Interferon Regulatory Factor 3-Mediated Signaling Limits Middle-East Respiratory Syndrome (MERS) Coronavirus Propagation in Cells from an Insectivorous Bat.
Identifieur interne : 000641 ( PubMed/Corpus ); précédent : 000640; suivant : 000642Interferon Regulatory Factor 3-Mediated Signaling Limits Middle-East Respiratory Syndrome (MERS) Coronavirus Propagation in Cells from an Insectivorous Bat.
Auteurs : Arinjay Banerjee ; Darryl Falzarano ; Noreen Rapin ; Jocelyne Lew ; Vikram MisraSource :
- Viruses [ 1999-4915 ] ; 2019.
English descriptors
- KwdEn :
- Animals, Cell Line, Chiroptera (virology), Gene Knockdown Techniques, Gene Knockout Techniques, Humans, Immune Evasion, Immunity, Innate, Interferon Regulatory Factor-3 (genetics), Interferon Regulatory Factor-3 (immunology), Interferon-beta (immunology), Kidney (cytology), Kidney (virology), Middle East Respiratory Syndrome Coronavirus (immunology), Middle East Respiratory Syndrome Coronavirus (pathogenicity), Phylogeny, Signal Transduction.
- MESH :
- chemical , genetics : Interferon Regulatory Factor-3.
- chemical , immunology : Interferon Regulatory Factor-3, Interferon-beta.
- cytology : Kidney.
- immunology : Middle East Respiratory Syndrome Coronavirus.
- pathogenicity : Middle East Respiratory Syndrome Coronavirus.
- virology : Chiroptera, Kidney.
- Animals, Cell Line, Gene Knockdown Techniques, Gene Knockout Techniques, Humans, Immune Evasion, Immunity, Innate, Phylogeny, Signal Transduction.
Abstract
Insectivorous bats are speculated to be ancestral hosts of Middle-East respiratory syndrome (MERS) coronavirus (CoV). MERS-CoV causes disease in humans with thirty-five percent fatality, and has evolved proteins that counteract human antiviral responses. Since bats experimentally infected with MERS-CoV do not develop signs of disease, we tested the hypothesis that MERS-CoV would replicate less efficiently in bat cells than in human cells because of its inability to subvert antiviral responses in bat cells. We infected human and bat (Eptesicus fuscus) cells with MERS-CoV and observed that the virus grew to higher titers in human cells. MERS-CoV also effectively suppressed the antiviral interferon beta (IFNβ) response in human cells, unlike in bat cells. To determine if IRF3, a critical mediator of the interferon response, also regulated the response in bats, we examined the response of IRF3 to poly(I:C), a synthetic analogue of viral double-stranded RNA. We observed that bat IRF3 responded to poly(I:C) by nuclear translocation and post-translational modifications, hallmarks of IRF3 activation. Suppression of IRF3 by small-interfering RNA (siRNA) demonstrated that IRF3 was critical for poly(I:C) and MERS-CoV induced induction of IFNβ in bat cells. Our study demonstrates that innate antiviral signaling in E. fuscus bat cells is resistant to MERS-CoV-mediated subversion.
