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

Viruses

Po-Yuan Ke¹ 

[1] Department of Biochemistry and Molecular Biology, College of Medicine, Chang Gung University, Taoyuan 33371, Taiwan, Republic of China;

关键词: HCV;    host factor;    cellular response;    autophagy;    ER stress;    unfolded protein response;    apoptosis;    DNA damage;    cell cycle arrest;    liver diseases;   

DOI  :  10.3390/v4102251

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
© 2012 by the authors; licensee MDPI, Basel, Switzerland.