Hepatitis C virus and intracellular antiviral response
- PMID: 34973476
- PMCID: PMC8844188
- DOI: 10.1016/j.coviro.2021.12.010
Hepatitis C virus and intracellular antiviral response
Abstract
To establish successful infection in cells, it is essential for hepatitis C virus (HCV) to overcome intracellular antiviral responses. The host cell mechanism that fights against the virus culminates in the production of interferons (IFNs), IFN-stimulated genes (ISGs) and pro-inflammatory cytokines as well as the induction of autophagy and apoptosis. HCV has developed multiple means to disrupt the host signaling pathways that lead to these antiviral responses. HCV impedes signaling pathways initiated by pattern-recognition receptors (PRRs), usurps and uses the antiviral autophagic response to enhance its replication, alters mitochondrial dynamics and metabolism to prevent cell death and attenuate IFN response, and dysregulates inflammasomal response to cause IFN resistance and immune tolerance. These effects of HCV allow HCV to successful replicate and persist in its host cells.
Copyright © 2021 Elsevier B.V. All rights reserved.
Conflict of interest statement
Declaration of Interest:
None.
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This article provides an updated review of recent studies on type I and type III IFNs signaling in HCV-infected hepatocytes and the impact of direct-acting antivirals on IFN responses to HCV infection.
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