DOI: 10.3390/v11020152
PubMed: 30781790
Links to Exploration step
pubmed:30781790Le document en format XML
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sortKey="Rapin, Noreen" sort="Rapin, Noreen" uniqKey="Rapin N" first="Noreen" last="Rapin">Noreen Rapin</name><affiliation><nlm:affiliation>Department of Veterinary Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK S7N 5B4, Canada. noreen.rapin@usask.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Lew, Jocelyne" sort="Lew, Jocelyne" uniqKey="Lew J" first="Jocelyne" last="Lew">Jocelyne Lew</name><affiliation><nlm:affiliation>Vaccine and Infectious Disease Organization-International Vaccine Centre (VIDO-Intervac), University of Saskatchewan, Saskatoon, SK S7N 5E3, Canada. jocelyne.lew@usask.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Misra, Vikram" sort="Misra, Vikram" uniqKey="Misra V" first="Vikram" last="Misra">Vikram Misra</name><affiliation><nlm:affiliation>Department of Veterinary Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK S7N 5B4, Canada. vikram.misra@usask.ca.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2019">2019</date><idno type="RBID">pubmed:30781790</idno><idno type="pmid">30781790</idno><idno type="doi">10.3390/v11020152</idno><idno type="wicri:Area/PubMed/Corpus">000641</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000641</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Interferon Regulatory Factor 3-Mediated Signaling Limits Middle-East Respiratory Syndrome (MERS) Coronavirus Propagation in Cells from an Insectivorous Bat.</title><author><name sortKey="Banerjee, Arinjay" sort="Banerjee, Arinjay" uniqKey="Banerjee A" first="Arinjay" last="Banerjee">Arinjay Banerjee</name><affiliation><nlm:affiliation>Department of Veterinary Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK S7N 5B4, Canada. banera9@mcmaster.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Falzarano, Darryl" sort="Falzarano, Darryl" uniqKey="Falzarano D" first="Darryl" last="Falzarano">Darryl Falzarano</name><affiliation><nlm:affiliation>Department of Veterinary Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK S7N 5B4, Canada. darryl.falzarano@usask.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Rapin, Noreen" sort="Rapin, Noreen" uniqKey="Rapin N" first="Noreen" last="Rapin">Noreen Rapin</name><affiliation><nlm:affiliation>Department of Veterinary Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK S7N 5B4, Canada. noreen.rapin@usask.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Lew, Jocelyne" sort="Lew, Jocelyne" uniqKey="Lew J" first="Jocelyne" last="Lew">Jocelyne Lew</name><affiliation><nlm:affiliation>Vaccine and Infectious Disease Organization-International Vaccine Centre (VIDO-Intervac), University of Saskatchewan, Saskatoon, SK S7N 5E3, Canada. jocelyne.lew@usask.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Misra, Vikram" sort="Misra, Vikram" uniqKey="Misra V" first="Vikram" last="Misra">Vikram Misra</name><affiliation><nlm:affiliation>Department of Veterinary Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK S7N 5B4, Canada. vikram.misra@usask.ca.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Viruses</title><idno type="eISSN">1999-4915</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Chiroptera (virology)</term><term>Gene Knockdown Techniques</term><term>Gene Knockout Techniques</term><term>Humans</term><term>Immune Evasion</term><term>Immunity, Innate</term><term>Interferon Regulatory Factor-3 (genetics)</term><term>Interferon Regulatory Factor-3 (immunology)</term><term>Interferon-beta (immunology)</term><term>Kidney (cytology)</term><term>Kidney (virology)</term><term>Middle East Respiratory Syndrome Coronavirus (immunology)</term><term>Middle East Respiratory Syndrome Coronavirus (pathogenicity)</term><term>Phylogeny</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interferon Regulatory Factor-3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Interferon Regulatory Factor-3</term><term>Interferon-beta</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Kidney</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Middle East Respiratory Syndrome Coronavirus</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Middle East Respiratory Syndrome Coronavirus</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Chiroptera</term><term>Kidney</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Gene Knockdown Techniques</term><term>Gene Knockout Techniques</term><term>Humans</term><term>Immune Evasion</term><term>Immunity, Innate</term><term>Phylogeny</term><term>Signal Transduction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Insectivorous bats are speculated to be ancestral hosts of Middle-East respiratory syndrome (MERS) coronavirus (CoV). MERS-CoV causes disease in humans with thirty-five percent fatality, and has evolved proteins that counteract human antiviral responses. Since bats experimentally infected with MERS-CoV do not develop signs of disease, we tested the hypothesis that MERS-CoV would replicate less efficiently in bat cells than in human cells because of its inability to subvert antiviral responses in bat cells. We infected human and bat (<i>Eptesicus fuscus</i>) cells with MERS-CoV and observed that the virus grew to higher titers in human cells. MERS-CoV also effectively suppressed the antiviral interferon beta (IFNβ) response in human cells, unlike in bat cells. To determine if IRF3, a critical mediator of the interferon response, also regulated the response in bats, we examined the response of IRF3 to poly(I:C), a synthetic analogue of viral double-stranded RNA. We observed that bat IRF3 responded to poly(I:C) by nuclear translocation and post-translational modifications, hallmarks of IRF3 activation. Suppression of IRF3 by small-interfering RNA (siRNA) demonstrated that IRF3 was critical for poly(I:C) and MERS-CoV induced induction of IFNβ in bat cells. Our study demonstrates that innate antiviral signaling in <i>E. fuscus</i> bat cells is resistant to MERS-CoV-mediated subversion.