Unique signatures of long noncoding RNA expression in response to virus infection and altered innate immune signaling.
Identifieur interne : 002239 ( Ncbi/Merge ); précédent : 002238; suivant : 002240Unique signatures of long noncoding RNA expression in response to virus infection and altered innate immune signaling.
Auteurs : Xinxia Peng [États-Unis] ; Lisa Gralinski ; Christopher D. Armour ; Martin T. Ferris ; Matthew J. Thomas ; Sean Proll ; Birgit G. Bradel-Tretheway ; Marcus J. Korth ; John C. Castle ; Matthew C. Biery ; Heather K. Bouzek ; David R. Haynor ; Matthew B. Frieman ; Mark Heise ; Christopher K. Raymond ; Ralph S. Baric ; Michael G. KatzeSource :
- mBio [ 2150-7511 ] ; 2010.
Descripteurs français
- KwdFr :
- ARN non traduit (biosynthèse), Analyse de profil d'expression de gènes, Animaux, Immunité innée, Modèles animaux de maladie humaine, Régulation de l'expression des gènes, Souris, Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (virologie), Transcription génétique, Transduction du signal, Virus du SRAS (immunologie), Virus du SRAS (pathogénicité).
- MESH :
- anatomopathologie : Syndrome respiratoire aigu sévère.
- biosynthèse : ARN non traduit.
- immunologie : Syndrome respiratoire aigu sévère, Virus du SRAS.
- pathogénicité : Virus du SRAS.
- virologie : Syndrome respiratoire aigu sévère.
- Analyse de profil d'expression de gènes, Animaux, Immunité innée, Modèles animaux de maladie humaine, Régulation de l'expression des gènes, Souris, Transcription génétique, Transduction du signal.
English descriptors
- KwdEn :
- Animals, Disease Models, Animal, Gene Expression Profiling, Gene Expression Regulation, Immunity, Innate, Mice, RNA, Untranslated (biosynthesis), SARS Virus (immunology), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (virology), Signal Transduction, Transcription, Genetic.
- MESH :
- chemical , biosynthesis : RNA, Untranslated.
- immunology : SARS Virus, Severe Acute Respiratory Syndrome.
- pathogenicity : SARS Virus.
- pathology : Severe Acute Respiratory Syndrome.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Disease Models, Animal, Gene Expression Profiling, Gene Expression Regulation, Immunity, Innate, Mice, Signal Transduction, Transcription, Genetic.
Abstract
Studies of the host response to virus infection typically focus on protein-coding genes. However, non-protein-coding RNAs (ncRNAs) are transcribed in mammalian cells, and the roles of many of these ncRNAs remain enigmas. Using next-generation sequencing, we performed a whole-transcriptome analysis of the host response to severe acute respiratory syndrome coronavirus (SARS-CoV) infection across four founder mouse strains of the Collaborative Cross. We observed differential expression of approximately 500 annotated, long ncRNAs and 1,000 nonannotated genomic regions during infection. Moreover, studies of a subset of these ncRNAs and genomic regions showed the following. (i) Most were similarly regulated in response to influenza virus infection. (ii) They had distinctive kinetic expression profiles in type I interferon receptor and STAT1 knockout mice during SARS-CoV infection, including unique signatures of ncRNA expression associated with lethal infection. (iii) Over 40% were similarly regulated in vitro in response to both influenza virus infection and interferon treatment. These findings represent the first discovery of the widespread differential expression of long ncRNAs in response to virus infection and suggest that ncRNAs are involved in regulating the host response, including innate immunity. At the same time, virus infection models provide a unique platform for studying the biology and regulation of ncRNAs.
DOI: 10.1128/mBio.00206-10
PubMed: 20978541
Links toward previous steps (curation, corpus...)
