SrasV1, PubMed, Checkpoint, bibRecord, 000E17

Genome Wide Identification of SARS-CoV Susceptibility Loci Using the Collaborative Cross.

Identifieur interne : 000E17 ( PubMed/Checkpoint ); précédent : 000E16; suivant : 000E18

Genome Wide Identification of SARS-CoV Susceptibility Loci Using the Collaborative Cross.

Auteurs : Lisa E. Gralinski [États-Unis] ; Martin T. Ferris [États-Unis] ; David L. Aylor [États-Unis] ; Alan C. Whitmore [États-Unis] ; Richard Green [États-Unis] ; Matthew B. Frieman [États-Unis] ; Damon Deming [États-Unis] ; Vineet D. Menachery [États-Unis] ; Darla R. Miller [États-Unis] ; Ryan J. Buus [États-Unis] ; Timothy A. Bell [États-Unis] ; Gary A. Churchill [États-Unis] ; David W. Threadgill [États-Unis] ; Michael G. Katze [États-Unis] ; Leonard Mcmillan [États-Unis] ; William Valdar [États-Unis] ; Mark T. Heise [États-Unis] ; Fernando Pardo-Manuel De Villena [États-Unis] ; Ralph S. Baric [États-Unis]

Source :

PLoS genetics [ 1553-7404 ] ; 2015.

RBID : pubmed:26452100

Descripteurs français

KwdFr :
- Animaux, Humains, Inflammation (anatomopathologie), Inflammation (génétique), Inflammation (virologie), Interactions hôte-pathogène, Modèles animaux de maladie humaine, Phénotype, Réplication virale (génétique), Souris, Susceptibilité à une maladie, Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (génétique), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (génétique), Virus du SRAS (pathogénicité).
MESH :
- anatomopathologie : Inflammation, Syndrome respiratoire aigu sévère.
- génétique : Inflammation, Réplication virale, Syndrome respiratoire aigu sévère, Virus du SRAS.
- pathogénicité : Virus du SRAS.
- virologie : Inflammation, Syndrome respiratoire aigu sévère.
- Animaux, Humains, Interactions hôte-pathogène, Modèles animaux de maladie humaine, Phénotype, Souris, Susceptibilité à une maladie.

English descriptors

KwdEn :
- Animals, Disease Models, Animal, Disease Susceptibility, Host-Pathogen Interactions, Humans, Inflammation (genetics), Inflammation (pathology), Inflammation (virology), Mice, Phenotype, SARS Virus (genetics), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (virology), Virus Replication (genetics).
MESH :
- genetics : Inflammation, SARS Virus, Severe Acute Respiratory Syndrome, Virus Replication.
- pathogenicity : SARS Virus.
- pathology : Inflammation, Severe Acute Respiratory Syndrome.
- virology : Inflammation, Severe Acute Respiratory Syndrome.
- Animals, Disease Models, Animal, Disease Susceptibility, Host-Pathogen Interactions, Humans, Mice, Phenotype.

Abstract

New systems genetics approaches are needed to rapidly identify host genes and genetic networks that regulate complex disease outcomes. Using genetically diverse animals from incipient lines of the Collaborative Cross mouse panel, we demonstrate a greatly expanded range of phenotypes relative to classical mouse models of SARS-CoV infection including lung pathology, weight loss and viral titer. Genetic mapping revealed several loci contributing to differential disease responses, including an 8.5Mb locus associated with vascular cuffing on chromosome 3 that contained 23 genes and 13 noncoding RNAs. Integrating phenotypic and genetic data narrowed this region to a single gene, Trim55, an E3 ubiquitin ligase with a role in muscle fiber maintenance. Lung pathology and transcriptomic data from mice genetically deficient in Trim55 were used to validate its role in SARS-CoV-induced vascular cuffing and inflammation. These data establish the Collaborative Cross platform as a powerful genetic resource for uncovering genetic contributions of complex traits in microbial disease severity, inflammation and virus replication in models of outbred populations.

