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Viruses 2012, 4(10), 2251-2290; doi:10.3390/v4102251
Review

Hepatitis C Virus and Cellular Stress Response: Implications to Molecular Pathogenesis of Liver Diseases

1,2
 and 2,*
Received: 31 August 2012; in revised form: 7 October 2012 / Accepted: 9 October 2012 / Published: 19 October 2012
(This article belongs to the Special Issue Hepatitis C Pathology)
View Full-Text   |   Download PDF [2053 KB, uploaded 19 October 2012]
Abstract: Infection with hepatitis C virus (HCV) is a leading risk factor for chronic liver disease progression, including steatosis, cirrhosis, and hepatocellular carcinoma. With approximately 3% of the human population infected worldwide, HCV infection remains a global public health challenge. The efficacy of current therapy is still limited in many patients infected with HCV, thus a greater understanding of pathogenesis in HCV infection is desperately needed. Emerging lines of evidence indicate that HCV triggers a wide range of cellular stress responses, including cell cycle arrest, apoptosis, endoplasmic reticulum (ER) stress/unfolded protein response (UPR), and autophagy. Also, recent studies suggest that these HCV-induced cellular responses may contribute to chronic liver diseases by modulating cell proliferation, altering lipid metabolism, and potentiating oncogenic pathways. However, the molecular mechanism underlying HCV infection in the pathogenesis of chronic liver diseases still remains to be determined. Here, we review the known stress response activation in HCV infection in vitro and in vivo, and also explore the possible relationship of a variety of cellular responses with the pathogenicity of HCV-associated diseases. Comprehensive knowledge of HCV-mediated disease progression shall shed new insights into the discovery of novel therapeutic targets and the development of new intervention strategy.
Keywords: HCV; host factor; cellular response; autophagy; ER stress; unfolded protein response; apoptosis; DNA damage; cell cycle arrest; liver diseases HCV; host factor; cellular response; autophagy; ER stress; unfolded protein response; apoptosis; DNA damage; cell cycle arrest; liver diseases
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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MDPI and ACS Style

Ke, P.-Y.; Chen, S.-L. Hepatitis C Virus and Cellular Stress Response: Implications to Molecular Pathogenesis of Liver Diseases. Viruses 2012, 4, 2251-2290.

AMA Style

Ke P-Y, Chen S-L. Hepatitis C Virus and Cellular Stress Response: Implications to Molecular Pathogenesis of Liver Diseases. Viruses. 2012; 4(10):2251-2290.

Chicago/Turabian Style

Ke, Po-Yuan; Chen, Steve S.-L. 2012. "Hepatitis C Virus and Cellular Stress Response: Implications to Molecular Pathogenesis of Liver Diseases." Viruses 4, no. 10: 2251-2290.


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