hepatitis B virus (HBV) infection do not eliminate viral replication once therapy is stopped, resulting in a rapid rebound of viremia in a majority of patients." | 1.32 | Use of adefovir in the treatment of the chronic hepatitis B virus infection with resistance to lamivudine. ( Barcena Marugan, R; Cid Gomez, L; Lopez Serrano, P, 2003) |
Research
Studies (87)
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 0 (0.00) | 18.7374 |
1990's | 5 (5.75) | 18.2507 |
2000's | 37 (42.53) | 29.6817 |
2010's | 37 (42.53) | 24.3611 |
2020's | 8 (9.20) | 2.80 |
Authors
Authors | Studies |
---|---|
Odayar, J | 1 |
Orrell, C | 2 |
Phillips, TK | 1 |
Hu, NC | 1 |
Kabanda, S | 1 |
Malaba, TR | 1 |
Allerton, J | 1 |
Wiesner, L | 1 |
Hsiao, NY | 2 |
Castillo-Mancilla, J | 1 |
Lesosky, M | 1 |
Myer, L | 2 |
Han, N | 1 |
Yan, LL | 1 |
Tang, H | 1 |
Jennings, L | 1 |
Robbins, RN | 1 |
Nguyen, N | 1 |
Ferraris, C | 1 |
Leu, CS | 1 |
Dolezal, C | 1 |
Mgbako, O | 1 |
Joska, J | 1 |
Castillo-Mancilla, JR | 2 |
Anderson, PL | 2 |
Remien, RH | 1 |
Winckelmann, A | 1 |
Fahnøe, U | 1 |
Bajpai, PS | 1 |
Dalegaard, MI | 1 |
Lundh, A | 1 |
Ryom, L | 1 |
Bukh, J | 1 |
Weis, N | 1 |
Chen, GJ | 1 |
Sun, HY | 1 |
Chen, LY | 1 |
Hsieh, SM | 1 |
Sheng, WH | 1 |
Liu, WD | 1 |
Chuang, YC | 1 |
Huang, YS | 1 |
Lin, KY | 1 |
Wu, PY | 1 |
Chang, HY | 1 |
Luo, YZ | 1 |
Su, YC | 1 |
Liu, WC | 1 |
Chang, SF | 1 |
Chang, SY | 1 |
Hung, CC | 1 |
Basso, M | 1 |
Battagin, G | 1 |
Nicolè, S | 1 |
Rossi, MC | 1 |
Colombo, F | 1 |
Pirola, N | 1 |
Baratti, S | 1 |
Storato, S | 1 |
Giovagnorio, F | 1 |
Malagnino, V | 1 |
Alessio, G | 1 |
Vinci, A | 1 |
Maurici, M | 1 |
Sarmati, L | 1 |
Parisi, SG | 1 |
Li, ZB | 1 |
Li, L | 1 |
Niu, XX | 1 |
Chen, SH | 1 |
Fu, YM | 1 |
Wang, CY | 1 |
Liu, Y | 2 |
Shao, Q | 1 |
Chen, G | 1 |
Ji, D | 1 |
Solano de la Asunción, C | 1 |
Terol, MJ | 1 |
Saus, A | 1 |
Olea, B | 1 |
Giménez, E | 1 |
Albert, E | 1 |
López-Jiménez, J | 1 |
Andreu, R | 1 |
García, D | 1 |
Fox, L | 1 |
Remigia, MJ | 1 |
Amat, P | 1 |
Solano, C | 1 |
Navarro, D | 1 |
Morrow, M | 1 |
MaWhinney, S | 1 |
Coyle, RP | 1 |
Coleman, SS | 1 |
Gardner, EM | 1 |
Zheng, JH | 1 |
Ellison, L | 1 |
Bushman, LR | 1 |
Kiser, JJ | 1 |
Childs, K | 1 |
Joshi, D | 1 |
Byrne, R | 1 |
Bruce, M | 1 |
Carey, I | 1 |
Agarwal, K | 1 |
Taylor, C | 1 |
Chun, TW | 1 |
Shawn Justement, J | 1 |
Murray, D | 1 |
Kim, CJ | 1 |
Blazkova, J | 1 |
Hallahan, CW | 1 |
Benko, E | 1 |
Costiniuk, CT | 1 |
Kandel, G | 1 |
Ostrowski, M | 1 |
Kaul, R | 1 |
Moir, S | 1 |
Casazza, JP | 1 |
Koup, RA | 1 |
Kovacs, C | 1 |
Fauci, AS | 2 |
Kitrinos, KM | 2 |
Corsa, A | 1 |
Flaherty, J | 1 |
Snow-Lampart, A | 1 |
Marcellin, P | 2 |
Borroto-Esoda, K | 1 |
Miller, MD | 4 |
González-Artacho, C | 1 |
Rodríguez Sicilia, MJ | 1 |
Alegría-Motte, C | 1 |
Gómez García, M | 1 |
Amancha, PK | 2 |
Hong, JJ | 2 |
Rogers, K | 1 |
Ansari, AA | 2 |
Villinger, F | 2 |
Berg, T | 3 |
Zoulim, F | 4 |
Moeller, B | 1 |
Trinh, H | 1 |
Chan, S | 1 |
Dinh, P | 1 |
Flaherty, JF | 1 |
McHutchison, JG | 1 |
Manns, M | 1 |
Hafkin, JS | 1 |
Osborn, MK | 1 |
Localio, AR | 1 |
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Clinical Trials (10)
Trial Overview
Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
A Prospective Cohort Study of Tenofovir Alafenamide Switch Therapy in Chronic Hepatitis B Patients Who Are Unsatisfied to Entecavir Therapy[NCT05583006] | 60 participants (Anticipated) | Observational | 2023-11-06 | Recruiting | |||
A Prospective Cohort Study of Tenofovir Alafenamide Switching Therapy in Kidney or Liver Transplant Recipients With Chronic Hepatitis B Virus Infection[NCT05410496] | Phase 4 | 50 participants (Anticipated) | Interventional | 2021-06-22 | Recruiting | ||
Quantifying Drug Adherence and Drug Exposure to Antiretroviral Therapy.[NCT02012621] | 807 participants (Actual) | Observational | 2013-12-31 | Completed | |||
A Randomized, Double-Blind, Controlled Evaluation of Tenofovir DF Versus Adefovir Dipivoxil for the Treatment of Presumed Pre-Core Mutant Chronic Hepatitis B[NCT00117676] | Phase 3 | 382 participants (Actual) | Interventional | 2005-02-28 | Completed | ||
A Randomized, Double-Blind, Controlled Evaluation of Tenofovir DF Versus Adefovir Dipivoxil for the Treatment of HBeAg Positive Chronic Hepatitis B[NCT00116805] | Phase 3 | 266 participants (Actual) | Interventional | 2005-06-30 | Completed | ||
Multi-center Study Evaluating Persistence of Hepatitis B Virus Replication, Long-term Prognostic Indicators and Their Clinical Relevance in Patients Co-infected With the Human Immunodeficiency Virus and Chronic Hepatitis B[NCT02889094] | 152 participants (Actual) | Observational | 2016-10-31 | Active, not recruiting | |||
Pilot Study Using 123I Radiolabeled 3BNC117 SPECT/CT to Image HIV Reservoir in Chronically Infected HIV Patients[NCT03468582] | Early Phase 1 | 6 participants (Actual) | Interventional | 2018-02-08 | Completed | ||
Prevention of Mother-to-child Transmission of Hepatitis B Virus: a One Arm, Open Label Intervention Study to Estimate the Optimal Timing of Tenofovir (TDF) in Pregnancy[NCT02995005] | Phase 1/Phase 2 | 98 participants (Actual) | Interventional | 2018-05-24 | Completed | ||
Entecavir Intensification for Persistent Hepatitis B Virus (HBV) Viremia in HIV-HBV Infection[NCT00662545] | Phase 4 | 10 participants (Actual) | Interventional | 2008-04-30 | Completed | ||
EuroSIDA Prospective Observational Cohort Study on Clinical and Virological Outcome of European Patients Infected With HIV[NCT02699736] | 23,000 participants (Actual) | Observational [Patient Registry] | 1994-01-31 | Enrolling by invitation | |||
[information is prepared from clinicaltrials.gov, extracted Sep-2024] |
Trial Outcomes
Adjusted Odds Ratio of Level of Tenofovir-diphosphate (TFV-DP) in Dried Blood Spots (DBS) Associated With Odds of HIV Viral Suppression at All Study Visits
HIV viral load, binary cutoff at assay level of detection (<20 copies/mL vs. >= 20 copies/mL); reference group: drug concentration (TFV-DP) < 350 femtomole (fmol)/punch vs. drug concentration (TFV-DP) >= 1850 fmol/punch; adjusted odds ratio calculated using generalized estimating equations; concentration cutoffs established in prior research of healthy volunteers (NCT02012621)
Timeframe: Up to 48 Weeks
Intervention | Adjusted odds ratio (aOR) (Number) |
---|---|
Study Cohort | 73.5 |
Adjusted Odds Ratio of Level of Tenofovir-diphosphate (TFV-DP) in Dried Blood Spots (DBS) Associated With Odds of HIV Viral Suppression at Next Study Visit
HIV viral load, binary cutoff at assay level of detection (<20 copies/mL vs. >= 20 copies/mL); drug concentration (TFV-DP) <800 femtomole (fmol)/punch) vs reference group of drug concentration (TFV-DP) >= 1650 fmol/punch; adjusted odds ratio calculated using generalized estimating equations (NCT02012621)
Timeframe: Up to 48 Weeks
Intervention | Adjusted odds ratio (aOR) (Number) |
---|---|
Study Cohort | 4.7 |
Adjusted Odds Ratio of Three-month Self-reported Adeherence Associated With Odds of HIV Viral Suppression at All Study Visits
HIV viral load, binary cutoff at assay level of detection (<20 copies/mL vs. >= 20 copies/mL); reference group: three-month self-reported adherence <28.5% vs. three-month self-reported adherence 100%; adherence cutoffs established in prior research (NCT02012621)
Timeframe: Up to 48 Weeks
Intervention | Adjusted odds ratio (aOR) (Number) |
---|---|
Study Cohort | 8.5 |
Percentage of Participants With ALT Normalization at Week 48
ALT normalization was defined as ALT > upper limit of normal (ULN) at baseline and within the normal range at the end of blinded treatment. The ULN was 43 U/L for males and 34 U/L for females aged 18 to < 69, and 35 U/L for males and 32 U/L for females aged ≥ 69. (NCT00117676)
Timeframe: Baseline; Week 48
Intervention | percentage of participants (Number) |
---|---|
TDF-TDF | 76.3 |
ADV-TDF | 77.1 |
Percentage of Participants With ALT Normalization at Weeks 96
ALT normalization was defined as ALT > ULN at baseline and within the normal range at Week 96. The ULN was 43 U/L for males and 34 U/L for females aged 18 to < 69, and 35 U/L for males and 32 U/L for females aged ≥ 69. (NCT00117676)
Timeframe: Baseline; Week 96
Intervention | percentage of participants (Number) |
---|---|
TDF-TDF | 72.4 |
ADV-TDF | 68.5 |
Percentage of Participants With HBV DNA < 400 Copies/mL at Week 48
(NCT00117676)
Timeframe: Week 48
Intervention | percentage of participants (Number) |
---|---|
TDF-TDF | 93.2 |
ADV-TDF | 63.2 |
Percentage of Participants With HBV DNA < 400 Copies/mL at Weeks 96
(NCT00117676)
Timeframe: Week 96
Intervention | percentage of participants (Number) |
---|---|
TDF-TDF | 90.6 |
ADV-TDF | 89.3 |
Change From Baseline in ALT at Weeks 48, 96, 144, 192, 240, 288, 336, 384, 432, and 480
(NCT00117676)
Timeframe: Baseline; Weeks 48, 96, 144, 192, 240, 288, 336, 384, 432, and 480
