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Hepatitis C Virus Infection: Host–Virus Interaction and Mechanisms of Viral Persistence

Department of Microbiology and Immunology, and the Institute for Molecular Medicine and Infectious Disease, Drexel University College of Medicine, 2900 West Queen Lane, Philadelphia, PA 19129, USA
Pennsylvania College of Optometry at Salus University, Elkins Park, PA 19027, USA
Immunology, Microenvironment & Metastasis Program, The Wistar Institute, Philadelphia, PA 19104, USA
Author to whom correspondence should be addressed.
Cells 2019, 8(4), 376;
Received: 30 October 2018 / Revised: 25 March 2019 / Accepted: 17 April 2019 / Published: 25 April 2019
(This article belongs to the Special Issue Hepatitis C Virus and Host Interactions)
Hepatitis C (HCV) is a major cause of liver disease, in which a third of individuals with chronic HCV infections may develop liver cirrhosis. In a chronic HCV infection, host immune factors along with the actions of HCV proteins that promote viral persistence and dysregulation of the immune system have an impact on immunopathogenesis of HCV-induced hepatitis. The genome of HCV encodes a single polyprotein, which is translated and processed into structural and nonstructural proteins. These HCV proteins are the target of the innate and adaptive immune system of the host. Retinoic acid-inducible gene-I (RIG-I)-like receptors and Toll-like receptors are the main pattern recognition receptors that recognize HCV pathogen-associated molecular patterns. This interaction results in a downstream cascade that generates antiviral cytokines including interferons. The cytolysis of HCV-infected hepatocytes is mediated by perforin and granzyme B secreted by cytotoxic T lymphocyte (CTL) and natural killer (NK) cells, whereas noncytolytic HCV clearance is mediated by interferon gamma (IFN-γ) secreted by CTL and NK cells. A host–HCV interaction determines whether the acute phase of an HCV infection will undergo complete resolution or progress to the development of viral persistence with a consequential progression to chronic HCV infection. Furthermore, these host–HCV interactions could pose a challenge to developing an HCV vaccine. This review will focus on the role of the innate and adaptive immunity in HCV infection, the failure of the immune response to clear an HCV infection, and the factors that promote viral persistence. View Full-Text
Keywords: HCV; immune dysregulation; viral persistence; dendritic cells; interferons; T cells; NK cells HCV; immune dysregulation; viral persistence; dendritic cells; interferons; T cells; NK cells
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Chigbu, D.I.; Loonawat, R.; Sehgal, M.; Patel, D.; Jain, P. Hepatitis C Virus Infection: Host–Virus Interaction and Mechanisms of Viral Persistence. Cells 2019, 8, 376.

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