Innate immunity and hepatitis C virus: eluding the host cell defense
Deborah R. Taylor1, Erica Silberstein1
1
Laboratory of Hepatitis and Related Emerging Agents, Division of Emerging and Transfusion-Transmitted Diseases, Office of Blood Research and Review, CBER FDA, 8800 Rockville Pike, HFM-310, NIH Building 29, 131,Bethesda, MD 20892
TABLE OF CONTENTS
- 1. Abstract
- 2. Introduction
- 3. IFN-Stimulated Genes
- 3.1. The IFN-induced dsRNA-activated protein kinase, PKR.
- 3.2. Adenosine deaminase that acts on dsRNA, ADAR1
- 4. Molecular Biology of HCV
- 4.1. HCV genotypes
- 4.2. in vitro systems for the study of HCV
- 5. Viral evasion of the IFN response
- 5.1. NS3/4A and evasion of IFN-beta induction
- 5.2. NS5A and IFN resistance
- 5.3. E2 and IFN resistance
- 5.4. HCV IRES and evasion of IFN
- 5.5. HCV inhibits IFN signaling
- 5.6. HCV and 2', 5' oligoadenylate synthetase
- 5.7. HCV and Mx
- 5.8. HCV and MHC class II
- 5.9. HCV and the IFN receptor
- 5.10. HCV and nitric oxide
- 6. Conclusions and future directions
- 7. Acknowledgments
- 8. References
1. ABSTRACT
Interferon-alpha (IFN-alpha) mono-therapy is largely ineffective for most of the hepatitis C virus (HCV)-infected patients that receive it. The addition of ribavirin to IFN therapy has increased the response rate dramatically. While many factors are implicated in determining the success rate for IFN therapy, viral genotype seems to play a crucial role. Examining differences in viral gene sequences has and will continue to advance our understanding as to how HCV and other viruses circumvent the IFN response. Here we review the different ways that HCV evades the immune response elicited by IFN.
