scholarly journals Hepatitis C Virus Is Primed by CD81 Protein for Low pH-dependent Fusion

2011 ◽  
Vol 286 (35) ◽  
pp. 30361-30376 ◽  
Author(s):  
Nishi R. Sharma ◽  
Guaniri Mateu ◽  
Marlene Dreux ◽  
Arash Grakoui ◽  
François-Loïc Cosset ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Low Ph ◽  
Ph Dependent

scholarly journals Hepatitis C Virus Glycoproteins Mediate Low pH-dependent Membrane Fusion with Liposomes

2006 ◽  
Vol 281 (7) ◽  
pp. 3909-3917 ◽  
Author(s):  
Dimitri Lavillette ◽  
Birke Bartosch ◽  
Delphine Nourrisson ◽  
Géraldine Verney ◽  
François-Loïc Cosset ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Membrane Fusion ◽  
Low Ph ◽  
Ph Dependent

Inactivation of Hepatitis C Virus in Low pH Intravenous Immunoglobulin

Biologicals ◽  
1994 ◽  
Vol 22 (1) ◽  
pp. 13-19 ◽  
Author(s):  
Robert E. Louie ◽  
Cynthia J. Galloway ◽  
Michael L. Dumas ◽  
Melvin F. Wong ◽  
G. Mitra
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Intravenous Immunoglobulin ◽  
Low Ph

scholarly journals Alternative endocytosis pathway for productive entry of hepatitis C virus

2014 ◽  
Vol 95 (12) ◽  
pp. 2658-2667 ◽  
Author(s):  
Mami Matsuda ◽  
Ryosuke Suzuki ◽  
Chikako Kataoka ◽  
Koichi Watashi ◽  
Hideki Aizaki ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Cell Types ◽  
Dominant Negative ◽  
Endocytic Pathway ◽  
Target Cells ◽  
Dominant Negative Form ◽  
Ph Dependent ◽  
P21 Activated Kinase ◽  
Infectious Entry

Previous studies have shown that hepatitis C virus (HCV) enters human hepatic cells through interaction with a series of cellular receptors, followed by clathrin-mediated, pH-dependent endocytosis. Here, we investigated the mechanisms of HCV entry into multiple HCV-permissive human hepatocyte-derived cells using trans-complemented HCV particles (HCVtcp). Knockdown of CD81 and claudin-1, or treatment with bafilomycin A1, reduced infection in Huh-7 and Huh7.5.1 cells, suggesting that HCV entered both cell types via receptor-mediated, pH-dependent endocytosis. Interestingly, knockdown of the clathrin heavy chain or dynamin-2 (Dyn2), as well as expression of the dominant-negative form of Dyn2, reduced infection of Huh-7 cells with HCVtcp, whereas infectious entry of HCVtcp into Huh7.5.1 cells was not impaired. Infection of Huh7.5.1 cells with culture-derived HCV (HCVcc) via a clathrin-independent pathway was also observed. Knockdown of caveolin-1, ADP-ribosylation factor 6 (Arf6), flotillin, p21-activated kinase 1 (PAK1) and the PAK1 effector C-terminal binding protein 1 of E1A had no inhibitory effects on HCVtcp infection into Huh7.5.1 cells, thus suggesting that the infectious entry pathway of HCV into Huh7.5.1 cells was not caveolae-mediated, or Arf6- and flotillin-mediated endocytosis and macropinocytosis, but rather may have occurred via an undefined endocytic pathway. Further analysis revealed that HCV entry was clathrin- and dynamin-dependent in ORL8c and HepCD81/miR122 cells, but productive entry of HCV was clathrin- and dynamin-independent in Hep3B/miR122 cells. Collectively, these data indicated that HCV entered different target cells through different entry routes.

scholarly journals Hepatitis C virus glycoproteins mediate pH-dependent cell entry of pseudotyped retroviral particles

2003 ◽  
Vol 100 (12) ◽  
pp. 7271-7276 ◽  
Author(s):  
M. Hsu ◽  
J. Zhang ◽  
M. Flint ◽  
C. Logvinoff ◽  
C. Cheng-Mayer ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Cell Entry ◽  
Dependent Cell ◽  
Ph Dependent

scholarly journals Time- and Temperature-Dependent Activation of Hepatitis C Virus for Low-pH-Triggered Entry