Intervention | units per liter (Mean) | |||||||||
---|---|---|---|---|---|---|---|---|---|---|
Week 48 | Week 96 | Week 144 | Week 192 | Week 240 | Week 288 | Week 336 | Week 384 | Week 432 | Week 480 | |
ADV-TDF | -124.4 | -138.5 | -140.0 | -140.3 | -139.5 | -134.7 | -143.1 | -132.6 | -131.9 | -129.2 |
TDF-TDF | -95.0 | -93.7 | -99.1 | -99.6 | -97.7 | -98.9 | -98.9 | -96.1 | -97.0 | -94.9 |
Change From Baseline in HBV DNA at Weeks 48, 96, 144, 192, 240, 288, 336, 384, 432, and 480
(NCT00117676)
Timeframe: Baseline; Weeks 48, 96, 144, 192, 240, 288, 336, 384, 432, and 480
Intervention | log10 copies/mL (Mean) | |||||||||
---|---|---|---|---|---|---|---|---|---|---|
Week 48 | Week 96 | Week 144 | Week 192 | Week 240 | Week 288 | Week 336 | Week 384 | Week 432 | Week 480 | |
ADV-TDF | -4.07 | -4.74 | -4.77 | -4.75 | -4.77 | -4.81 | -4.81 | -4.79 | -4.69 | -4.75 |
TDF-TDF | -4.57 | -4.54 | -4.61 | -4.56 | -4.59 | -4.61 | -4.61 | -4.56 | -4.60 | -4.57 |
Change From Baseline in Knodell and Ishak Necroinflammatory Scores at Week 240
The Knodell necroinflammatory score is the combined score for necrosis and inflammation domains of the Knodell scoring system, and ranges from 0 (best) to 14 (worst). The Ishak score measures the degree of liver fibrosis (scarring) caused by chronic necroinflammation (inflammation leading to cell death) and ranges from 0 (best) to 6 (worst). (NCT00117676)
Timeframe: Baseline; Week 240
Intervention | units on a scale (Mean) | |
---|---|---|
Knodell Score | Ishak Score | |
ADV-TDF | -4.9 | -4.2 |
TDF-TDF | -4.6 | -4.0 |
Change From Baseline in Knodell and Ishak Necroinflammatory Scores at Week 48
The Knodell necroinflammatory score is the combined score for necrosis and inflammation domains of the Knodell scoring system, and ranges from 0 (best) to 14 (worst). The Ishak score measures the degree of liver fibrosis (scarring) caused by chronic necroinflammation (inflammation leading to cell death) and ranges from 0 (best) to 6 (worst). (NCT00117676)
Timeframe: Baseline; Week 48
Intervention | units on a scale (Mean) | |
---|---|---|
Knodell Necroinflammatory Score | Ishak Necroinflammatory Score | |
ADV-TDF | -3.4 | -2.6 |
TDF-TDF | -3.5 | -2.6 |
Change From Week 48 in ALT at Weeks 96, 144, 192, 240, 288, 336, 384, 432, and 480
(NCT00117676)
Timeframe: Week 48; Weeks 96, 144, 192, 240, 288, 336, 384, 432, and 480
Intervention | units per liter (Mean) | ||||||||
---|---|---|---|---|---|---|---|---|---|
Week 96 | Week 144 | Week 192 | Week 240 | Week 288 | Week 336 | Week 384 | Week 432 | Week 480 | |
ADV-TDF | -0.6 | -0.3 | -3.6 | -3.9 | -4.1 | -2.0 | -3.9 | -8.9 | -5.9 |
TDF-TDF | 2.4 | -0.6 | 0.7 | -2.5 | -3.9 | -2.6 | -2.9 | -4.6 | -2.8 |
Change From Week 48 in HBV DNA at Weeks 96, 144, 192, 240, 288, 336, 384, 432, and 480
(NCT00117676)
Timeframe: Week 48; Weeks 96, 144, 192, 240, 288, 336, 384, 432, and 480
Intervention | log10 copies/mL (Mean) | ||||||||
---|---|---|---|---|---|---|---|---|---|
Week 96 | Week 144 | Week 192 | Week 240 | Week 288 | Week 336 | Week 384 | Week 432 | Week 480 | |
ADV-TDF | -0.60 | -0.63 | -0.61 | -0.61 | -0.64 | -0.65 | -0.66 | -0.67 | -0.72 |
TDF-TDF | 0.02 | -0.03 | 0.01 | -0.04 | -0.04 | -0.05 | -0.02 | -0.04 | -0.05 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 144 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 144 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 96 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 96 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 97 to 144
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites within HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to genotype | |
ADV-TDF | 0 | 0 | 0 | 0 | 0 |
TDF-TDF | 4 | 0 | 1 | 2 | 1 |
TDF-TDF With Addition of FTC | 0 | 0 | 0 | 0 | 0 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 192 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 192 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 144 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 144 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 145 to 192
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites within HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to genotype | |
ADV-TDF | 0 | 0 | 0 | 0 | 0 |
TDF-TDF | 3 | 0 | 1 | 1 | 1 |
TDF-TDF With Addition of FTC | 1 | 0 | 0 | 1 | 0 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 240 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 240 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 192 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 192 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 193 to 240
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites within HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to genotype | |
ADV-TDF | 2 | 0 | 0 | 0 | 2 |
TDF-TDF | 1 | 1 | 0 | 0 | 0 |
TDF-TDF With Addition of FTC | 2 | 0 | 2 | 0 | 0 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 288 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 288 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 240 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 240 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 241 to 288
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites within HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to genotype | |
ADV-TDF | 1 | 0 | 1 | 0 | 0 |
TDF-TDF | 3 | 0 | 2 | 1 | 0 |
TDF-TDF With Addition of FTC | 1 | 0 | 1 | 0 | 0 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 336 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 336 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 288 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 288 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 289 to 336
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites within HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to genotype | |
ADV-TDF | 1 | 0 | 0 | 0 | 1 |
TDF-TDF | 0 | 0 | 0 | 0 | 0 |
TDF-TDF With Addition of FTC | 1 | 0 | 0 | 1 | 0 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 384 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 384 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 336 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 336 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 337 to 384
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites within HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to genotype | |
ADV-TDF | 0 | 0 | 0 | 0 | 0 |
TDF-TDF | 1 | 0 | 0 | 0 | 1 |
TDF-TDF With Addition of FTC | 0 | 0 | 0 | 0 | 0 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 432 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 432 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 384 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 384 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 385 to 432
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites within HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to genotype | |
ADV-TDF | 1 | 0 | 1 | 0 | 0 |
TDF-TDF | 2 | 0 | 0 | 2 | 0 |
TDF-TDF With Addition of FTC | 0 | 0 | 0 | 0 | 0 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 48 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 48, those with viral breakthrough, and those who discontinued after Week 24 with HBV DNA ≥ 400 copies/mL. (NCT00117676)
Timeframe: Baseline; Week 48
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites in HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to be genotyped | |
ADV-TDF | 42 | 7 | 14 | 20 | 1 |
TDF-TDF | 8 | 0 | 3 | 4 | 1 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 480 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 480 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 432 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 432 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 433 to 480
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites within HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to genotype | |
ADV-TDF | 0 | 0 | 0 | 0 | 0 |
TDF-TDF | 0 | 0 | 0 | 0 | 0 |
TDF-TDF With Addition of FTC | 0 | 0 | 0 | 0 | 0 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 96 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 96 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 48 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00117676)
Timeframe: Baseline; Weeks 49 to 96
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites within HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to be genotyped | |
ADV-TDF | 0 | 0 | 0 | 0 | 0 |
TDF-TDF | 6 | 0 | 2 | 4 | 0 |
TDF-TDF With Addition of FTC | 1 | 0 | 1 | 0 | 0 |
Percentage of Participants With ALT Normalization at Weeks 144, 192, 240, 288, 336, and 384
ALT normalization was defined as ALT > ULN at baseline and within the normal range at the subsequent time point. The ULN was 43 U/L for males and 34 U/L for females aged 18 to < 69, and 35 U/L for males and 32 U/L for females aged ≥ 69. (NCT00117676)
