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Murine Coronavirus Cell Type Dependent Interaction with the Type I Interferon Response

Coronaviruses infect many species of animal including humans, causing acute and chronic diseases of many organ systems. Murine coronavirus, mouse hepatitis virus (MHV) infection of the mouse, provides animal models for the study of central nervous system disease, including encephalitis and demyelina...

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Autores principales: Rose, Kristine M., Weiss, Susan R.
Formato: Texto
Lenguaje:English
Publicado: Molecular Diversity Preservation International (MDPI) 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835314/
https://www.ncbi.nlm.nih.gov/pubmed/20221421
http://dx.doi.org/10.3390/v1030689
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author Rose, Kristine M.
Weiss, Susan R.
author_facet Rose, Kristine M.
Weiss, Susan R.
author_sort Rose, Kristine M.
collection PubMed
description Coronaviruses infect many species of animal including humans, causing acute and chronic diseases of many organ systems. Murine coronavirus, mouse hepatitis virus (MHV) infection of the mouse, provides animal models for the study of central nervous system disease, including encephalitis and demyelinating diseases such as Multiple Sclerosis and for hepatitis. While there are many studies of the adaptive immune response to MHV, there has until recently been scant information on the type I interferon (IFN) response to MHV. The relationship between MHV and the IFN-α/β response is paradoxical. While the type I IFN response is a crucial aspect of host defense against MHV in its natural host, there is little if any induction of IFN following infection of mouse fibroblast cell lines in vitro. Furthermore, MHV is relatively resistant to the antiviral effects of IFN-α/β in mouse fibroblast cell lines and in human 293T cells. MHV can, under some circumstances, compromise the antiviral effects of IFN signaling. The nucleocapsid protein as well as the nsp1 and nsp3 proteins of MHV has been reported to have IFN antagonist activity. However, in primary cell types such as plasmacytoid dendritic cells (pDC) and macrophages, IFN is induced by MHV infection and an antiviral state is established. Other primary cell types such as neurons, astrocytes and hepatocytes fail to produce IFN following infection and, in vivo, likely depend on IFN produced by pDCs and macrophages for protection from MHV. Thus MHV induction of IFN-α/β and the ability to induce an antiviral state in response to interferon is extremely cell type dependent. IFN induced protection from MHV pathogenesis likely requires the orchestrated activities of several cell types, however, the cell types involved in limiting MHV replication may be different in the liver and in the immune privileged CNS.
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spelling pubmed-28353142010-03-09 Murine Coronavirus Cell Type Dependent Interaction with the Type I Interferon Response Rose, Kristine M. Weiss, Susan R. Viruses Review Coronaviruses infect many species of animal including humans, causing acute and chronic diseases of many organ systems. Murine coronavirus, mouse hepatitis virus (MHV) infection of the mouse, provides animal models for the study of central nervous system disease, including encephalitis and demyelinating diseases such as Multiple Sclerosis and for hepatitis. While there are many studies of the adaptive immune response to MHV, there has until recently been scant information on the type I interferon (IFN) response to MHV. The relationship between MHV and the IFN-α/β response is paradoxical. While the type I IFN response is a crucial aspect of host defense against MHV in its natural host, there is little if any induction of IFN following infection of mouse fibroblast cell lines in vitro. Furthermore, MHV is relatively resistant to the antiviral effects of IFN-α/β in mouse fibroblast cell lines and in human 293T cells. MHV can, under some circumstances, compromise the antiviral effects of IFN signaling. The nucleocapsid protein as well as the nsp1 and nsp3 proteins of MHV has been reported to have IFN antagonist activity. However, in primary cell types such as plasmacytoid dendritic cells (pDC) and macrophages, IFN is induced by MHV infection and an antiviral state is established. Other primary cell types such as neurons, astrocytes and hepatocytes fail to produce IFN following infection and, in vivo, likely depend on IFN produced by pDCs and macrophages for protection from MHV. Thus MHV induction of IFN-α/β and the ability to induce an antiviral state in response to interferon is extremely cell type dependent. IFN induced protection from MHV pathogenesis likely requires the orchestrated activities of several cell types, however, the cell types involved in limiting MHV replication may be different in the liver and in the immune privileged CNS. Molecular Diversity Preservation International (MDPI) 2009-11-04 /pmc/articles/PMC2835314/ /pubmed/20221421 http://dx.doi.org/10.3390/v1030689 Text en © 2009 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0 This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Review
Rose, Kristine M.
Weiss, Susan R.
Murine Coronavirus Cell Type Dependent Interaction with the Type I Interferon Response
title Murine Coronavirus Cell Type Dependent Interaction with the Type I Interferon Response
title_full Murine Coronavirus Cell Type Dependent Interaction with the Type I Interferon Response
title_fullStr Murine Coronavirus Cell Type Dependent Interaction with the Type I Interferon Response
title_full_unstemmed Murine Coronavirus Cell Type Dependent Interaction with the Type I Interferon Response
title_short Murine Coronavirus Cell Type Dependent Interaction with the Type I Interferon Response
title_sort murine coronavirus cell type dependent interaction with the type i interferon response
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835314/
https://www.ncbi.nlm.nih.gov/pubmed/20221421
http://dx.doi.org/10.3390/v1030689
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