Hepatitis C Virus: Strategies to Evade Antiviral Responses

ABSTRACT 

Hepatitis C virus (HCV) causes chronic liver disease and poses a major clinical and economic burden worldwide. HCV is an RNA virus that is sensed as nonself in the infected liver by host pattern recognition receptors, triggering downstream signaling to interferons (IFNs). The type III IFNs play an important role in immunity to HCV, and human genetic variation in their gene loci is associated with differential HCV infection outcomes. HCV evades host antiviral innate immune responses to mediate a persistent infection in the liver. This review focuses on anti-HCV innate immune sensing, signaling and effectors and the processes and proteins used by HCV to evade and regulate host innate immunity.

KEYWORDS :

• HCV
• IFN
• immune evasion
• MAVS
• NS3/4A
• RIG-I
• ISGs

Disclaimer

The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

Acknowledgements

We would like to thank Mounavya Aligeti and Allison Roder for critical reading of the manuscript and helpful discussions.

Financial & competeing interests disclosure

Research in the Horner lab is supported by the National Institute of Allergy and Infectious Diseases of the National Institutes of Health under Award Number K22AI100935, the Duke University Center for AIDS Research (CFAR), an NIH funded program (5P30 AI064518), and a Duke School of Medicine Whitehead Scholarship. C Vazquez is supported by a Ford Foundation Fellowship. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

Research in the Horner lab is supported by the National Institute of Allergy and Infectious Diseases of the National Institutes of Health under Award Number K22AI100935, the Duke University Center for AIDS Research (CFAR), an NIH funded program (5P30 AI064518), and a Duke School of Medicine Whitehead Scholarship. C Vazquez is supported by a Ford Foundation Fellowship. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.