Hepatitis C Virus Infection: Host–Virus Interaction and Mechanisms of Viral Persistence
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 h...
Main Authors: | , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
MDPI AG
2019-04-01
|
Series: | Cells |
Subjects: | |
Online Access: | https://www.mdpi.com/2073-4409/8/4/376 |
id |
doaj-ef626e0362444239afd018420cccd234 |
---|---|
record_format |
Article |
spelling |
doaj-ef626e0362444239afd018420cccd2342020-11-25T01:23:18ZengMDPI AGCells2073-44092019-04-018437610.3390/cells8040376cells8040376Hepatitis C Virus Infection: Host–Virus Interaction and Mechanisms of Viral PersistenceDeGaulle I. Chigbu0Ronak Loonawat1Mohit Sehgal2Dip Patel3Pooja Jain4Department 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, USADepartment 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, USAImmunology, Microenvironment & Metastasis Program, The Wistar Institute, Philadelphia, PA 19104, USADepartment 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, USADepartment 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, USAHepatitis 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.https://www.mdpi.com/2073-4409/8/4/376HCVimmune dysregulationviral persistencedendritic cellsinterferonsT cellsNK cells |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
DeGaulle I. Chigbu Ronak Loonawat Mohit Sehgal Dip Patel Pooja Jain |
spellingShingle |
DeGaulle I. Chigbu Ronak Loonawat Mohit Sehgal Dip Patel Pooja Jain Hepatitis C Virus Infection: Host–Virus Interaction and Mechanisms of Viral Persistence Cells HCV immune dysregulation viral persistence dendritic cells interferons T cells NK cells |
author_facet |
DeGaulle I. Chigbu Ronak Loonawat Mohit Sehgal Dip Patel Pooja Jain |
author_sort |
DeGaulle I. Chigbu |
title |
Hepatitis C Virus Infection: Host–Virus Interaction and Mechanisms of Viral Persistence |
title_short |
Hepatitis C Virus Infection: Host–Virus Interaction and Mechanisms of Viral Persistence |
title_full |
Hepatitis C Virus Infection: Host–Virus Interaction and Mechanisms of Viral Persistence |
title_fullStr |
Hepatitis C Virus Infection: Host–Virus Interaction and Mechanisms of Viral Persistence |
title_full_unstemmed |
Hepatitis C Virus Infection: Host–Virus Interaction and Mechanisms of Viral Persistence |
title_sort |
hepatitis c virus infection: host–virus interaction and mechanisms of viral persistence |
publisher |
MDPI AG |
series |
Cells |
issn |
2073-4409 |
publishDate |
2019-04-01 |
description |
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. |
topic |
HCV immune dysregulation viral persistence dendritic cells interferons T cells NK cells |
url |
https://www.mdpi.com/2073-4409/8/4/376 |
work_keys_str_mv |
AT degaulleichigbu hepatitiscvirusinfectionhostvirusinteractionandmechanismsofviralpersistence AT ronakloonawat hepatitiscvirusinfectionhostvirusinteractionandmechanismsofviralpersistence AT mohitsehgal hepatitiscvirusinfectionhostvirusinteractionandmechanismsofviralpersistence AT dippatel hepatitiscvirusinfectionhostvirusinteractionandmechanismsofviralpersistence AT poojajain hepatitiscvirusinfectionhostvirusinteractionandmechanismsofviralpersistence |
_version_ |
1725123157248966656 |