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pubmed:20978541Le document en format XML
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Katze</name></author></analytic><series><title level="j">mBio</title><idno type="eISSN">2150-7511</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Gene Expression Profiling</term><term>Gene Expression Regulation</term><term>Immunity, Innate</term><term>Mice</term><term>RNA, Untranslated (biosynthesis)</term><term>SARS Virus (immunology)</term><term>SARS Virus (pathogenicity)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe Acute Respiratory Syndrome (pathology)</term><term>Severe Acute Respiratory Syndrome (virology)</term><term>Signal Transduction</term><term>Transcription, Genetic</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN non traduit (biosynthèse)</term><term>Analyse de profil d'expression de gènes</term><term>Animaux</term><term>Immunité innée</term><term>Modèles animaux de maladie humaine</term><term>Régulation de l'expression des gènes</term><term>Souris</term><term>Syndrome respiratoire aigu sévère (anatomopathologie)</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Syndrome respiratoire aigu sévère (virologie)</term><term>Transcription génétique</term><term>Transduction du signal</term><term>Virus du SRAS (immunologie)</term><term>Virus du SRAS (pathogénicité)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>RNA, Untranslated</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>ARN non traduit</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Gene Expression Profiling</term><term>Gene Expression Regulation</term><term>Immunity, Innate</term><term>Mice</term><term>Signal Transduction</term><term>Transcription, Genetic</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term><term>Animaux</term><term>Immunité innée</term><term>Modèles animaux de maladie humaine</term><term>Régulation de l'expression des gènes</term><term>Souris</term><term>Transcription génétique</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Studies of the host response to virus infection typically focus on protein-coding genes. However, non-protein-coding RNAs (ncRNAs) are transcribed in mammalian cells, and the roles of many of these ncRNAs remain enigmas. Using next-generation sequencing, we performed a whole-transcriptome analysis of the host response to severe acute respiratory syndrome coronavirus (SARS-CoV) infection across four founder mouse strains of the Collaborative Cross. We observed differential expression of approximately 500 annotated, long ncRNAs and 1,000 nonannotated genomic regions during infection. Moreover, studies of a subset of these ncRNAs and genomic regions showed the following. (i) Most were similarly regulated in response to influenza virus infection. (ii) They had distinctive kinetic expression profiles in type I interferon receptor and STAT1 knockout mice during SARS-CoV infection, including unique signatures of ncRNA expression associated with lethal infection. (iii) Over 40% were similarly regulated in vitro in response to both influenza virus infection and interferon treatment. These findings represent the first discovery of the widespread differential expression of long ncRNAs in response to virus infection and suggest that ncRNAs are involved in regulating the host response, including innate immunity. At the same time, virus infection models provide a unique platform for studying the biology and regulation of ncRNAs.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20978541</PMID><DateCompleted><Year>2011</Year><Month>08</Month><Day>26</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>04</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2150-7511</ISSN><JournalIssue CitedMedium="Internet"><Volume>1</Volume><Issue>5</Issue><PubDate><Year>2010</Year><Month>Oct</Month><Day>26</Day></PubDate></JournalIssue><Title>mBio</Title><ISOAbbreviation>mBio</ISOAbbreviation></Journal><ArticleTitle>Unique signatures of long noncoding RNA expression in response to virus infection and altered innate immune signaling.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1128/mBio.00206-10</ELocationID><ELocationID EIdType="pii" ValidYN="Y">e00206-10</ELocationID><Abstract><AbstractText>Studies of the host response to virus infection typically focus on protein-coding genes. However, non-protein-coding RNAs (ncRNAs) are transcribed in mammalian cells, and the roles of many of these ncRNAs remain enigmas. Using next-generation sequencing, we performed a whole-transcriptome analysis of the host response to severe acute respiratory syndrome coronavirus (SARS-CoV) infection across four founder mouse strains of the Collaborative Cross. We observed differential expression of approximately 500 annotated, long ncRNAs and 1,000 nonannotated genomic regions during infection. Moreover, studies of a subset of these ncRNAs and genomic regions showed the following. (i) Most were similarly regulated in response to influenza virus infection. (ii) They had distinctive kinetic expression profiles in type I interferon receptor and STAT1 knockout mice during SARS-CoV infection, including unique signatures of ncRNA expression associated with lethal infection. (iii) Over 40% were similarly regulated in vitro in response to both influenza virus infection and interferon treatment. These findings represent the first discovery of the widespread differential expression of long ncRNAs in response to virus infection and suggest that ncRNAs are involved in regulating the host response, including innate immunity. At the same time, virus infection models provide a unique platform for studying the biology and regulation of ncRNAs.