SARS-CoV-Encoded Small RNAs Contribute to Infection-Associated Lung Pathology.
Identifieur interne : 000B52 ( PubMed/Corpus ); précédent : 000B51; suivant : 000B53SARS-CoV-Encoded Small RNAs Contribute to Infection-Associated Lung Pathology.
Auteurs : Lucía Morales ; Juan Carlos Oliveros ; Raúl Fernandez-Delgado ; Benjamin Robert Tenoever ; Luis Enjuanes ; Isabel SolaSource :
- Cell host & microbe [ 1934-6069 ] ; 2017.
English descriptors
- KwdEn :
- Animals, Cytokines (biosynthesis), Disease Models, Animal, High-Throughput Nucleotide Sequencing, Lung (pathology), Mice, RNA, Small Untranslated (genetics), RNA, Small Untranslated (metabolism), RNA, Viral (genetics), RNA, Viral (metabolism), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (virology).
- MESH :
- chemical , biosynthesis : Cytokines.
- chemical , genetics : RNA, Small Untranslated, RNA, Viral.
- chemical , metabolism : RNA, Small Untranslated, RNA, Viral.
- pathogenicity : SARS Virus.
- pathology : Lung, Severe Acute Respiratory Syndrome.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Disease Models, Animal, High-Throughput Nucleotide Sequencing, Mice.
Abstract
Severe acute respiratory syndrome coronavirus (SARS-CoV) causes lethal disease in humans, which is characterized by exacerbated inflammatory response and extensive lung pathology. To address the relevance of small non-coding RNAs in SARS-CoV pathology, we deep sequenced RNAs from the lungs of infected mice and discovered three 18-22 nt small viral RNAs (svRNAs). The three svRNAs were derived from the nsp3 (svRNA-nsp3.1 and -nsp3.2) and N (svRNA-N) genomic regions of SARS-CoV. Biogenesis of CoV svRNAs was RNase III, cell type, and host species independent, but it was dependent on the extent of viral replication. Antagomir-mediated inhibition of svRNA-N significantly reduced in vivo lung pathology and pro-inflammatory cytokine expression. Taken together, these data indicate that svRNAs contribute to SARS-CoV pathogenesis and highlight the potential of svRNA-N antagomirs as antivirals.
DOI: 10.1016/j.chom.2017.01.015
PubMed: 28216251
Links to Exploration step
pubmed:28216251Le document en format XML
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Electronic address: l.enjuanes@cnb.csic.es.</nlm:affiliation></affiliation></author><author><name sortKey="Sola, Isabel" sort="Sola, Isabel" uniqKey="Sola I" first="Isabel" last="Sola">Isabel Sola</name><affiliation><nlm:affiliation>Department of Molecular and Cell Biology, National Center of Biotechnology (CNB-CSIC), Madrid, 28049, Spain.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:28216251</idno><idno type="pmid">28216251</idno><idno type="doi">10.1016/j.chom.2017.01.015</idno><idno type="wicri:Area/PubMed/Corpus">000B52</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000B52</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">SARS-CoV-Encoded Small RNAs Contribute to Infection-Associated Lung Pathology.</title><author><name sortKey="Morales, Lucia" sort="Morales, Lucia" uniqKey="Morales L" first="Lucía" last="Morales">Lucía Morales</name><affiliation><nlm:affiliation>Department of Molecular and Cell Biology, National Center of Biotechnology (CNB-CSIC), Madrid, 28049, Spain.</nlm:affiliation></affiliation></author><author><name sortKey="Oliveros, Juan Carlos" sort="Oliveros, Juan Carlos" uniqKey="Oliveros J" first="Juan Carlos" last="Oliveros">Juan Carlos Oliveros</name><affiliation><nlm:affiliation>Computational Genomics Service, National Center of Biotechnology (CNB-CSIC), Madrid, 28049, Spain.</nlm:affiliation></affiliation></author><author><name sortKey="Fernandez Delgado, Raul" sort="Fernandez Delgado, Raul" uniqKey="Fernandez Delgado R" first="Raúl" last="Fernandez-Delgado">Raúl Fernandez-Delgado</name><affiliation><nlm:affiliation>Department of Molecular and Cell Biology, National Center of Biotechnology (CNB-CSIC), Madrid, 28049, Spain.</nlm:affiliation></affiliation></author><author><name sortKey="Tenoever, Benjamin Robert" sort="Tenoever, Benjamin Robert" uniqKey="Tenoever B" first="Benjamin Robert" last="Tenoever">Benjamin Robert Tenoever</name><affiliation><nlm:affiliation>Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Enjuanes, Luis" sort="Enjuanes, Luis" uniqKey="Enjuanes L" first="Luis" last="Enjuanes">Luis Enjuanes</name><affiliation><nlm:affiliation>Department of Molecular and Cell Biology, National Center of Biotechnology (CNB-CSIC), Madrid, 28049, Spain. Electronic address: l.enjuanes@cnb.csic.es.</nlm:affiliation></affiliation></author><author><name sortKey="Sola, Isabel" sort="Sola, Isabel" uniqKey="Sola I" first="Isabel" last="Sola">Isabel Sola</name><affiliation><nlm:affiliation>Department of Molecular and Cell Biology, National Center of Biotechnology (CNB-CSIC), Madrid, 28049, Spain.