2006 ◽  
Vol 80 (4) ◽  
pp. 1734-1741 ◽  
Author(s):  
Donna M. Tscherne ◽  
Christopher T. Jones ◽  
Matthew J. Evans ◽  
Brett D. Lindenbach ◽  
Jane A. McKeating ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Viral Entry ◽  
Ebola Virus ◽  
Virus Production ◽  
Low Ph ◽  
Acidic Ph ◽  
Prolonged Incubation ◽  
Diarrhea Virus ◽  
Concanamycin A

ABSTRACT Hepatitis C virus (HCV) is an important human pathogen associated with chronic liver disease. Recently, based on a genotype 2a isolate, tissue culture systems supporting complete replication and infectious virus production have been developed. In this study, we used cell culture-produced infectious HCV to analyze the viral entry pathway into Huh-7.5 cells. Bafilomycin A1 and concanamycin A, inhibitors of vacuolar ATPases, prevented HCV entry when they were present prior to infection and had minimal effect on downstream replication events. HCV entry therefore appears to be pH dependent, requiring an acidified intracellular compartment. For many other enveloped viruses, acidic pH triggers an irreversible conformational change, which promotes virion-endosomal membrane fusion. Such viruses are often inactivated by low pH. In the case of HCV, exposure of virions to acidic pH followed by return to neutral pH did not affect their infectivity. This parallels the observation made for the related pestivirus bovine viral diarrhea virus. Low pH could activate the entry of cell surface-bound HCV but only after prolonged incubation at 37°C. This suggests that there are rate-limiting, postbinding events that are needed to render HCV competent for low-pH-triggered entry. Such events may involve interaction with a cellular coreceptor or other factors but do not require cathepsins B and L, late endosomal proteases that activate Ebola virus and reovirus for entry.

scholarly journals Hepatitis C Virus Entry Requires a Critical Postinternalization Step and Delivery to Early Endosomes via Clathrin-Coated Vesicles

2006 ◽  
Vol 80 (23) ◽  
pp. 11571-11578 ◽  
Author(s):  
Laurent Meertens ◽  
Claire Bertaux ◽  
Tatjana Dragic
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Low Ph ◽  
Dominant Negative ◽  
Coated Vesicles ◽  
Target Cells ◽  
Bafilomycin A1 ◽  
Late Endosomes ◽  
Early Endosomes ◽  
Life Threatening

ABSTRACT Hepatitis C virus (HCV) is a major human pathogen associated with life-threatening liver disease. Entry into hepatocytes requires CD81 and a putative second receptor. In this study, we elucidated the postreceptor attachment stages of HCV entry using HCV pseudoparticles (HCVpp) as a model system. By means of dominant-negative mutants and short interfering RNAs of various cellular proteins, we showed that HCVpp enter via clathrin-coated vesicles and require delivery to early but not to late endosomes. However, the kinetics of HCV envelope glycoprotein-mediated fusion are delayed compared to those of other viruses that enter in early endosomes. Entry of HCVpp can be efficiently blocked by bafilomycin A1, which neutralizes the pH in early endosomes and impairs progression of endocytosis beyond this stage. However, low-pH exposure of bafilomycin A1-treated target cells does not induce entry of HCVpp at the plasma membrane or in the early stages of endocytosis. These observations indicate that, subsequent to internalization, HCVpp entry necessitates additional, low-pH-dependent interactions, modifications, or trafficking, and that these events are irreversibly disrupted by bafilomycin A1 treatment.

HEPATITIS C VIRUS INFECTION (AND ADDITIONAL NEOPLASMS) AMONG MARGINAL ZONE LYMPHOMAS

1997 ◽  
Vol 96 (2) ◽  
pp. 427-428 ◽  
Author(s):  
FREDERICO SILVESTRI ◽  
GIOVANNI BARILLARI ◽  
RENATO FANIN ◽  
FLAVIA SALMASO ◽  
LAURA INFANTI ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Infection ◽  
Marginal Zone ◽  
Hepatitis C Virus Infection
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