Journal
BIOLOGICAL CHEMISTRY
Volume 389, Issue 10, Pages 1283-1298Publisher
WALTER DE GRUYTER GMBH
DOI: 10.1515/BC.2008.147
Keywords
hepatitis C; innate immunity; interferon signaling; pathogen-associated molecular pattern; pathogen recognition receptors; retinoic acid-inducible gene I
Categories
Funding
- Deutsche Forschungsgemeinschaft
- Heisenberg program of the Deutsche Forschungsgemeinschaft
- Priority 1 'Life Sciences, Genomics and Biotechnology for Health' program (FP6) [LSHMCT-2004-503359]
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Hepatitis C virus (HCV) is a serious global health problem which accounts for approximately 40% of chronic liver diseases worldwide. HCV frequently establishes a persistent infection, although it is recognized and targeted by innate immunity as well as cellular and humoral immune mechanisms. This suggests that HCV has developed powerful strategies to escape elimination by innate and adaptive immunity. HCV-induced liver injury is thought to be mainly immune-mediated rather than due to direct cytopathic effects of the virus. Hence, therapeutic strategies should target those mechanisms favoring viral persistence since unspecific enhancement of host antiviral immunity may theoretically also promote liver injury. The present review summarizes our current understanding of how the hepatitis C virus interferes with the innate antiviral host-response to establish persistent infection.
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