期刊
FEMS MICROBIOLOGY LETTERS
卷 202, 期 2, 页码 149-156出版社
OXFORD UNIV PRESS
DOI: 10.1016/S0378-1097(01)00286-5
关键词
hepatitis C virus; core protein; gene regulation; apoptosis; cell growth regulation; immune response
类别
资金
- NIAID NIH HHS [AI45250, AI45144] Funding Source: Medline
- NIDDK NIH HHS [DK58023, DK5614301] Funding Source: Medline
Hepatitis C virus (HCV) often causes a prolonged and persistent infection, and an association between hepatocellular carcinoma (HCC) and HCV infection has been noted. The pathogenesis of liver damage. is at least in part related to virus-mediated factors. Understanding the molecular basis of pathogenesis is a major challenge in gaining insight into HCV-associated disease progression. Recent experimental evidence using HCV cloned genomic regions suggests that the core protein has numerous functional activities. These include its likely role in encapsidation of viral RNA, a regulatory effect on cellular and unrelated viral promoters, interactions with a number of cellular proteins, an modulatory role in programmed cell death or apoptosis under certain conditions, involvement in cell growth promotion and immortalization, induction of HCC in transgenic mice, and a possible immunoregulatory role. These intriguing properties suggest that the core protein, in concert with cellular factors, may contribute to pathogenesis during persistent HCV infection. (C) 2001 Federation of European Microbiological Societies. Published by Elsevier Science B.V. All rights reserved.
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