DOI: 10.1371/journal.pgen.1005504
PubMed: 26452100

Affiliations:

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Le document en format XML

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<author><name sortKey="Katze, Michael G" sort="Katze, Michael G" uniqKey="Katze M" first="Michael G" last="Katze">Michael G. Katze</name>
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<author><name sortKey="Mcmillan, Leonard" sort="Mcmillan, Leonard" uniqKey="Mcmillan L" first="Leonard" last="Mcmillan">Leonard Mcmillan</name>
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<author><name sortKey="Valdar, William" sort="Valdar, William" uniqKey="Valdar W" first="William" last="Valdar">William Valdar</name>
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<country xml:lang="fr">États-Unis</country>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Genome Wide Identification of SARS-CoV Susceptibility Loci Using the Collaborative Cross.</title>
<author><name sortKey="Gralinski, Lisa E" sort="Gralinski, Lisa E" uniqKey="Gralinski L" first="Lisa E" last="Gralinski">Lisa E. Gralinski</name>
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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Ferris, Martin T" sort="Ferris, Martin T" uniqKey="Ferris M" first="Martin T" last="Ferris">Martin T. Ferris</name>
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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Aylor, David L" sort="Aylor, David L" uniqKey="Aylor D" first="David L" last="Aylor">David L. Aylor</name>
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<author><name sortKey="Green, Richard" sort="Green, Richard" uniqKey="Green R" first="Richard" last="Green">Richard Green</name>
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<author><name sortKey="Deming, Damon" sort="Deming, Damon" uniqKey="Deming D" first="Damon" last="Deming">Damon Deming</name>
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<author><name sortKey="Menachery, Vineet D" sort="Menachery, Vineet D" uniqKey="Menachery V" first="Vineet D" last="Menachery">Vineet D. Menachery</name>
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<author><name sortKey="Miller, Darla R" sort="Miller, Darla R" uniqKey="Miller D" first="Darla R" last="Miller">Darla R. Miller</name>
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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Buus, Ryan J" sort="Buus, Ryan J" uniqKey="Buus R" first="Ryan J" last="Buus">Ryan J. Buus</name>
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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Bell, Timothy A" sort="Bell, Timothy A" uniqKey="Bell T" first="Timothy A" last="Bell">Timothy A. Bell</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Genetics, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina, United States of America; Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina</wicri:regionArea>
<placeName><region type="state">Caroline du Nord</region>
</placeName>
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<author><name sortKey="Churchill, Gary A" sort="Churchill, Gary A" uniqKey="Churchill G" first="Gary A" last="Churchill">Gary A. Churchill</name>
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<country xml:lang="fr">États-Unis</country>
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<placeName><region type="state">Maine (État)</region>
</placeName>
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<author><name sortKey="Threadgill, David W" sort="Threadgill, David W" uniqKey="Threadgill D" first="David W" last="Threadgill">David W. Threadgill</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Veterinary Pathobiology, Texas A&M University, College Station, Texas</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
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<author><name sortKey="Katze, Michael G" sort="Katze, Michael G" uniqKey="Katze M" first="Michael G" last="Katze">Michael G. Katze</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Microbiology, University of Washington, Seattle, Washington</wicri:regionArea>
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<settlement type="city">Seattle</settlement>
</placeName>
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</affiliation>
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<series><title level="j">PLoS genetics</title>
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<front><div type="abstract" xml:lang="en">New systems genetics approaches are needed to rapidly identify host genes and genetic networks that regulate complex disease outcomes. Using genetically diverse animals from incipient lines of the Collaborative Cross mouse panel, we demonstrate a greatly expanded range of phenotypes relative to classical mouse models of SARS-CoV infection including lung pathology, weight loss and viral titer. Genetic mapping revealed several loci contributing to differential disease responses, including an 8.5Mb locus associated with vascular cuffing on chromosome 3 that contained 23 genes and 13 noncoding RNAs. Integrating phenotypic and genetic data narrowed this region to a single gene, Trim55, an E3 ubiquitin ligase with a role in muscle fiber maintenance. Lung pathology and transcriptomic data from mice genetically deficient in Trim55 were used to validate its role in SARS-CoV-induced vascular cuffing and inflammation. These data establish the Collaborative Cross platform as a powerful genetic resource for uncovering genetic contributions of complex traits in microbial disease severity, inflammation and virus replication in models of outbred populations. </div>
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<DateCompleted><Year>2016</Year>
<Month>05</Month>
<Day>03</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>02</Month>
<Day>02</Day>
</DateRevised>
<Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1553-7404</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>11</Volume>
<Issue>10</Issue>
