Analysis of the host transcriptome from demyelinating spinal cord of murine coronavirus-infected mice.

Persistent infection of the mouse central nervous system (CNS) with mouse hepatitis virus (MHV) induces a demyelinating disease pathologically similar to multiple sclerosis and is therefore used as a model system. There is little information regarding the host factors that correlate with and contrib...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Ruth Elliott, Fan Li, Isabelle Dragomir, Ming Ming W Chua, Brian D Gregory, Susan R Weiss
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/2b9cc7769c2a4720b66ba1c5c3df9195
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:2b9cc7769c2a4720b66ba1c5c3df9195
record_format	dspace
spelling	oai:doaj.org-article:2b9cc7769c2a4720b66ba1c5c3df91952021-11-18T08:54:40ZAnalysis of the host transcriptome from demyelinating spinal cord of murine coronavirus-infected mice.1932-620310.1371/journal.pone.0075346https://doaj.org/article/2b9cc7769c2a4720b66ba1c5c3df91952013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24058676/?tool=EBIhttps://doaj.org/toc/1932-6203Persistent infection of the mouse central nervous system (CNS) with mouse hepatitis virus (MHV) induces a demyelinating disease pathologically similar to multiple sclerosis and is therefore used as a model system. There is little information regarding the host factors that correlate with and contribute to MHV-induced demyelination. Here, we detail the genes and pathways associated with MHV-induced demyelinating disease in the spinal cord. High-throughput sequencing of the host transcriptome revealed that demyelination is accompanied by numerous transcriptional changes indicative of immune infiltration as well as changes in the cytokine milieu and lipid metabolism. We found evidence that a Th1-biased cytokine/chemokine response and eicosanoid-derived inflammation accompany persistent MHV infection and that antigen presentation is ongoing. Interestingly, increased expression of genes involved in lipid transport, processing, and catabolism, including some with known roles in neurodegenerative diseases, coincided with demyelination. Lastly, expression of several genes involved in osteoclast or bone-resident macrophage function, most notably TREM2 and DAP12, was upregulated in persistently infected mouse spinal cord. This study highlights the complexity of the host antiviral response, which accompany MHV-induced demyelination, and further supports previous findings that MHV-induced demyelination is immune-mediated. Interestingly, these data suggest a parallel between bone reabsorption by osteoclasts and myelin debris clearance by microglia in the bone and the CNS, respectively. To our knowledge, this is the first report of using an RNA-seq approach to study the host CNS response to persistent viral infection.Ruth ElliottFan LiIsabelle DragomirMing Ming W ChuaBrian D GregorySusan R WeissPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 9, p e75346 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Ruth Elliott Fan Li Isabelle Dragomir Ming Ming W Chua Brian D Gregory Susan R Weiss Analysis of the host transcriptome from demyelinating spinal cord of murine coronavirus-infected mice.
description	Persistent infection of the mouse central nervous system (CNS) with mouse hepatitis virus (MHV) induces a demyelinating disease pathologically similar to multiple sclerosis and is therefore used as a model system. There is little information regarding the host factors that correlate with and contribute to MHV-induced demyelination. Here, we detail the genes and pathways associated with MHV-induced demyelinating disease in the spinal cord. High-throughput sequencing of the host transcriptome revealed that demyelination is accompanied by numerous transcriptional changes indicative of immune infiltration as well as changes in the cytokine milieu and lipid metabolism. We found evidence that a Th1-biased cytokine/chemokine response and eicosanoid-derived inflammation accompany persistent MHV infection and that antigen presentation is ongoing. Interestingly, increased expression of genes involved in lipid transport, processing, and catabolism, including some with known roles in neurodegenerative diseases, coincided with demyelination. Lastly, expression of several genes involved in osteoclast or bone-resident macrophage function, most notably TREM2 and DAP12, was upregulated in persistently infected mouse spinal cord. This study highlights the complexity of the host antiviral response, which accompany MHV-induced demyelination, and further supports previous findings that MHV-induced demyelination is immune-mediated. Interestingly, these data suggest a parallel between bone reabsorption by osteoclasts and myelin debris clearance by microglia in the bone and the CNS, respectively. To our knowledge, this is the first report of using an RNA-seq approach to study the host CNS response to persistent viral infection.
format	article
author	Ruth Elliott Fan Li Isabelle Dragomir Ming Ming W Chua Brian D Gregory Susan R Weiss
author_facet	Ruth Elliott Fan Li Isabelle Dragomir Ming Ming W Chua Brian D Gregory Susan R Weiss
author_sort	Ruth Elliott
title	Analysis of the host transcriptome from demyelinating spinal cord of murine coronavirus-infected mice.
title_short	Analysis of the host transcriptome from demyelinating spinal cord of murine coronavirus-infected mice.
title_full	Analysis of the host transcriptome from demyelinating spinal cord of murine coronavirus-infected mice.
title_fullStr	Analysis of the host transcriptome from demyelinating spinal cord of murine coronavirus-infected mice.
title_full_unstemmed	Analysis of the host transcriptome from demyelinating spinal cord of murine coronavirus-infected mice.
title_sort	analysis of the host transcriptome from demyelinating spinal cord of murine coronavirus-infected mice.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/2b9cc7769c2a4720b66ba1c5c3df9195
work_keys_str_mv	AT ruthelliott analysisofthehosttranscriptomefromdemyelinatingspinalcordofmurinecoronavirusinfectedmice AT fanli analysisofthehosttranscriptomefromdemyelinatingspinalcordofmurinecoronavirusinfectedmice AT isabelledragomir analysisofthehosttranscriptomefromdemyelinatingspinalcordofmurinecoronavirusinfectedmice AT mingmingwchua analysisofthehosttranscriptomefromdemyelinatingspinalcordofmurinecoronavirusinfectedmice AT briandgregory analysisofthehosttranscriptomefromdemyelinatingspinalcordofmurinecoronavirusinfectedmice AT susanrweiss analysisofthehosttranscriptomefromdemyelinatingspinalcordofmurinecoronavirusinfectedmice
_version_	1718421131814240256

Analysis of the host transcriptome from demyelinating spinal cord of murine coronavirus-infected mice.

Ejemplares similares