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Published, Version of Record (VoR)CC BY V4.0, Open
Journal article
Hepatitis C Virus Infection: Host-Virus Interaction and Mechanisms of Viral Persistence
Cells (Basel, Switzerland), v 8(4), 376
01 Apr 2019
PMID: 31027278
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
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-) 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.
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Details
- Title
- Hepatitis C Virus Infection: Host-Virus Interaction and Mechanisms of Viral Persistence
- Creators
- DeGaulle I. Chigbu - Drexel University, Microbiology and ImmunologyRonak Loonawat - Drexel University, Microbiology and ImmunologyMohit Sehgal - The Wistar InstituteDip Patel - Drexel University, Microbiology and ImmunologyPooja Jain - Drexel University
- Publication Details
- Cells (Basel, Switzerland), v 8(4), 376
- Publisher
- MDPI
- Number of pages
- 27
- Grant note
- R01NS097147 / NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Neurological Disorders & Stroke (NINDS) R01CA054559 / NATIONAL CANCER INSTITUTE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Cancer Institute (NCI) NINDS R01NS097147; NCI R01CA054559 / NIH; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Microbiology and Immunology; Pennsylvania College of Optometry (PCO)
- Web of Science ID
- WOS:000467304300090
- Scopus ID
- 2-s2.0-85070545036
- Other Identifier
- 991019168086504721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Cell Biology