Timeframe: Baseline; Weeks 144, 192, 240, 288, 336, and 384
Intervention | percentage of participants (Number) | |||||
---|---|---|---|---|---|---|
Week 144 | Week 192 | Week 240 | Week 288 | Week 336 | Week 384 | |
ADV-TDF | 70.0 | 76.4 | 75.7 | 72.9 | 65.4 | 69.2 |
TDF-TDF | 74.3 | 68.2 | 70.3 | 69.9 | 65.9 | 65.3 |
Percentage of Participants With ALT Normalization at Weeks 432 and 480
ALT normalization was defined as ALT > ULN at baseline and within the normal range at the subsequent time point. The ULN was 43 U/L for males and 34 U/L for females aged 18 to < 69, and 35 U/L for males and 32 U/L for females aged ≥ 69. (NCT00117676)
Timeframe: Baseline; Weeks 432 and 480
Intervention | percentage of participants (Number) | |
---|---|---|
Week 432 | Week 480 | |
ADV-TDF | 87.2 | 88.9 |
TDF-TDF | 86.5 | 80.0 |
Percentage of Participants With HBsAg Loss and/or Seroconversion to Anti-HBs at Week 96
HBsAg loss was defined as HBsAg positive at baseline and HBsAg negative at Week 96. Seroconversion to anti-HBs was defined as change of detectable antibody to HBsAg from negative at baseline to positive at Week 96. (NCT00117676)
Timeframe: Baseline; Week 96
Intervention | percentage of participants (Number) | |
---|---|---|
HBsAg Loss | Anti-HBs Seroconversion | |
ADV-TDF | 0 | 0 |
TDF-TDF | 0 | 0 |
Percentage of Participants With HBsAg Loss and/or Seroconversion to Anti-HBs at Weeks 144, 192, 240, 288, 336, 384, 432, and 480
HBsAg loss was defined as HBsAg positive at baseline and HBsAg negative at the subsequent time point. Seroconversion to anti-HBs was defined as change of detectable antibody to HBsAg from negative at baseline to positive at the subsequent time point. (NCT00117676)
Timeframe: Baseline; Weeks 144, 192, 240, 288, 336, 384, 432, and 480
Intervention | percentage of participants (Number) | |||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
HBsAg Loss - Week 144 | Anti-HBs Seroconversion - Week 144 | HBsAg Loss - Week 192 | Anti-HBs Seroconversion - Week 192 | HBsAg Loss - Week 240 | Anti-HBs Seroconversion - Week 240 | HBsAg Loss - Week 288 | Anti-HBs Seroconversion - Week 288 | HBsAg Loss - Week 336 | Anti-HBs Seroconversion - Week 336 | HBsAg Loss - Week 384 | Anti-HBs Seroconversion - Week 384 | HBsAg Loss - Week 432 | Anti-HBs Seroconversion - Week 432 | HBsAg Loss - Week 480 | Anti-HBs Seroconversion - Week 480 | |
ADV-TDF | 0 | 0 | 0 | 0 | 0.8 | 0 | 0.8 | 0.8 | 0.8 | 0.8 | 0.8 | 0.8 | 1.6 | 0.8 | 2.4 | 0.8 |
TDF-TDF | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0.8 | 0.4 | 1.2 | 0.4 | 1.2 | 0.8 |
Percentage of Participants With HBV DNA < 400 Copies/mL and Histological Improvement (2-point Reduction in Knodell Necroinflammatory Score Without Worsening in Knodell Fibrosis Score) at Week 48
"Complete response was a composite endpoint defined as histological response and HBV DNA < 400 copies/mL. Histological response was based on the Knodell numerical scoring of liver biopsy specimens and defined as at least a 2-point reduction in Knodell necroinflammatory score without worsening in Knodell fibrosis score. The Knodell necroinflammatory score is the combined necrosis and inflammation domain scores and ranges from 0 to 14; the Knodell fibrosis domain score ranges from 0 to 4.~A participant was a nonresponder for the primary endpoint if either biopsy (baseline or end-of-treatment) was missing or if there was not an HBV DNA value available at or beyond Week 40." (NCT00117676)
Timeframe: Baseline; Week 48
Intervention | percentage of participants (Number) | |
---|---|---|
Yes | No | |
ADV-TDF | 48.8 | 51.2 |
TDF-TDF | 70.8 | 29.2 |
Percentage of Participants With HBV DNA < 400 Copies/mL at Weeks 144, 192, 240, 288, 336, and 384
(NCT00117676)
Timeframe: Weeks 144, 192, 240, 288, 336, and 384
Intervention | percentage of participants (Number) | |||||
---|---|---|---|---|---|---|
Week 144 | Week 192 | Week 240 | Week 288 | Week 336 | Week 384 | |
ADV-TDF | 88.4 | 86.8 | 83.9 | 82.9 | 78.0 | 76.3 |
TDF-TDF | 86.7 | 84.0 | 82.8 | 80.5 | 77.0 | 74.3 |
Percentage of Participants With HBV DNA < 400 Copies/mL at Weeks 432 and 480
(NCT00117676)
Timeframe: Weeks 432 and 480
Intervention | percentage of participants (Number) | |
---|---|---|
Week 432 | Week 480 | |
ADV-TDF | 97.7 | 100.0 |
TDF-TDF | 97.6 | 100.0 |
Percentage of Participants With Hepatitis B S-Antigen (HBsAg) Loss or Seroconversion Antibody to HBs (Anti-HBs) at Week 48
HBsAg loss was defined as HBsAg positive at baseline and HBsAg negative at Week 48. Seroconversion to anti-HBs was defined as change of detectable antibody to HBsAg from negative at baseline to positive at Week 48. (NCT00117676)
Timeframe: Baseline; Week 48
Intervention | percentage of participants (Number) | |
---|---|---|
HBsAg Loss | Seroconversion to anti-HBs | |
ADV-TDF | 0 | 0 |
TDF-TDF | 0 | 0 |
Percentage of Participants With Histological Response at Week 240
Histological response was based on the Knodell numerical scoring of liver biopsy specimens and defined as at least a 2-point reduction in Knodell necroinflammatory score without worsening in Knodell fibrosis score. The Knodell necroinflammatory score is the combined necrosis and inflammation domain scores and ranges from 0 to 14; the Knodell fibrosis domain score ranges from 0 to 4. (NCT00117676)
Timeframe: Baseline; Week 240
Intervention | percentage of participants (Number) | |
---|---|---|
Yes | No | |
ADV-TDF | 85.1 | 14.9 |
TDF-TDF | 87.3 | 12.7 |
Percentage of Participants With Histological Response at Week 48
Histological response was based on the Knodell numerical scoring of liver biopsy specimens and defined as at least a 2-point reduction in Knodell necroinflammatory score without worsening in Knodell fibrosis score. The Knodell necroinflammatory score is the combined necrosis and inflammation domain scores and ranges from 0 to 14; the Knodell fibrosis domain score ranges from 0 to 4. (NCT00117676)
Timeframe: Baseline; Week 48
Intervention | percentage of participants (Number) | |
---|---|---|
Yes | No | |
ADV-TDF | 68.8 | 31.2 |
TDF-TDF | 72.4 | 27.6 |
Ranked Assessment of Necroinflammation and Fibrosis at Week 240
Participants were ranked as having improvement, no change, worsening, or missing data (compared to Baseline) based on the Knodell scoring system, and results are presented as the percentage of participants in each category. The Knodell necroinflammatory score is the combined score for necrosis and inflammation domains of the Knodell scoring system, which ranges from 0 (best) to 14 (worst). The Knodell fibrosis domain score ranges from 0 (best) to 4 (worst). A decrease of 1 point or more indicated improvement, and an increase of 1 point or more indicated worsening. (NCT00117676)
Timeframe: Baseline; Week 240
Intervention | percentage of participants (Number) | |||||
---|---|---|---|---|---|---|
Improvement - Necroinflammation | No Change - Necroinflammation | Worsening - Necroinflammation | Improvement - Fibrosis | No Change - Fibrosis | Worsening - Fibrosis | |
ADV-TDF | 94.6 | 1.4 | 4.1 | 59.5 | 33.8 | 6.8 |
TDF-TDF | 96.7 | 2.7 | 0.7 | 62.0 | 34.0 | 4.0 |
Ranked Assessment of Necroinflammation and Fibrosis at Week 48
Participants were ranked as having improvement, no change, worsening, or missing data (compared to Baseline) based on the Knodell scoring system, and results are presented as the percentage of participants in each category. The Knodell necroinflammatory score is the combined score for necrosis and inflammation domains of the Knodell scoring system, which ranges from 0 (best) to 14 (worst). The Knodell fibrosis domain score ranges from 0 (best) to 4 (worst). A decrease of 1 point or more indicated improvement, and an increase of 1 point or more indicated worsening. (NCT00117676)
Timeframe: Baseline; Week 48
Intervention | percentage of participants (Number) | |||||||
---|---|---|---|---|---|---|---|---|
Improvement - Necroinflammation | No Change - Necroinflammation | Worsening - Necroinflammation | Missing Data - Necroinflammation | Improvement - Fibrosis | No Change - Fibrosis | Worsening - Fibrosis | Missing Data - Fibrosis | |
ADV-TDF | 81.6 | 8.0 | 0.8 | 9.6 | 25.6 | 54.4 | 10.4 | 9.6 |
TDF-TDF | 82.0 | 6.8 | 4.8 | 6.4 | 22.0 | 63.2 | 8.4 | 6.4 |
Percentage of Participants With Alanine Aminotransferase (ALT) Normalization at Week 48
ALT normalization was defined as ALT > upper limit of normal (ULN) at baseline and within the normal range at the end of blinded treatment. The ULN was 43 U/L for males and 34 U/L for females aged 18 to < 69, and 35 U/L for males and 32 U/L for females aged ≥ 69. (NCT00116805)
Timeframe: Baseline; Week 48
Intervention | percentage of participants (Number) |
---|---|
TDF-TDF | 68.0 |
ADV-TDF | 54.4 |
Percentage of Participants With ALT Normalization at Week 96