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Cell host & microbe</title><idno type="eISSN">1934-6069</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cytokines (biosynthesis)</term><term>Disease Models, Animal</term><term>High-Throughput Nucleotide Sequencing</term><term>Lung (pathology)</term><term>Mice</term><term>RNA, Small Untranslated (genetics)</term><term>RNA, Small Untranslated (metabolism)</term><term>RNA, Viral (genetics)</term><term>RNA, Viral (metabolism)</term><term>SARS Virus (pathogenicity)</term><term>Severe Acute Respiratory Syndrome (pathology)</term><term>Severe Acute Respiratory Syndrome (virology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>RNA, Small Untranslated</term><term>RNA, Viral</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>RNA, Small Untranslated</term><term>RNA, Viral</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term><term>Severe Acute Respiratory Syndrome</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>High-Throughput Nucleotide Sequencing</term><term>Mice</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome coronavirus (SARS-CoV) causes lethal disease in humans, which is characterized by exacerbated inflammatory response and extensive lung pathology. To address the relevance of small non-coding RNAs in SARS-CoV pathology, we deep sequenced RNAs from the lungs of infected mice and discovered three 18-22 nt small viral RNAs (svRNAs). The three svRNAs were derived from the nsp3 (svRNA-nsp3.1 and -nsp3.2) and N (svRNA-N) genomic regions of SARS-CoV. Biogenesis of CoV svRNAs was RNase III, cell type, and host species independent, but it was dependent on the extent of viral replication. Antagomir-mediated inhibition of svRNA-N significantly reduced in vivo lung pathology and pro-inflammatory cytokine expression. Taken together, these data indicate that svRNAs contribute to SARS-CoV pathogenesis and highlight the potential of svRNA-N antagomirs as antivirals.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28216251</PMID><DateCompleted><Year>2017</Year><Month>08</Month><Day>29</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1934-6069</ISSN><JournalIssue CitedMedium="Internet"><Volume>21</Volume><Issue>3</Issue><PubDate><Year>2017</Year><Month>Mar</Month><Day>08</Day></PubDate></JournalIssue><Title>Cell host & microbe</Title><ISOAbbreviation>Cell Host Microbe</ISOAbbreviation></Journal><ArticleTitle>SARS-CoV-Encoded Small RNAs Contribute to Infection-Associated Lung Pathology.</ArticleTitle><Pagination><MedlinePgn>344-355</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S1931-3128(17)30037-9</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.chom.2017.01.015</ELocationID><Abstract><AbstractText>Severe acute respiratory syndrome coronavirus (SARS-CoV) causes lethal disease in humans, which is characterized by exacerbated inflammatory response and extensive lung pathology. To address the relevance of small non-coding RNAs in SARS-CoV pathology, we deep sequenced RNAs from the lungs of infected mice and discovered three 18-22 nt small viral RNAs (svRNAs). The three svRNAs were derived from the nsp3 (svRNA-nsp3.1 and -nsp3.2) and N (svRNA-N) genomic regions of SARS-CoV. Biogenesis of CoV svRNAs was RNase III, cell type, and host species independent, but it was dependent on the extent of viral replication. Antagomir-mediated inhibition of svRNA-N significantly reduced in vivo lung pathology and pro-inflammatory cytokine expression. Taken together, these data indicate that svRNAs contribute to SARS-CoV pathogenesis and highlight the potential of svRNA-N antagomirs as antivirals.</AbstractText><CopyrightInformation>Copyright © 2017 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Morales</LastName><ForeName>Lucía</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Molecular and Cell Biology, National Center of Biotechnology (CNB-CSIC), Madrid, 28049, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Oliveros</LastName><ForeName>Juan Carlos</ForeName><Initials>JC</Initials><AffiliationInfo><Affiliation>Computational Genomics Service, National Center of Biotechnology (CNB-CSIC), Madrid, 28049, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fernandez-Delgado</LastName><ForeName>Raúl</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Molecular and Cell Biology, National Center of Biotechnology (CNB-CSIC), Madrid, 28049, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>tenOever</LastName><ForeName>Benjamin Robert</ForeName><Initials>BR</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Enjuanes</LastName><ForeName>Luis</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Molecular and Cell Biology, National Center of Biotechnology (CNB-CSIC), Madrid, 28049, Spain. Electronic address: l.enjuanes@cnb.csic.es.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sola</LastName><ForeName>Isabel</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Department of Molecular and Cell Biology, National Center of Biotechnology (CNB-CSIC), Madrid, 28049, Spain.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HHSN266200700010C</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 AI060699</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>02</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Cell Host 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