scholarly journals Hepatitis C Virus Entry: An Intriguingly Complex and Highly Regulated Process

2020 ◽  
Vol 21 (6) ◽  
pp. 2091 ◽  
Author(s):  
Che Colpitts ◽  
Pei-Ling Tsai ◽  
Mirjam Zeisel
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Viral Entry ◽  
Chronic Infection ◽  
Molecular Mechanisms ◽  
Therapeutic Potential ◽  
Virus Entry ◽  
Host Factors ◽  
Entry Inhibitors

Hepatitis C virus (HCV) is a major cause of chronic hepatitis and liver disease worldwide. Its tissue and species tropism are largely defined by the viral entry process that is required for subsequent productive viral infection and establishment of chronic infection. This review provides an overview of the viral and host factors involved in HCV entry into hepatocytes, summarizes our understanding of the molecular mechanisms governing this process and highlights the therapeutic potential of host-targeting entry inhibitors.

scholarly journals Hepatitis C Virus Glycan-Dependent Interactions and the Potential for Novel Preventative Strategies

Pathogens ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 685
Author(s):  
Emmanuelle V. LeBlanc ◽  
Youjin Kim ◽  
Chantelle J. Capicciotti ◽  
Che C. Colpitts
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Immune Evasion ◽  
Hcv Infection ◽  
Major Contributor ◽  
Effective Management ◽  
Hcv Treatment ◽  
Entry Inhibitors ◽  
Chronic Hepatitis C Virus

Chronic hepatitis C virus (HCV) infections continue to be a major contributor to liver disease worldwide. HCV treatment has become highly effective, yet there are still no vaccines or prophylactic strategies available to prevent infection and allow effective management of the global HCV burden. Glycan-dependent interactions are crucial to many aspects of the highly complex HCV entry process, and also modulate immune evasion. This review provides an overview of the roles of viral and cellular glycans in HCV infection and highlights glycan-focused advances in the development of entry inhibitors and vaccines to effectively prevent HCV infection.

scholarly journals Reply to Padmanabhan and Dixit: Hepatitis C virus entry inhibitors for optimally boosting direct-acting antiviral-based treatments

2017 ◽  
Vol 114 (23) ◽  
pp. E4527-E4529 ◽  
Author(s):  
Hirofumi Ohashi ◽  
Yoshiki Koizumi ◽  
Kento Fukano ◽  
Takaji Wakita ◽  
Alan S. Perelson ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Entry ◽  
Direct Acting Antiviral ◽  
Entry Inhibitors ◽  
Virus Entry Inhibitors ◽  
Direct Acting

Identification of a series of 1,3,4-trisubstituted pyrazoles as novel hepatitis C virus entry inhibitors

2013 ◽  
Vol 23 (23) ◽  
pp. 6467-6473 ◽  
Author(s):  
Jong Yeon Hwang ◽  
Hee-Young Kim ◽  
Dong-Sik Park ◽  
Jihyun Choi ◽  
Sung Min Baek ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Entry ◽  
Entry Inhibitors ◽  
Virus Entry Inhibitors

Hepatitis C virus resistance to interferon therapy: an alarming situation

2014 ◽  
Vol 9 (12) ◽  
pp. 1155-1167
Author(s):  
Sobia Kanwal ◽  
Tariq Mahmood
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Social Factors ◽  
Molecular Mechanisms ◽  
Public Health Problem ◽  
Pegylated Interferon ◽  
Host Factors ◽  
Interferon Α ◽  
Major Public Health Problem ◽  
Choice Of Treatment

AbstractHepatitis C virus is presently a major public health problem across the globe. The main objective in treating hepatitis C virus (HCV) infection is to achieve a sustained virological response (SVR). Interferon-α (IFN-α) and pegylated interferon (PegIFN) in combination with Ribavirin (RBV) are the choice of treatment nowadays against chronic hepatitis C. There are several mechanisms evolved by the hepatitis C virus that facilitate the persistence of virus and further lead the patient’s status as non responder. Various factors involved in patient’s lack ofresponse to the therapy include: (1) viral factors, (2) host factors, (3) molecular mechanisms related to the lack of response and (4) social factors. Herein we have made an attempt to summarize all the related predictors of drug resistance in one article so that the future polices can be planned to overcome this obstacle and potential therapies can be designed by considering these factors.

scholarly journals Tight Junction Proteins Claudin-1 and Occludin Control Hepatitis C Virus Entry and Are Downregulated during Infection To Prevent Superinfection

2008 ◽  
Vol 83 (4) ◽  
pp. 2011-2014 ◽  
Author(s):  
Shufeng Liu ◽  
Wei Yang ◽  
Le Shen ◽  
Jerrold R. Turner ◽  
Carolyn B. Coyne ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Tight Junction ◽  
Viral Entry ◽  
Virus Entry ◽  
Tight Junction Proteins ◽  
Functional Changes ◽  
Key Factor ◽  
Junction Proteins ◽  
Mutational Study

ABSTRACT A tight junction (TJ) protein, claudin-1 (CLDN1), was identified recently as a key factor for hepatitis C virus (HCV) entry. Here, we show that another TJ protein, occludin, is also required for HCV entry. Mutational study of CLDN1 revealed that its tight junctional distribution plays an important role in mediating viral entry. Together, these data support the model in which HCV enters liver cells from the TJ. Interestingly, HCV infection of Huh-7 hepatoma cells downregulated the expression of CLDN1 and occludin, preventing superinfection. The altered TJ protein expression may contribute to the morphological and functional changes observed in HCV-infected hepatocytes.

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