ALT normalization was defined as ALT > ULN at baseline and within the normal range at Week 96. The ULN was 43 U/L for males and 34 U/L for females aged 18 to < 69, and 35 U/L for males and 32 U/L for females aged ≥ 69. (NCT00116805)
Timeframe: Baseline; Week 96
Intervention | percentage of participants (Number) |
---|---|
TDF-TDF | 65.2 |
ADV-TDF | 74.4 |
Percentage of Participants With HBV DNA < 400 Copies/mL and Histological Improvement (2-point Reduction in Knodell Necroinflammatory Score Without Worsening in Knodell Fibrosis Score) at Week 48
"Complete response was a composite endpoint defined as histological response and HBV DNA < 400 copies/mL. Histological response was based on the Knodell numerical scoring of liver biopsy specimens and defined as at least a 2-point reduction in Knodell necroinflammatory score without worsening in Knodell fibrosis score. The Knodell necroinflammatory score is the combined necrosis and inflammation domain scores and ranges from 0 to 14; the Knodell fibrosis domain score ranges from 0 to 4.~A participant was a nonresponder for the primary endpoint if either biopsy (baseline or end-of-treatment) was missing or if there was not an HBV DNA value available at or beyond Week 40." (NCT00116805)
Timeframe: Baseline; Week 48
Intervention | percentage of participants (Number) |
---|---|
TDF-TDF | 66.5 |
ADV 10 mg | 12.2 |
Percentage of Participants With HBV DNA < 400 Copies/mL at Week 48
(NCT00116805)
Timeframe: Week 48
Intervention | percentage of participants (Number) |
---|---|
TDF-TDF | 76.1 |
ADV-TDF | 13.3 |
Percentage of Participants With HBV DNA < 400 Copies/mL at Week 96
(NCT00116805)
Timeframe: Week 96
Intervention | percentage of participants (Number) |
---|---|
TDF-TDF | 77.6 |
ADV-TDF | 77.9 |
Change From Baseline in ALT at Weeks 48, 96, 144, 192, 240, 288, 336, 384, 432, and 480
(NCT00116805)
Timeframe: Baseline; Weeks 48, 96, 144, 192, 240, 288, 336, 384, 432, and 480
Intervention | U/L (Mean) | |||||||||
---|---|---|---|---|---|---|---|---|---|---|
Week 48 | Week 96 | Week 144 | Week 192 | Week 240 | Week 288 | Week 336 | Week 384 | Week 432 | Week 480 | |
ADV-TDF | -106.1 | -120.4 | -126.2 | -139.6 | -134.8 | -130.9 | -132.3 | -133.7 | -162.1 | -157.5 |
TDF-TDF | -107.2 | -107.8 | -100.7 | -101.4 | -95.9 | -102.3 | -101.9 | -108.1 | -105.0 | -92.3 |
Change From Baseline in HBV DNA at Weeks 48, 96, 144, 192, 240, 288, 336, 384, 432, and 480
(NCT00116805)
Timeframe: Baseline; Weeks 48, 96, 144, 192, 240, 288, 336, 384, 432, and 480
Intervention | log10 IU/mL (Mean) | |||||||||
---|---|---|---|---|---|---|---|---|---|---|
Week 48 | Week 96 | Week 144 | Week 192 | Week 240 | Week 288 | Week 336 | Week 384 | Week 432 | Week 480 | |
ADV-TDF | -3.93 | -6.38 | -6.31 | -6.49 | -6.45 | -6.49 | -6.46 | -6.28 | -6.45 | -6.37 |
TDF-TDF | -6.17 | -6.26 | -6.32 | -6.30 | -6.22 | -6.27 | -6.35 | -6.38 | -6.13 | -6.18 |
Change From Baseline in Knodell and Ishak Necroinflammatory Scores at Week 240
The Knodell necroinflammatory score is the combined score for necrosis and inflammation domains of the Knodell scoring system, and ranges from 0 (best) to 14 (worst). The Ishak score measures the degree of liver fibrosis (scarring) caused by chronic necroinflammation (inflammation leading to cell death) and ranges from 0 (best) to 6 (worst). (NCT00116805)
Timeframe: Baseline; Week 240
Intervention | units on a scale (Mean) | |
---|---|---|
Knodell Necroinflammatory Score | Ishak Necroinflammatory Score | |
ADV-TDF | -5.1 | -4.5 |
TDF-TDF | -4.8 | -4.1 |
Change From Baseline in Knodell and Ishak Necroinflammatory Scores at Week 48
The Knodell necroinflammatory score is the combined score for necrosis and inflammation domains of the Knodell scoring system, and ranges from 0 (best) to 14 (worst). The Ishak score measures the degree of liver fibrosis (scarring) caused by chronic necroinflammation (inflammation leading to cell death) and ranges from 0 (best) to 6 (worst). (NCT00116805)
Timeframe: Baseline; Week 48
Intervention | units on a scale (Mean) | |
---|---|---|
Knodell Necroinflammatory Score | Ishak Necroinflammatory Score | |
ADV-TDF | -3.2 | -2.6 |
TDF-TDF | -3.6 | -2.7 |
Change From Week 48 in ALT at Weeks 96, 144, 192, 240, 288, 336, 384, 432, and 480
(NCT00116805)
Timeframe: Week 48; Weeks 96, 144, 192, 240, 288, 336, 384, 432, and 480
Intervention | U/L (Mean) | ||||||||
---|---|---|---|---|---|---|---|---|---|
Week 96 | Week 144 | Week 192 | Week 240 | Week 288 | Week 336 | Week 384 | Week 432 | Week 480 | |
ADV-TDF | -6.9 | -0.7 | -7.8 | -8.1 | -10.3 | -9.3 | -6.9 | -11.6 | -7.1 |
TDF-TDF | -2.0 | -0.4 | -1.3 | 3.7 | -1.6 | -1.2 | -4.4 | -4.3 | -5.5 |
Change From Week 48 in HBV DNA at Weeks 96, 144, 192, 240, 288, 336, 384, 432, and 480
(NCT00116805)
Timeframe: Week 48; Weeks 96, 144, 192, 240, 288, 336, 384, 432, and 480
Intervention | log10 IU/mL (Mean) | ||||||||
---|---|---|---|---|---|---|---|---|---|
Week 96 | Week 144 | Week 192 | Week 240 | Week 288 | Week 336 | Week 384 | Week 432 | Week 480 | |
ADV-TDF | -2.43 | -2.27 | -2.41 | -2.49 | -2.62 | -2.59 | -2.34 | -2.32 | -2.16 |
TDF-TDF | -0.10 | -0.19 | -0.20 | -0.14 | -0.18 | -0.25 | -0.29 | -0.13 | -0.24 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 144 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 144 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 96 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 96 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 97 to 144
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites in HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to be genotyped | |
ADV-TDF | 5 | 2 | 3 | 0 | 0 |
ADV-TDF With Addition of FTC | 5 | 0 | 0 | 3 | 1 |
TDF-TDF | 2 | 1 | 0 | 1 | 0 |
TDF-TDF With Addition of FTC | 7 | 2 | 3 | 2 | 0 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 192 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 192 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 144 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 144 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 145 to 192
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites in HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to be genotyped | |
ADV-TDF | 1 | 0 | 1 | 0 | 0 |
ADV-TDF With Addition of FTC | 1 | 0 | 1 | 0 | 0 |
TDF-TDF | 2 | 0 | 1 | 0 | 1 |
TDF-TDF With Addition of FTC | 5 | 0 | 0 | 1 | 3 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 240 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 240 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 192 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 192 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 193 to 240
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites in HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to be genotyped | |
ADV-TDF | 0 | 0 | 0 | 0 | 0 |
ADV-TDF With Addition of FTC | 1 | 1 | 0 | 0 | 0 |
TDF-TDF | 3 | 0 | 2 | 1 | 0 |
TDF-TDF With Addition of FTC | 3 | 0 | 0 | 2 | 1 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 288 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 288 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 240 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 240 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 241 to 288
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites in HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to be genotyped | |
ADV-TDF | 0 | 0 | 0 | 0 | 0 |
ADV-TDF With Addition of FTC | 0 | 0 | 0 | 0 | 0 |
TDF-TDF | 3 | 0 | 0 | 2 | 1 |
TDF-TDF With Addition of FTC | 0 | 0 | 0 | 0 | 0 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 336 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 336 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 288 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 288 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 289 to 336
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites in HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to be genotyped | |
ADV-TDF | 1 | 0 | 0 | 1 | 0 |
ADV-TDF With Addition of FTC | 0 | 0 | 0 | 0 | 0 |
TDF-TDF | 1 | 0 | 0 | 0 | 1 |
TDF-TDF With Addition of FTC | 0 | 0 | 0 | 0 | 0 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 384 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 384 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 336 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 336 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 337 to 384
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites in HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to be genotyped | |
ADV-TDF | 2 | 1 | 1 | 0 | 0 |
ADV-TDF With Addition of FTC | 2 | 0 | 1 | 1 | 0 |
TDF-TDF | 1 | 0 | 0 | 0 | 1 |
TDF-TDF With Addition of FTC | 0 | 0 | 0 | 0 | 0 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 432 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 432 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 384 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 384 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 385 to 432