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Peng</LastName><ForeName>Xinxia</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Microbiology, School of Medicine, University of Washington, Seattle, Washington, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gralinski</LastName><ForeName>Lisa</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Armour</LastName><ForeName>Christopher D</ForeName><Initials>CD</Initials></Author><Author ValidYN="Y"><LastName>Ferris</LastName><ForeName>Martin T</ForeName><Initials>MT</Initials></Author><Author ValidYN="Y"><LastName>Thomas</LastName><ForeName>Matthew J</ForeName><Initials>MJ</Initials></Author><Author ValidYN="Y"><LastName>Proll</LastName><ForeName>Sean</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Bradel-Tretheway</LastName><ForeName>Birgit G</ForeName><Initials>BG</Initials></Author><Author ValidYN="Y"><LastName>Korth</LastName><ForeName>Marcus J</ForeName><Initials>MJ</Initials></Author><Author ValidYN="Y"><LastName>Castle</LastName><ForeName>John C</ForeName><Initials>JC</Initials></Author><Author ValidYN="Y"><LastName>Biery</LastName><ForeName>Matthew C</ForeName><Initials>MC</Initials></Author><Author ValidYN="Y"><LastName>Bouzek</LastName><ForeName>Heather K</ForeName><Initials>HK</Initials></Author><Author ValidYN="Y"><LastName>Haynor</LastName><ForeName>David R</ForeName><Initials>DR</Initials></Author><Author ValidYN="Y"><LastName>Frieman</LastName><ForeName>Matthew B</ForeName><Initials>MB</Initials></Author><Author ValidYN="Y"><LastName>Heise</LastName><ForeName>Mark</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Raymond</LastName><ForeName>Christopher K</ForeName><Initials>CK</Initials></Author><Author ValidYN="Y"><LastName>Baric</LastName><ForeName>Ralph S</ForeName><Initials>RS</Initials></Author><Author ValidYN="Y"><LastName>Katze</LastName><ForeName>Michael G</ForeName><Initials>MG</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HHSN272200800060C</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U54 AI081680</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2010</Year><Month>10</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>mBio</MedlineTA><NlmUniqueID>101519231</NlmUniqueID></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D022661">RNA, Untranslated</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020869" MajorTopicYN="Y">Gene Expression Profiling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007113" MajorTopicYN="Y">Immunity, Innate</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D022661" MajorTopicYN="N">RNA, Untranslated</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014158" MajorTopicYN="Y">Transcription, Genetic</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2010</Year><Month>08</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2010</Year><Month>09</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2010</Year><Month>10</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2010</Year><Month>10</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>8</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">20978541</ArticleId><ArticleId IdType="doi">10.1128/mBio.00206-10</ArticleId><ArticleId IdType="pmc">PMC2962437</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Methods Mol Biol. 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IdType="pubmed">12184808</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Washington (État)</li></region><settlement><li>Seattle</li></settlement><orgName><li>Université de Washington</li></orgName></list><tree><noCountry><name sortKey="Armour, Christopher D" sort="Armour, Christopher D" uniqKey="Armour C" first="Christopher D" last="Armour">Christopher D. Armour</name><name sortKey="Baric, Ralph S" sort="Baric, Ralph S" uniqKey="Baric R" first="Ralph S" last="Baric">Ralph S. Baric</name><name sortKey="Biery, Matthew C" sort="Biery, Matthew C" uniqKey="Biery M" first="Matthew C" last="Biery">Matthew C. Biery</name><name sortKey="Bouzek, Heather K" sort="Bouzek, Heather K" uniqKey="Bouzek H" first="Heather K" last="Bouzek">Heather K. Bouzek</name><name sortKey="Bradel Tretheway, Birgit G" sort="Bradel Tretheway, Birgit G" uniqKey="Bradel Tretheway B" first="Birgit G" last="Bradel-Tretheway">Birgit G. Bradel-Tretheway</name><name sortKey="Castle, John C" sort="Castle, John C" uniqKey="Castle J" first="John C" last="Castle">John C. Castle</name><name sortKey="Ferris, Martin T" sort="Ferris, Martin T" uniqKey="Ferris M" first="Martin T" last="Ferris">Martin T. Ferris</name><name sortKey="Frieman, Matthew B" sort="Frieman, Matthew B" uniqKey="Frieman M" first="Matthew B" last="Frieman">Matthew B. Frieman</name><name sortKey="Gralinski, Lisa" sort="Gralinski, Lisa" uniqKey="Gralinski L" first="Lisa" last="Gralinski">Lisa Gralinski</name><name sortKey="Haynor, David R" sort="Haynor, David R" uniqKey="Haynor D" first="David R" last="Haynor">David R. Haynor</name><name sortKey="Heise, Mark" sort="Heise, Mark" uniqKey="Heise M" first="Mark" last="Heise">Mark Heise</name><name sortKey="Katze, Michael G" sort="Katze, Michael G" uniqKey="Katze M" first="Michael G" last="Katze">Michael G. Katze</name><name sortKey="Korth, Marcus J" sort="Korth, Marcus J" uniqKey="Korth M" first="Marcus J" last="Korth">Marcus J. Korth</name><name sortKey="Proll, Sean" sort="Proll, Sean" uniqKey="Proll S" first="Sean" last="Proll">Sean Proll</name><name sortKey="Raymond, Christopher K" sort="Raymond, Christopher K" uniqKey="Raymond C" first="Christopher K" last="Raymond">Christopher K. Raymond</name><name sortKey="Thomas, Matthew J" sort="Thomas, Matthew J" uniqKey="Thomas M" first="Matthew J" last="Thomas">Matthew J. Thomas</name></noCountry><country name="États-Unis"><region name="Washington (État)"><name sortKey="Peng, Xinxia" sort="Peng, Xinxia" uniqKey="Peng X" first="Xinxia" last="Peng">Xinxia Peng</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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