Abstract
Activation and viral control of the innate immune response are hallmarks of hepatitis C virus (HCV) infection and are major determinants of spontaneous clearance or progression to chronic infection and liver disease. In this review, we provide a contemporary overview of how HCV is sensed by the host cell to trigger innate immune activation and the mechanisms deployed by the virus to evade this response. Type I and III interferons (IFNs) are crucial mediators of antiviral innate immunity against HCV, and we specifically highlight the importance of IFN-λ host genetics for the outcome of HCV infection. Last, we focus on the proin-flammatory responses elicited by HCV infection and describe our current understanding of how interleukin (IL)-1β signaling and cross talk between the IL-1β and IFN signaling pathways lead to sustained inflammation and increased risk of liver pathology.
| Original language | English (US) |
|---|---|
| Article number | a036988 |
| Pages (from-to) | 1-15 |
| Number of pages | 15 |
| Journal | Cold Spring Harbor Perspectives in Medicine |
| Volume | 11 |
| Issue number | 2 |
| DOIs | |
| State | Published - Feb 2021 |
| Externally published | Yes |
Bibliographical note
Publisher Copyright:© 2021 Cold Spring Harbor Laboratory Press; all rights reserved;.
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
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