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites in HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to be genotyped | |
ADV-TDF | 0 | 0 | 0 | 0 | 0 |
ADV-TDF With Addition of FTC | 1 | 0 | 0 | 1 | 0 |
TDF-TDF | 1 | 0 | 1 | 0 | 0 |
TDF-TDF With Addition of FTC | 3 | 0 | 0 | 3 | 0 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 48 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL, those with viral breakthrough, and those who discontinued after Week 24 with HBV DNA ≥ 400 copies/mL. (NCT00116805)
Timeframe: Baseline; Week 48
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites in HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to be genotyped | |
ADV-TDF | 75 | 8 | 17 | 43 | 7 |
TDF-TDF | 31 | 2 | 13 | 7 | 9 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 480 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 480 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 432 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen after Week 432 and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 433 to 480
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites in HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to be genotyped | |
ADV-TDF | 1 | 0 | 0 | 1 | 0 |
ADV-TDF With Addition of FTC | 0 | 0 | 0 | 0 | 0 |
TDF-TDF | 0 | 0 | 0 | 0 | 0 |
TDF-TDF With Addition of FTC | 3 | 0 | 1 | 2 | 0 |
Number of Participants With HBV Genotypic Changes From Baseline at Week 96 (Resistance Surveillance)
Of the total number analyzed, participants evaluated for resistance included those with HBV DNA ≥ 400 copies/mL at Week 96 on TDF monotherapy, those with viral breakthrough, those who discontinued after Week 48 with HBV DNA ≥ 400 copies/mL, and those who added emtricitabine to the open-label TDF regimen and had HBV DNA ≥ 400 copies/mL at the time of the addition. (NCT00116805)
Timeframe: Baseline; Weeks 49 to 96
Intervention | participants (Number) | ||||
---|---|---|---|---|---|
Participants evaluated | Changes at conserved sites in HBV polymerase | Changes at polymorphic sites in HBV polymerase | No genotypic changes (wild-type virus) | Unable to be genotyped | |
ADV-TDF | 16 | 2 | 1 | 12 | 1 |
ADV-TDF With Addition of FTC | 10 | 3 | 2 | 3 | 2 |
TDF-TDF | 18 | 2 | 3 | 10 | 3 |
TDF-TDF With Addition of FTC | 13 | 0 | 1 | 5 | 7 |
Percentage of Participants With ALT Normalization at Weeks 144, 192, 240, 288, 336, and 384
ALT normalization was defined as ALT > ULN at baseline and within the normal range at the subsequent time point. The ULN was 43 U/L for males and 34 U/L for females aged 18 to < 69, and 35 U/L for males and 32 U/L for females aged ≥ 69. (NCT00116805)
Timeframe: Baseline; Weeks 144, 192, 240, 288, 336, and 384
Intervention | percentage of participants (Number) | |||||
---|---|---|---|---|---|---|
Week 144 | Week 192 | Week 240 | Week 288 | Week 336 | Week 384 | |
ADV-TDF | 67.8 | 69.4 | 65.9 | 70.1 | 67.9 | 67.1 |
TDF-TDF | 60.2 | 59.6 | 50.0 | 51.3 | 46.2 | 52.6 |
Percentage of Participants With ALT Normalization at Weeks 432 and 480
ALT normalization was defined as ALT > ULN at baseline and within the normal range at the subsequent time point. The ULN was 43 U/L for males and 34 U/L for females aged 18 to < 69, and 35 U/L for males and 32 U/L for females aged ≥ 69. (NCT00116805)
Timeframe: Baseline; Weeks 432 and 480
Intervention | percentage of participants (Number) | |
---|---|---|
Week 432 | Week 480 | |
ADV-TDF | 78.6 | 82.8 |
TDF-TDF | 79.6 | 75.0 |
Percentage of Participants With HBeAg Loss or Seroconversion to Anti-HBe at Week 96
HBeAg loss was defined as HBeAg positive at baseline and HBeAg negative at Week 96. Seroconversion to anti-HBe was defined as change of detectable antibody to HBeAg from negative at baseline to positive at Week 96. (NCT00116805)
Timeframe: Baseline; Week 96
Intervention | percentage of participants (Number) | |
---|---|---|
HBeAg Loss | Seroconversion to Anti-HBe | |
ADV-TDF | 25.6 | 22.0 |
TDF-TDF | 25.9 | 22.8 |
Percentage of Participants With HBsAg Loss or Seroconversion to Anti-HBs at Week 96
HBsAg loss was defined as HBsAg positive at baseline and HBsAg negative at the subsequent time point. Seroconversion to anti-HBs was defined as change of detectable antibody to HBsAg from negative at baseline to positive at the subsequent time point. (NCT00116805)
Timeframe: Baseline; Week 96
Intervention | percentage of participants (Number) | |
---|---|---|
HBsAg Loss | Anti-HBs Seroconversion | |
ADV-TDF | 5.8 | 4.7 |
TDF-TDF | 5.3 | 4.1 |
Percentage of Participants With HBsAg Loss or Seroconversion to Anti-HBs at Weeks 144, 192, 240, 288, 336, 384, 432, and 480
HBsAg loss was defined as HBsAg positive at baseline and HBsAg negative at the subsequent time point. Seroconversion to anti-HBs was defined as change of detectable antibody to HBsAg from negative at baseline to positive at the subsequent time point. (NCT00116805)
Timeframe: Baseline; Weeks 144, 192, 240, 288, 336, 384, 432, and 480
Intervention | percentage of participants (Number) | |||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
HBsAg Loss - Week 144 | Anti-HBs Seroconversion - Week 144 | HBsAg Loss - Week 192 | Anti-HBs Seroconversion - Week 192 | HBsAg Loss - Week 240 | Anti-HBs Seroconversion - Week 240 | HBsAg Loss - Week 288 | Anti-HBs Seroconversion - Week 288 | HBsAg Loss - Week 336 | Anti-HBs Seroconversion - Week 336 | HBsAg Loss - Week 384 | Anti-HBs Seroconversion - Week 384 | HBsAg Loss - Week 432 | Anti-HBs Seroconversion - Week 432 | HBsAg Loss - Week 480 | Anti-HBs Seroconversion - Week 480 | |
ADV-TDF | 8.0 | 6.8 | 7.9 | 6.7 | 8.0 | 8.0 | 8.0 | 8.0 | 7.9 | 7.9 | 9.0 | 7.9 | 10.2 | 8.0 | 10.1 | 7.9 |
TDF-TDF | 7.5 | 5.2 | 9.4 | 6.4 | 9.2 | 6.3 | 9.2 | 6.4 | 10.3 | 7.5 | 11.0 | 8.1 | 10.9 | 7.6 | 10.9 | 8.0 |
Percentage of Participants With HBV DNA < 400 Copies/mL at Weeks 144, 192, 240, 288, 336, and 384
(NCT00116805)
Timeframe: Weeks 144, 192, 240, 288, 336, and 384
Intervention | percentage of participants (Number) | |||||
---|---|---|---|---|---|---|
Week 144 | Week 192 | Week 240 | Week 288 | Week 336 | Week 384 | |
ADV-TDF | 70.5 | 71.6 | 66.3 | 64.8 | 62.1 | 60.5 |
TDF-TDF | 71.7 | 67.9 | 63.4 | 61.3 | 59.4 | 56.1 |
Percentage of Participants With HBV DNA < 400 Copies/mL at Weeks 432 and 480
(NCT00116805)
Timeframe: Weeks 432 and 480
Intervention | percentage of participants (Number) | |
---|---|---|
Week 432 | Week 480 | |
ADV-TDF | 100.0 | 96.6 |
TDF-TDF | 93.0 | 98.0 |
Percentage of Participants With Hepatitis B e Antigen (HBeAg) Loss/Seroconversion at Week 48
HBeAg loss was defined as HBeAg positive at baseline and HBeAg negative at Week 48. Seroconversion to anti-HBe was defined as change of detectable antibody to HBeAg from negative at baseline to positive at Week 48. (NCT00116805)
Timeframe: Baseline; Week 48
Intervention | percentage of participants (Number) | |
---|---|---|
HBeAg Loss | HBeAg Seroconversion | |
ADV-TDF | 17.5 | 17.5 |
TDF-TDF | 22.2 | 20.9 |
Percentage of Participants With Hepatitis B S-Antigen (HBsAg) Loss or Seroconversion at Week 48
HBsAg loss was defined as HBsAg positive at baseline and HBsAg negative at Week 48. Seroconversion to anti-HBs was defined as change of detectable antibody to HBsAg from negative at baseline to positive at Week 48. (NCT00116805)
Timeframe: Baseline; Week 48
Intervention | percentage of participants (Number) | |
---|---|---|
HBsAg Loss | HBsAg Seroconversion | |
ADV-TDF | 0 | 0 |
TDF-TDF | 3.2 | 1.3 |
Percentage of Participants With Histological Response at Week 240
Histological response was based on the Knodell numerical scoring of liver biopsy specimens and defined as at least a 2-point reduction in Knodell necroinflammatory score without worsening in Knodell fibrosis score. The Knodell necroinflammatory score is the combined necrosis and inflammation domain scores and ranges from 0 to 14; the Knodell fibrosis domain score ranges from 0 to 4. (NCT00116805)
Timeframe: Baseline; Week 240
Intervention | percentage of participants (Number) | |
---|---|---|
Yes | No | |
ADV-TDF | 89.6 | 10.4 |
TDF-TDF | 88.2 | 11.8 |
Percentage of Participants With Histological Response at Week 48
Histological response was based on the Knodell numerical scoring of liver biopsy specimens and defined as at least a 2-point reduction in Knodell necroinflammatory score without worsening in Knodell fibrosis score. The Knodell necroinflammatory score is the combined necrosis and inflammation domain scores and ranges from 0 to 14; the Knodell fibrosis domain score ranges from 0 to 4. (NCT00116805)
Timeframe: Baseline; Week 48
Intervention | percentage of participants (Number) | |
---|---|---|
Yes | No | |
ADV-TDF | 67.8 | 32.2 |
TDF-TDF | 74.4 | 25.6 |
Ranked Assessment of Necroinflammation and Fibrosis at Week 240
