HBV Bypasses the Innate Immune Response and Does Not Protect HCV From Antiviral Activity of Interferon.
Fiche publication
Date publication
mai 2018
Journal
Gastroenterology
Auteurs
Membres identifiés du Cancéropôle Est :
Pr BAUMERT Thomas
Tous les auteurs :
Mutz P, Metz P, Lempp FA, Bender S, Qu B, Schöneweis K, Seitz S, Tu T, Restuccia A, Frankish J, Dächert C, Schusser B, Koschny R, Polychronidis G, Schemmer P, Hoffmann K, Baumert TF, Binder M, Urban S, Bartenschlager R
Lien Pubmed
Résumé
Hepatitis C virus (HCV) infection is sensitive to interferon (IFN)-based therapy, whereas hepatitis B virus (HBV) infection is not. It is unclear whether HBV escapes detection by the IFN-mediated immune response or actively suppresses it. Moreover, little is known on how HBV and HCV influence each other in coinfected cells. We investigated interactions between HBV and the IFN-mediated immune response using HepaRG cells and primary human hepatocytes (PHHs). We analyzed the effects of HBV on HCV replication, and vice versa, at the single-cell level.
Mots clés
Antiviral Agents, pharmacology, Coinfection, drug therapy, DNA, Viral, drug effects, Hepacivirus, drug effects, Hepatitis B, drug therapy, Hepatitis B virus, drug effects, Hepatitis C, drug therapy, Hepatocytes, drug effects, Humans, Immunity, Innate, immunology, Interferons, pharmacology, Liver, cytology, Virus Replication, drug effects
Référence
Gastroenterology. 2018 05;154(6):1791-1804.e22