vasoactive-intestinal-peptide has been researched along with Zika-Virus-Infection* in 2 studies
1 review(s) available for vasoactive-intestinal-peptide and Zika-Virus-Infection
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Vasoactive intestinal peptide: a potential target for antiviral therapy.
Viral infection is clinically common and some viral diseases, such as the ongoing global outbreak of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), have high morbidity and mortality. However, most viral infections are currently lacking in specific therapeutic agents and effective prophylactic vaccines, due to inadequate response, increased rate of drug resistance and severe adverse side effects. Therefore, it is urgent to find new specific therapeutic targets for antiviral defense among which "peptide-based therapeutics" is an emerging field. Peptides may be promising antiviral drugs because of their high efficacy and low toxic side effects. Vasoactive intestinal peptide (VIP) is a prospective antiviral peptide. Since its successful isolation in 1970, VIP has been reported to be involved in infections of SARS-CoV-2, human immune deficiency virus (HIV), vesicular stomatitis virus (VSV), respiratory syncytial virus (RSV), Zika virus (ZIKV) and cytomegalovirus (CMV). Additionally, given that viral attacks sometimes cause severe complications due to overaction of inflammatory and immune responses, the potent anti-inflammatory and immunoregulator properties of VIP facilitate it to be a powerful and promising candidate. This review summarizes the role and mechanisms of VIP in all reported viral infections and suggests its clinical potential as an antiviral therapeutic target. Topics: Antiviral Agents; COVID-19 Drug Treatment; Humans; Prospective Studies; SARS-CoV-2; Vasoactive Intestinal Peptide; Zika Virus; Zika Virus Infection | 2022 |
1 other study(ies) available for vasoactive-intestinal-peptide and Zika-Virus-Infection
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Zika virus infection of first trimester trophoblast cells affects cell migration, metabolism and immune homeostasis control.
Zika virus (ZIKV) re-emerged after circulating almost undetected for many years and the last spread in 2015 was the major outbreak reported. ZIKV infection was associated with congenital fetal growth anomalies such as microcephaly, brain calcifications, and low birth weight related to fetal growth restriction. In this study, we investigated the effect of ZIKV infection on first trimester trophoblast cell function and metabolism. We also studied the interaction of trophoblast cells with decidual immune populations. Results presented here demonstrate that ZIKV infection triggered a strong antiviral response in first trimester cytotrophoblast-derived cells, impaired cell migration, increased glucose uptake and GLUT3 expression, and reduced brain derived neurotrophic factor (BDNF) expression. ZIKV infection also conditioned trophoblast cells to favor a tolerogenic response since an increased recruitment of CD14+ monocytes bearing an anti-inflammatory profile, increased CD4+ T cells and NK CD56 Topics: Brain-Derived Neurotrophic Factor; CD4-Positive T-Lymphocytes; Cell Movement; Cells, Cultured; Congenital Abnormalities; Energy Metabolism; Female; Fetus; Glucose; Glucose Transporter Type 3; Humans; Placenta; Placentation; Pregnancy; Pregnancy Trimester, First; Trophoblasts; Vasoactive Intestinal Peptide; Zika Virus; Zika Virus Infection | 2021 |