Participants were ranked as having improvement, no change, worsening, or missing data (compared to Baseline) based on the Knodell scoring system, and results are presented as the percentage of participants in each category. The Knodell necroinflammatory score is the combined score for necrosis and inflammation domains of the Knodell scoring system, which ranges from 0 (best) to 14 (worst). The Knodell fibrosis domain score ranges from 0 (best) to 4 (worst). A decrease of 1 point or more indicated improvement, and an increase of 1 point or more indicated worsening. (NCT00116805)
Timeframe: Baseline; Week 240
Intervention | percentage of participants (Number) | |||||
---|---|---|---|---|---|---|
Improvement - Necroinflammation | No Change - Necroinflammation | Worsening - Necroinflammation | Improvement - Fibrosis | No Change - Fibrosis | Worsening - Fibrosis | |
ADV-TDF | 97.9 | 2.1 | 0 | 58.3 | 39.6 | 2.1 |
TDF-TDF | 96.1 | 3.9 | 0 | 56.6 | 39.5 | 3.9 |
Ranked Assessment of Necroinflammation and Fibrosis at Week 48
Participants were ranked as having improvement, no change, worsening, or missing data (compared to Baseline) based on the Knodell scoring system, and results are presented as the percentage of participants in each category. The Knodell necroinflammatory score is the combined score for necrosis and inflammation domains of the Knodell scoring system, which ranges from 0 (best) to 14 (worst). The Knodell fibrosis domain score ranges from 0 (best) to 4 (worst). A decrease of 1 point or more indicated improvement, and an increase of 1 point or more indicated worsening. (NCT00116805)
Timeframe: Baseline; Week 48
Intervention | percentage of participants (Number) | |||||||
---|---|---|---|---|---|---|---|---|
Improvement - Necroinflammation | No Change - Necroinflammation | Worsening - Necroinflammation | Missing Data - Necroinflammation | Improvement - Fibrosis | No Change - Fibrosis | Worsening - Fibrosis | Missing Data - Fibrosis | |
ADV-TDF | 78.9 | 3.3 | 5.6 | 12.2 | 20.0 | 61.1 | 6.7 | 12.2 |
TDF-TDF | 81.3 | 4.5 | 3.4 | 10.8 | 19.9 | 63.6 | 5.1 | 11.4 |
Hepatitis B Virus (HBV) DNA
"HBV DNA carries the genetic blueprint of the virus. How many HBV DNA particles or copies are found in the blood indicates how rapidly the virus is reproducing in the liver." (NCT00662545)
Timeframe: week 24
Intervention | log 10 IU/ml (Median) |
---|---|
Entecavir Intensification | 2.4 |
Standard of Care | 0.8 |
HIV RNA < 75 Copies/ml
(NCT00662545)
Timeframe: entry, week 12, and week 24
Intervention | participants (Number) |
---|---|
Entecavir Intensification | 5 |
Standard of Care | 5 |
Incidence of ALT Flares
ALT flare: sudden increase in blood level of alanine transaminase (ALT) (NCT00662545)
Timeframe: every 4 weeks for 24 weeks
Intervention | participants (Number) |
---|---|
Entecavir Intensification | 0 |
Standard of Care | 0 |
Incidence of New Hepatic Decompensation( Ascites, Variceal Hemorrhage, Encephalopathy)
(NCT00662545)
Timeframe: every 4 weeks for 24 weeks
Intervention | participants (Number) |
---|---|
Entecavir Intensification | 0 |
Standard of Care | 0 |
Incidence of Permanent Discontinuation Due to Toxicity
(NCT00662545)
Timeframe: 24 weeks
Intervention | participants (Number) |
---|---|
Entecavir Intensification | 0 |
Standard of Care | 0 |
Reviews
1 review available for adenine and Viremia
Article | Year |
---|---|
The risk of HIV drug resistance following implementation of pre-exposure prophylaxis.
Topics: Adenine; Animals; Anti-HIV Agents; Deoxycytidine; Drug Administration Schedule; Drug Resistance, Vir | 2010 |
Trials
13 trials available for adenine and Viremia
Article | Year |
---|---|
No detectable resistance to tenofovir disoproxil fumarate after 6 years of therapy in patients with chronic hepatitis B.
Topics: Adenine; Antiviral Agents; DNA, Viral; Double-Blind Method; Drug Resistance, Viral; Genotype; Hepati | 2014 |
No detectable resistance to tenofovir disoproxil fumarate after 6 years of therapy in patients with chronic hepatitis B.
Topics: Adenine; Antiviral Agents; DNA, Viral; Double-Blind Method; Drug Resistance, Viral; Genotype; Hepati | 2014 |
No detectable resistance to tenofovir disoproxil fumarate after 6 years of therapy in patients with chronic hepatitis B.
Topics: Adenine; Antiviral Agents; DNA, Viral; Double-Blind Method; Drug Resistance, Viral; Genotype; Hepati | 2014 |
No detectable resistance to tenofovir disoproxil fumarate after 6 years of therapy in patients with chronic hepatitis B.
Topics: Adenine; Antiviral Agents; DNA, Viral; Double-Blind Method; Drug Resistance, Viral; Genotype; Hepati | 2014 |
Long-term efficacy and safety of emtricitabine plus tenofovir DF vs. tenofovir DF monotherapy in adefovir-experienced chronic hepatitis B patients.
Topics: Adenine; Antiviral Agents; Deoxycytidine; DNA, Viral; Double-Blind Method; Drug Resistance, Viral; D | 2014 |
Persistent viremia in human immunodeficiency virus/hepatitis B coinfected patients undergoing long-term tenofovir: virological and clinical implications.
Topics: Adenine; Adult; Coinfection; DNA, Viral; Drug Resistance, Viral; Female; Follow-Up Studies; Genotype | 2014 |
Use of tenofovir disoproxil fumarate in highly viremic, hepatitis B mono-infected pregnant women.
Topics: Adenine; Adolescent; Adult; Antiviral Agents; DNA, Viral; Female; Hepatitis B; Humans; Infant, Newbo | 2014 |
Five years of treatment with adefovir dipivoxil in Chinese patients with HBeAg-positive chronic hepatitis B.
Topics: Adenine; Adolescent; Adult; Antiviral Agents; Asian People; DNA, Viral; Drug Resistance, Viral; Fema | 2012 |
A randomized study of tenofovir disoproxil fumarate in treatment-experienced HIV-1 infected adolescents.
Topics: Adenine; Adolescent; Anti-HIV Agents; Child; Double-Blind Method; Drug Resistance, Viral; Drug Thera | 2012 |
Augmentation of hepatitis B virus-specific cellular immunity with programmed death receptor-1/programmed death receptor-L1 blockade in hepatitis B virus and HIV/hepatitis B virus coinfected patients treated with adefovir.
Topics: Adenine; Adult; Antiviral Agents; B7-H1 Antigen; CD8-Positive T-Lymphocytes; Double-Blind Method; He | 2013 |
Early virological failure with a combination of tenofovir, didanosine and efavirenz.
Topics: Adenine; Adult; Aged; Alkynes; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; Benzoxazines; | 2005 |
Clinical and virological response to adefovir dipovixil for lamivudine-resistant HBeAg-negative hepatitis B.
Topics: Adenine; Administration, Oral; Adult; Alanine Transaminase; Antiviral Agents; DNA, Viral; Drug Resis | 2005 |
Efficacy and safety of adefovir dipivoxil in kidney recipients, hemodialysis patients, and patients with renal insufficiency.
Topics: Adenine; Adult; Aged; Antiviral Agents; Drug Resistance, Viral; Female; Hepatitis B virus; Hepatitis | 2005 |
Low-dose tenofovir is more potent than adefovir and is effective in controlling HBV viremia in chronic HBeAg-negative hepatitis B.
Topics: Adenine; Adult; Aged; Antiviral Agents; Dose-Response Relationship, Drug; Drug Resistance, Viral; Fe | 2007 |
Impact of early viral kinetics on T-cell reactivity during antiviral therapy in chronic hepatitis B.
Topics: Adenine; Adult; Antiviral Agents; Deoxycytidine; DNA, Viral; Double-Blind Method; Drug Therapy, Comb | 2007 |
A placebo-controlled phase I/II study of adefovir dipivoxil in patients with chronic hepatitis B virus infection.
Topics: Adenine; Adult; Alanine Transaminase; Antiviral Agents; DNA, Viral; Double-Blind Method; Female; Hep | 1999 |
Other Studies
73 other studies available for adenine and Viremia
Article | Year |
---|---|
Use of Tenofovir Diphosphate Levels to Predict Viremia During the Postpartum Period in Women Living With Human Immunodeficiency Virus (HIV): A Nested Case-Control Study.
Topics: Adenine; Anti-HIV Agents; Case-Control Studies; Female; HIV; HIV Infections; Humans; Organophosphate | 2022 |
[Clinical significance and management strategies of low-level viremia during the treatment of chronic hepatitis B].
Topics: Adenine; Antiviral Agents; Hepatitis B virus; Hepatitis B, Chronic; Humans; Tenofovir; Treatment Out | 2021 |
Tenofovir diphosphate in dried blood spots predicts future viremia in persons with HIV taking antiretroviral therapy in South Africa.
Topics: Adenine; Adult; Anti-HIV Agents; Biomarkers; Female; HIV Infections; Humans; Male; Medication Adhere | 2022 |
Novel hepatitis B virus reverse transcriptase mutations in patients with sustained viremia despite long-term tenofovir treatment.
Topics: Adenine; Antiviral Agents; DNA, Viral; Drug Resistance, Viral; Hepatitis B virus; Hepatitis B, Chron | 2022 |
Low-level viraemia and virologic failure among people living with HIV who received maintenance therapy with co-formulated bictegravir, emtricitabine and tenofovir alafenamide versus dolutegravir-based regimens.