<PubDate><Year>2015</Year>
<Month>Oct</Month>
</PubDate>
</JournalIssue>
<Title>PLoS genetics</Title>
<ISOAbbreviation>PLoS Genet.</ISOAbbreviation>
</Journal>
<ArticleTitle>Genome Wide Identification of SARS-CoV Susceptibility Loci Using the Collaborative Cross.</ArticleTitle>
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</Pagination>
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<Abstract><AbstractText>New systems genetics approaches are needed to rapidly identify host genes and genetic networks that regulate complex disease outcomes. Using genetically diverse animals from incipient lines of the Collaborative Cross mouse panel, we demonstrate a greatly expanded range of phenotypes relative to classical mouse models of SARS-CoV infection including lung pathology, weight loss and viral titer. Genetic mapping revealed several loci contributing to differential disease responses, including an 8.5Mb locus associated with vascular cuffing on chromosome 3 that contained 23 genes and 13 noncoding RNAs. Integrating phenotypic and genetic data narrowed this region to a single gene, Trim55, an E3 ubiquitin ligase with a role in muscle fiber maintenance. Lung pathology and transcriptomic data from mice genetically deficient in Trim55 were used to validate its role in SARS-CoV-induced vascular cuffing and inflammation. These data establish the Collaborative Cross platform as a powerful genetic resource for uncovering genetic contributions of complex traits in microbial disease severity, inflammation and virus replication in models of outbred populations. </AbstractText>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gralinski</LastName>
<ForeName>Lisa E</ForeName>
<Initials>LE</Initials>
<AffiliationInfo><Affiliation>Department of Epidemiology, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ferris</LastName>
<ForeName>Martin T</ForeName>
<Initials>MT</Initials>
<AffiliationInfo><Affiliation>Department of Genetics, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina, United States of America.</Affiliation>
</AffiliationInfo>
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<ForeName>David L</ForeName>
<Initials>DL</Initials>
<AffiliationInfo><Affiliation>Department of Genetics, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina, United States of America.</Affiliation>
</AffiliationInfo>
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<ForeName>Alan C</ForeName>
<Initials>AC</Initials>
<AffiliationInfo><Affiliation>Department of Genetics, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina, United States of America.</Affiliation>
</AffiliationInfo>
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<ForeName>Richard</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology, University of Washington, Seattle, Washington, United States of America.</Affiliation>
</AffiliationInfo>
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<ForeName>Matthew B</ForeName>
<Initials>MB</Initials>
<AffiliationInfo><Affiliation>Department of Epidemiology, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina, United States of America.</Affiliation>
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<ForeName>Damon</ForeName>
<Initials>D</Initials>
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</AffiliationInfo>
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<Initials>DR</Initials>
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</AffiliationInfo>
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<ForeName>Ryan J</ForeName>
<Initials>RJ</Initials>
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</AffiliationInfo>
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<ForeName>Timothy A</ForeName>
<Initials>TA</Initials>
<AffiliationInfo><Affiliation>Department of Genetics, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina, United States of America; Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina, United States of America.</Affiliation>
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<ForeName>Gary A</ForeName>
<Initials>GA</Initials>
<AffiliationInfo><Affiliation>The Jackson Laboratory, Bar Harbor, Maine, United States of America.</Affiliation>
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</Author>
<Author ValidYN="Y"><LastName>Threadgill</LastName>
<ForeName>David W</ForeName>
<Initials>DW</Initials>
<AffiliationInfo><Affiliation>Department of Veterinary Pathobiology, Texas A&M University, College Station, Texas, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Katze</LastName>
<ForeName>Michael G</ForeName>
<Initials>MG</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology, University of Washington, Seattle, Washington, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>McMillan</LastName>
<ForeName>Leonard</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Computer Science, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Valdar</LastName>
<ForeName>William</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>Department of Genetics, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Heise</LastName>
<ForeName>Mark T</ForeName>
<Initials>MT</Initials>
<AffiliationInfo><Affiliation>Department of Genetics, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pardo-Manuel de Villena</LastName>
<ForeName>Fernando</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>Department of Genetics, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina, United States of America; Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Baric</LastName>
<ForeName>Ralph S</ForeName>
<Initials>RS</Initials>
<AffiliationInfo><Affiliation>Department of Epidemiology, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina, United States of America.</Affiliation>
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Genome Wide Identification of SARS-CoV Susceptibility Loci Using the Collaborative Cross.

Genome Wide Identification of SARS-CoV Susceptibility Loci Using the Collaborative Cross.

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