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30781790</PMID><DateCompleted><Year>2019</Year><Month>08</Month><Day>20</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>09</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1999-4915</ISSN><JournalIssue CitedMedium="Internet"><Volume>11</Volume><Issue>2</Issue><PubDate><Year>2019</Year><Month>02</Month><Day>13</Day></PubDate></JournalIssue><Title>Viruses</Title><ISOAbbreviation>Viruses</ISOAbbreviation></Journal><ArticleTitle>Interferon Regulatory Factor 3-Mediated Signaling Limits Middle-East Respiratory Syndrome (MERS) Coronavirus Propagation in Cells from an Insectivorous Bat.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">E152</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3390/v11020152</ELocationID><Abstract><AbstractText>Insectivorous bats are speculated to be ancestral hosts of Middle-East respiratory syndrome (MERS) coronavirus (CoV). MERS-CoV causes disease in humans with thirty-five percent fatality, and has evolved proteins that counteract human antiviral responses. Since bats experimentally infected with MERS-CoV do not develop signs of disease, we tested the hypothesis that MERS-CoV would replicate less efficiently in bat cells than in human cells because of its inability to subvert antiviral responses in bat cells. We infected human and bat (<i>Eptesicus fuscus</i>) cells with MERS-CoV and observed that the virus grew to higher titers in human cells. MERS-CoV also effectively suppressed the antiviral interferon beta (IFNβ) response in human cells, unlike in bat cells. To determine if IRF3, a critical mediator of the interferon response, also regulated the response in bats, we examined the response of IRF3 to poly(I:C), a synthetic analogue of viral double-stranded RNA. We observed that bat IRF3 responded to poly(I:C) by nuclear translocation and post-translational modifications, hallmarks of IRF3 activation. Suppression of IRF3 by small-interfering RNA (siRNA) demonstrated that IRF3 was critical for poly(I:C) and MERS-CoV induced induction of IFNβ in bat cells. Our study demonstrates that innate antiviral signaling in <i>E. fuscus</i> bat cells is resistant to MERS-CoV-mediated subversion.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Banerjee</LastName><ForeName>Arinjay</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-2821-8357</Identifier><AffiliationInfo><Affiliation>Department of Veterinary Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK S7N 5B4, Canada. banera9@mcmaster.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Falzarano</LastName><ForeName>Darryl</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Veterinary Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK S7N 5B4, Canada. darryl.falzarano@usask.ca.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Vaccine and Infectious Disease Organization-International Vaccine Centre (VIDO-Intervac), University of Saskatchewan, Saskatoon, SK S7N 5E3, Canada. darryl.falzarano@usask.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rapin</LastName><ForeName>Noreen</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Veterinary Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK S7N 5B4, Canada. noreen.rapin@usask.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lew</LastName><ForeName>Jocelyne</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Vaccine and Infectious Disease Organization-International Vaccine Centre (VIDO-Intervac), University of Saskatchewan, Saskatoon, SK S7N 5E3, Canada. jocelyne.lew@usask.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Misra</LastName><ForeName>Vikram</ForeName><Initials>V</Initials><Identifier Source="ORCID">0000-0001-6818-7156</Identifier><AffiliationInfo><Affiliation>Department of Veterinary Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK S7N 5B4, Canada. vikram.misra@usask.ca.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>02</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Viruses</MedlineTA><NlmUniqueID>101509722</NlmUniqueID><ISSNLinking>1999-4915</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C494232">IRF3 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050838">Interferon Regulatory 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MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010802" MajorTopicYN="N">Phylogeny</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">IRF3</Keyword><Keyword MajorTopicYN="Y">MERS-CoV</Keyword><Keyword MajorTopicYN="Y">bat</Keyword><Keyword MajorTopicYN="Y">interferon</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>12</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2019</Year><Month>02</Month><Day>08</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>02</Month><Day>11</Day></PubMedPubDate><PubMedPubDate 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