Topics: Adenine; Alanine; Amides; Anti-HIV Agents; Emtricitabine; Heterocyclic Compounds, 3-Ring; Heterocycl | 2022 |
Predicting Factors of Plasma HIV RNA Undetectability after Switching to Co-Formulated Bictegravir, Emtricitabine, and Tenofovir Alafenamide in Experienced HIV-1 Patients: A Multicenter Study.
Topics: Adenine; Emtricitabine; Follow-Up Studies; Heterocyclic Compounds, 4 or More Rings; HIV Seropositivi | 2023 |
Switching from entecavir to tenofovir alafenamide for chronic hepatitis B patients with low-level viraemia.
Topics: Adenine; Alanine; Antiviral Agents; Guanine; Hepatitis B virus; Hepatitis B, Chronic; Humans; Prospe | 2021 |
Switching from entecavir to tenofovir alafenamide for chronic hepatitis B patients with low-level viraemia.
Topics: Adenine; Alanine; Antiviral Agents; Guanine; Hepatitis B virus; Hepatitis B, Chronic; Humans; Prospe | 2021 |
Switching from entecavir to tenofovir alafenamide for chronic hepatitis B patients with low-level viraemia.
Topics: Adenine; Alanine; Antiviral Agents; Guanine; Hepatitis B virus; Hepatitis B, Chronic; Humans; Prospe | 2021 |
Switching from entecavir to tenofovir alafenamide for chronic hepatitis B patients with low-level viraemia.
Topics: Adenine; Alanine; Antiviral Agents; Guanine; Hepatitis B virus; Hepatitis B, Chronic; Humans; Prospe | 2021 |
Cytomegalovirus-specific T-cell immunity and DNAemia in patients with chronic lymphocytic leukaemia undergoing treatment with ibrutinib.
Topics: Adenine; Aged; Aged, 80 and over; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Cytomegalo | 2021 |
Predictive Value of Tenofovir Diphosphate in Dried Blood Spots for Future Viremia in Persons Living With HIV.
Topics: Adenine; Adult; Anti-HIV Agents; Biomarkers; Female; HIV; HIV Infections; Humans; Male; Medication A | 2019 |
Tenofovir-based combination therapy for HIV/HBV co-infection: factors associated with a partial HBV virological response in patients with undetectable HIV viraemia.
Topics: Adenine; Adult; Anti-HIV Agents; Case-Control Studies; Coinfection; Deoxycytidine; DNA, Viral; Drug | 2013 |
Effect of antiretroviral therapy on HIV reservoirs in elite controllers.
Topics: Adenine; Anti-HIV Agents; Asymptomatic Diseases; CD4-CD8 Ratio; CD4-Positive T-Lymphocytes; Deoxycyt | 2013 |
[Outcome of chronic hepatitis B and C in patients with inflammatory bowel disease treated with immunosuppressive drugs and anti-TNF agents].
Topics: Adalimumab; Adenine; Adult; Antibodies, Monoclonal, Humanized; Antiviral Agents; Azathioprine; Crohn | 2014 |
In vivo blockade of the programmed cell death-1 pathway using soluble recombinant PD-1-Fc enhances CD4+ and CD8+ T cell responses but has limited clinical benefit.
Topics: Adenine; Animals; Anti-Retroviral Agents; Antibodies, Monoclonal; Apoptosis; CD4-Positive T-Lymphocy | 2013 |
Incidence and risk factors for incomplete HBV DNA suppression in HIV/HBV-co-infected patients initiating tenofovir-based therapy.
Topics: Adenine; Adult; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; Cohort Studies; Coinfection; | 2014 |
Reduction of infectivity in chronic hepatitis B virus carriers among healthcare providers and pregnant women by antiviral therapy.
Topics: Adenine; Antiviral Agents; DNA, Viral; Female; Guanine; Health Personnel; Hepatitis B e Antigens; He | 2014 |
BCX4430, a novel nucleoside analog, effectively treats yellow fever in a Hamster model.
Topics: Adenine; Adenosine; Alanine Transaminase; Animals; Antibodies, Neutralizing; Antibodies, Viral; Anti | 2014 |
Whole-body immunoPET reveals active SIV dynamics in viremic and antiretroviral therapy-treated macaques.
Topics: Adenine; Animals; Anti-Retroviral Agents; Copper Radioisotopes; Deoxycytidine; Emtricitabine; Immuno | 2015 |
Variability in long-term hepatitis B virus dynamics under antiviral therapy.
Topics: Adenine; Antiviral Agents; DNA, Viral; Female; Follow-Up Studies; Hepatitis B; Hepatitis B virus; Hu | 2016 |
Efficacy of the broad-spectrum antiviral compound BCX4430 against Zika virus in cell culture and in a mouse model.
Topics: Adenine; Adenosine; Animals; Antiviral Agents; Brain; Cell Line; Disease Models, Animal; Humans; Mal | 2017 |
Drug-susceptible HIV-1 infection despite intermittent fixed-dose combination tenofovir/emtricitabine as prophylaxis is associated with low-level viremia, delayed seroconversion, and an attenuated clinical course.
Topics: Adenine; Adult; Amino Acid Sequence; Anti-HIV Agents; CD4 Lymphocyte Count; Chemoprevention; Deoxycy | 2008 |
Effect of tenofovir subtraction on HIV plasma viraemia, CD4+ T-cell count and resistance in a patient with baseline K65R and M184V mutations.
Topics: Adenine; Adult; Anti-HIV Agents; CD4 Lymphocyte Count; Drug Administration Schedule; Drug Resistance | 2008 |
Prolonged use of tenofovir in HIV/hepatitis B virus (HBV)-coinfected individuals does not lead to HBV polymerase mutations and is associated with persistence of lamivudine HBV polymerase mutations.
Topics: Adenine; Adult; Aged; Antiretroviral Therapy, Highly Active; Antiviral Agents; Cross-Sectional Studi | 2009 |
Initiation of antiretroviral therapy 48 hours after infection with simian immunodeficiency virus potently suppresses acute-phase viremia and blocks the massive loss of memory CD4+ T cells but fails to prevent disease.
Topics: Adenine; Amino Acid Sequence; Animals; Anti-HIV Agents; CD4-Positive T-Lymphocytes; Cells, Cultured; | 2009 |
Salvage therapy with tenofovir followed by adefovir maintenance in a cirrhotic patient with a lamivudine resistant HBV flare.
Topics: Adenine; Adult; Antiviral Agents; DNA, Viral; Drug Resistance, Viral; Drug Therapy, Combination; Hep | 2009 |
The absence of HIV mutations in cerebrospinal fluid and in peripheral blood mononuclear cells during a regimen containing Trizivir plus tenofovir.
Topics: Adenine; Anti-HIV Agents; Cohort Studies; Drug Combinations; Drug Therapy, Combination; HIV Infectio | 2009 |
Tenofovir: new indication. In chronic hepatitis B: beware bone toxicity.
Topics: Adenine; Antiviral Agents; Bone and Bones; Bone Diseases; Double-Blind Method; Drug Approval; Europe | 2009 |
Selection and counterselection of the rtI233V adefovir resistance mutation during antiviral therapy.
Topics: Adenine; Adult; Amino Acid Sequence; Amino Acid Substitution; Antiviral Agents; Drug Resistance, Vir | 2010 |
Low-abundance HIV species and their impact on mutational profiles in patients with virological failure on once-daily abacavir/lamivudine/zidovudine and tenofovir.
Topics: Adenine; Adolescent; Adult; Aged; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; Dideoxynuc | 2010 |
Lamivudine-resistance mutations can be selected even at very low levels of hepatitis B viraemia.
Topics: Adenine; Adult; Aged; Antiviral Agents; DNA, Viral; Drug Resistance, Viral; Female; Hepatitis B viru | 2010 |
Rapid HIV-RNA decline following addition of raltegravir and tenofovir to ongoing highly active antiretroviral therapy in a woman presenting with high-level HIV viraemia at week 38 of pregnancy.
Topics: Adenine; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; Female; HIV Infections; Humans; Org | 2010 |
More research needed to find new HIV-suppressive functions of cytotoxic T cells.
Topics: Adenine; Animals; Combined Modality Therapy; Deoxycytidine; Emtricitabine; HIV Infections; Humans; L | 2010 |
Tenofovir (TDF)-selected or abacavir (ABC)-selected low-frequency HIV type 1 subpopulations during failure with persistent viremia as detected by ultradeep pyrosequencing.
Topics: Adenine; Dideoxynucleosides; HIV-1; Humans; Organophosphonates; Reverse Transcriptase Inhibitors; Te | 2011 |
Parallel decline of CD8+CD38+ lymphocytes and viremia in treated hepatitis B patients.
Topics: Adenine; ADP-ribosyl Cyclase 1; Adult; CD3 Complex; Female; Hepatitis B, Chronic; Humans; Male; Memb | 2011 |
Successful switch to tenofovir after suboptimal response to entecavir in an immunocompromised patient with chronic hepatitis B and without genotypic hepatitis B virus resistance.
Topics: Adenine; Adult; Alanine Transaminase; Antiviral Agents; Bone Marrow; DNA, Viral; Drug Therapy, Combi | 2011 |
HIV-HBV vaccine escape mutant infection with loss of HBV surface antibody and persistent HBV viremia on tenofovir/emtricitabine without antiviral resistance.
Topics: Adenine; Antiviral Agents; Coinfection; Deoxycytidine; Drug Resistance, Viral; Emtricitabine; Hepati | 2011 |
Predictors of HBeAg status and hepatitis B viraemia in HIV-infected patients with chronic hepatitis B in the HAART era in Brazil.
Topics: Adenine; Adult; Alanine Transaminase; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; Brazil | 2011 |
Entecavir plus tenofovir combination as rescue therapy in pre-treated chronic hepatitis B patients: an international multicenter cohort study.
Topics: Adenine; Adult; Aged; Antiviral Agents; Cohort Studies; Drug Resistance, Viral; Drug Therapy, Combin | 2012 |
Tenofovir disoproxil fumarate for prevention of vertical transmission of hepatitis B virus infection by highly viremic pregnant women: a case series.
Topics: Adenine; Adult; Alanine Transaminase; Antiviral Agents; Drug Administration Routes; Female; Hepatiti | 2012 |
A highly intensified ART regimen induces long-term viral suppression and restriction of the viral reservoir in a simian AIDS model.
Topics: Adenine; Animals; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; Cyclohexanes; Darunavir; D | 2012 |
Reduced inflammation and CD4 loss in acute SHIV infection during oral pre-exposure prophylaxis.
Topics: Adenine; Alanine; Animals; Anti-HIV Agents; CD4 Lymphocyte Count; CD4-Positive T-Lymphocytes; Cytoki | 2012 |
Prolonged tenofovir treatment of macaques infected with K65R reverse transcriptase mutants of SIV results in the development of antiviral immune responses that control virus replication after drug withdrawal.
Topics: Adenine; Alleles; Animals; Antibodies, Viral; Antibody Formation; Antiviral Agents; CD4 Lymphocyte C | 2012 |
Evolution of adefovir-resistant HBV polymerase gene variants after switching to tenofovir disoproxil fumarate monotherapy.
Topics: Adenine; Adult; Aged; Antiviral Agents; Cloning, Molecular; DNA, Viral; Drug Resistance, Viral; Drug | 2012 |
Outcome of lamivudine-resistant chronic hepatitis B after up to 5 years of combination therapy with adefovir.
Topics: Adenine; Adult; Aged; Alanine Transaminase; Antiviral Agents; DNA, Viral; Drug Resistance, Viral; Dr | 2012 |
Evaluation of single and combination therapies with tenofovir disoproxil fumarate and emtricitabine in vitro and in a robust mouse model supporting high levels of hepatitis B virus replication.
Topics: Adenine; Animals; Antiviral Agents; Cell Line; Deoxycytidine; Drug Combinations; Drug Interactions; | 2012 |
Antiviral effect of adefovir in combination with a DNA vaccine in the duck hepatitis B virus infection model.
Topics: Adenine; Animals; Antibody Formation; Antiviral Agents; Ducks; Hepadnaviridae Infections; Hepatitis | 2003 |
Use of adefovir in the treatment of the chronic hepatitis B virus infection with resistance to lamivudine.
Topics: Adenine; Antiviral Agents; DNA, Viral; Drug Resistance, Viral; Female; Hepatitis B virus; Hepatitis | 2003 |
Transient early post-inoculation anti-retroviral treatment facilitates controlled infection with sparing of CD4+ T cells in gut-associated lymphoid tissues in SIVmac239-infected rhesus macaques, but not resistance to rechallenge.
Topics: Adenine; Animals; Anti-HIV Agents; CD4-Positive T-Lymphocytes; DNA Primers; Gene Products, env; Gene | 2003 |
Highly uneven distribution of tenofovir-selected simian immunodeficiency virus in different anatomical sites of rhesus macaques.
Topics: Adenine; Animals; DNA Mutational Analysis; Drug Resistance, Viral; Genotype; Longitudinal Studies; M | 2004 |
CD8+-cell-mediated suppression of virulent simian immunodeficiency virus during tenofovir treatment.
Topics: Adenine; Animals; Antiviral Agents; CD8-Positive T-Lymphocytes; Macaca mulatta; Organophosphonates; | 2004 |
Virologic outcome after switching from a nucleoside reverse transcriptase inhibitor to tenofovir in patients with undetectable HIV-1 RNA plasma level.
Topics: Adenine; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; Drug Resistance, Viral; HIV Infecti | 2004 |
Suppression of lamivudine-resistant B-domain mutants by adefovir dipivoxil in the woodchuck hepatitis virus model.
Topics: Adenine; Administration, Oral; Amino Acid Motifs; Amino Acid Substitution; Animals; Antiviral Agents | 2004 |
Predictors of residual viremia in HIV-infected patients successfully treated with efavirenz and lamivudine plus either tenofovir or stavudine.
Topics: Adenine; Adolescent; Adult; Alkynes; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; Benzoxa | 2005 |
SIV-specific T lymphocyte responses in PBMC and lymphoid tissues of SIV-infected pigtailed macaques during suppressive combination antiretroviral therapy.
Topics: Adenine; Animals; Anti-Retroviral Agents; Drug Therapy, Combination; Emtricitabine; Immunity, Cellul | 2005 |
Adherence to trizivir and tenofovir as a simplified salvage regimen is associated with suppression of viraemia and a decreased cholesterol.
Topics: Acquired Immunodeficiency Syndrome; Adenine; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; | 2005 |
Antiviral effect of oral administration of tenofovir disoproxil fumarate in woodchucks with chronic woodchuck hepatitis virus infection.
Topics: Adenine; Administration, Oral; Animals; Antiviral Agents; Dose-Response Relationship, Drug; Hepatiti | 2005 |
Impact of tenofovir-containing antiretroviral therapy on chronic hepatitis B in a cohort co-infected with human immunodeficiency virus.
Topics: Adenine; Adult; Aged; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; Cohort Studies; DNA, V | 2005 |
DNA immunization in combination with effective antiretroviral drug therapy controls viral rebound and prevents simian AIDS after treatment is discontinued.
Topics: Adenine; Animals; Anti-HIV Agents; CD4 Lymphocyte Count; CD8-Positive T-Lymphocytes; Cell Proliferat | 2006 |
Variant of hepatitis B virus with primary resistance to adefovir.
Topics: Adenine; Amino Acid Sequence; Antiviral Agents; DNA, Viral; Drug Resistance, Viral; Female; Hepatiti | 2006 |
Relationship between antiretrovirals used as part of a cART regimen and CD4 cell count increases in patients with suppressed viremia.
Topics: Adenine; Adult; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; CD4 Lymphocyte Count; Female | 2006 |
Nonresponse to adefovir: host or virus dependent?
Topics: Adenine; Adult; Antiviral Agents; Female; Hepatitis B; Hepatitis B virus; Humans; Organophosphonates | 2006 |
Administration of fludarabine-loaded autologous red blood cells in simian immunodeficiency virus-infected sooty mangabeys depletes pSTAT-1-expressing macrophages and delays the rebound of viremia after suspension of antiretroviral therapy.
Topics: Adenine; Animals; Antiretroviral Therapy, Highly Active; Antiviral Agents; Cercocebus atys; Drug Car | 2006 |
COBAS AmpliPrep-COBAS TaqMan hepatitis B virus (HBV) test: a novel automated real-time PCR assay for quantification of HBV DNA in plasma.
Topics: Adenine; Antiviral Agents; Automation; Biopsy; DNA, Viral; Drug Resistance, Viral; Hepatitis B Surfa | 2007 |
Induction therapy with enfuvirtide-based highly active antiretroviral therapy in a patient with acute HIV-1 infection.
Topics: Adenine; Adult; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; Deoxycytidine; Emtricitabine | 2007 |
Sequential emergence and clinical implications of viral mutants with K70E and K65R mutation in reverse transcriptase during prolonged tenofovir monotherapy in rhesus macaques with chronic RT-SHIV infection.
Topics: Adenine; Amino Acid Substitution; Animals; Anti-HIV Agents; CD8-Positive T-Lymphocytes; Disease Mode | 2007 |
Evolution of viral load and changes of polymerase and precore/core promoter sequences in lamivudine-resistant hepatitis B virus during adefovir therapy.
Topics: Adenine; Adult; Antiviral Agents; Base Sequence; DNA Mutational Analysis; DNA Primers; DNA, Viral; D | 2007 |
Emergence of hepatitis B virus quasispecies with lower susceptibility to nucleos(t)ide analogues during lamivudine treatment.
Topics: Adenine; Adult; Aged; Antiviral Agents; DNA-Directed DNA Polymerase; DNA, Viral; Drug Resistance, Vi | 2007 |
Short communication: no evidence of occult SHIV infection as demonstrated by CD8+ cell depletion after chemoprophylaxis-induced protection from mucosal infection in rhesus macaques.
Topics: Adenine; Animals; Anti-HIV Agents; Antibodies; Antibody Specificity; Antiviral Agents; CD8-Positive | 2008 |
Viral dynamics of primary viremia and antiretroviral therapy in simian immunodeficiency virus infection.
Topics: Adenine; AIDS Vaccines; Animals; Antiviral Agents; Cells, Cultured; Humans; Kinetics; Lymphocytes; M | 1997 |
Two doses of PMPA protect newborn macaques against oral simian immunodeficiency virus infection.
Topics: Adenine; Animals; Animals, Newborn; Anti-HIV Agents; Antibodies, Viral; Dose-Response Relationship, | 1998 |
Hybridization-AT-tailing (HybrAT) method for sensitive and strand-specific detection of DNA and RNA.
Topics: Adenine; Base Sequence; DNA; DNA-Directed DNA Polymerase; Hepatitis C; Hepatitis C Antibodies; Human | 1998 |
Control of SIV rebound through structured treatment interruptions during early infection.
Topics: Adenine; Animals; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; CD4 Lymphocyte Count; CD8- | 2000 |
Vaccines. Monkey puzzles.
Topics: Acquired Immunodeficiency Syndrome; Adenine; AIDS Vaccines; Animals; Anti-HIV Agents; Clinical Trial | 2002 |
Transplacental antiretroviral therapy with 9-(2-phosphonylmethoxyethyl)adenine is embryotoxic in transgenic mice.
Topics: Adenine; Animals; Antiviral Agents; Embryo, Mammalian; Female; Fetal Resorption; Litter Size; Matern | 1991 |