The ORF4b-encoded accessory proteins of Middle East respiratory syndrome coronavirus and two related bat coronaviruses localize to the nucleus and inhibit innate immune signalling.
Identifieur interne : 001067 ( PubMed/Curation ); précédent : 001066; suivant : 001068The ORF4b-encoded accessory proteins of Middle East respiratory syndrome coronavirus and two related bat coronaviruses localize to the nucleus and inhibit innate immune signalling.
Auteurs : Krystal L. Matthews [États-Unis] ; Christopher M. Coleman [États-Unis] ; Yvonne Van Der Meer [Pays-Bas] ; Eric J. Snijder [Pays-Bas] ; Matthew B. Frieman [États-Unis]Source :
- The Journal of general virology [ 1465-2099 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux, Chiroptera, Coronavirus (immunologie), Facteur de transcription NF-kappa B (antagonistes et inhibiteurs), Humains, Interactions hôte-pathogène, Interféron de type I (antagonistes et inhibiteurs), Noyau de la cellule (), Noyau de la cellule (virologie), Protéines virales régulatrices ou accessoires (immunologie), Échappement immunitaire.
- MESH :
- antagonistes et inhibiteurs : Facteur de transcription NF-kappa B, Interféron de type I.
- immunologie : Coronavirus, Protéines virales régulatrices ou accessoires.
- virologie : Noyau de la cellule.
- Animaux, Chiroptera, Humains, Interactions hôte-pathogène, Noyau de la cellule, Échappement immunitaire.
English descriptors
- KwdEn :
- MESH :
- chemical , antagonists & inhibitors : Interferon Type I, NF-kappa B.
- chemistry : Cell Nucleus.
- immunology : Coronavirus, Viral Regulatory and Accessory Proteins.
- virology : Cell Nucleus.
- Animals, Chiroptera, Host-Pathogen Interactions, Humans, Immune Evasion.
Abstract
The recently emerged Middle East respiratory syndrome coronavirus (MERS-CoV), a betacoronavirus, is associated with severe pneumonia and renal failure. The environmental origin of MERS-CoV is as yet unknown; however, its genome sequence is closely related to those of two bat coronaviruses, named BtCoV-HKU4 and BtCoV-HKU5, which were derived from Chinese bat samples. A hallmark of highly pathogenic respiratory viruses is their ability to evade the innate immune response of the host. CoV accessory proteins, for example those from severe acute respiratory syndrome CoV (SARS-CoV), have been shown to block innate antiviral signalling pathways. MERS-CoV, similar to SARS-CoV, has been shown to inhibit type I IFN induction in a variety of cell types in vitro. We therefore hypothesized that MERS-CoV and the phylogenetically related BtCoV-HKU4 and BtCoV-HKU5 may encode proteins with similar capabilities. In this study, we have demonstrated that the ORF4b-encoded accessory protein (p4b) of MERS-CoV, BtCoV-HKU4 and BtCoV-HKU5 may indeed facilitate innate immune evasion by inhibiting the type I IFN and NF-κB signalling pathways. We also analysed the subcellular localization of p4b from MERS-CoV, BtCoV-HKU4 and BtCoV-HKU5 and demonstrated that all are localized to the nucleus.
DOI: 10.1099/vir.0.062059-0
PubMed: 24443473
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Snijder</name><affiliation wicri:level="1"><nlm:affiliation>Molecular Virology Laboratory, Department of Medical Microbiology, Leiden University Medical Center, PO Box 9600, 2300RC Leiden, The Netherlands.</nlm:affiliation><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Molecular Virology Laboratory, Department of Medical Microbiology, Leiden University Medical Center, PO Box 9600, 2300RC Leiden</wicri:regionArea></affiliation></author><author><name sortKey="Frieman, Matthew B" sort="Frieman, Matthew B" uniqKey="Frieman M" first="Matthew B" last="Frieman">Matthew B. Frieman</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, University of Maryland at Baltimore, 685 West Baltimore St, Room 380, Baltimore, MD 21201, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, University of Maryland at Baltimore, 685 West Baltimore St, Room 380, Baltimore, MD 21201</wicri:regionArea></affiliation></author></analytic><series><title level="j">The Journal of general virology</title><idno type="eISSN">1465-2099</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cell Nucleus (chemistry)</term><term>Cell Nucleus (virology)</term><term>Chiroptera</term><term>Coronavirus (immunology)</term><term>Host-Pathogen Interactions</term><term>Humans</term><term>Immune Evasion</term><term>Interferon Type I (antagonists & inhibitors)</term><term>NF-kappa B (antagonists & inhibitors)</term><term>Viral Regulatory and Accessory Proteins (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Chiroptera</term><term>Coronavirus (immunologie)</term><term>Facteur de transcription NF-kappa B (antagonistes et inhibiteurs)</term><term>Humains</term><term>Interactions hôte-pathogène</term><term>Interféron de type I (antagonistes et inhibiteurs)</term><term>Noyau de la cellule ()</term><term>Noyau de la cellule (virologie)</term><term>Protéines virales régulatrices ou accessoires (immunologie)</term><term>Échappement immunitaire</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Interferon Type I</term><term>NF-kappa B</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Facteur de transcription NF-kappa B</term><term>Interféron de type I</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Cell Nucleus</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Coronavirus</term><term>Protéines virales régulatrices ou accessoires</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Coronavirus</term><term>Viral Regulatory and Accessory Proteins</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Noyau de la cellule</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Cell Nucleus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Chiroptera</term><term>Host-Pathogen Interactions</term><term>Humans</term><term>Immune Evasion</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Chiroptera</term><term>Humains</term><term>Interactions hôte-pathogène</term><term>Noyau de la cellule</term><term>Échappement immunitaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The recently emerged Middle East respiratory syndrome coronavirus (MERS-CoV), a betacoronavirus, is associated with severe pneumonia and renal failure. The environmental origin of MERS-CoV is as yet unknown; however, its genome sequence is closely related to those of two bat coronaviruses, named BtCoV-HKU4 and BtCoV-HKU5, which were derived from Chinese bat samples. A hallmark of highly pathogenic respiratory viruses is their ability to evade the innate immune response of the host. CoV accessory proteins, for example those from severe acute respiratory syndrome CoV (SARS-CoV), have been shown to block innate antiviral signalling pathways. MERS-CoV, similar to SARS-CoV, has been shown to inhibit type I IFN induction in a variety of cell types in vitro. We therefore hypothesized that MERS-CoV and the phylogenetically related BtCoV-HKU4 and BtCoV-HKU5 may encode proteins with similar capabilities. In this study, we have demonstrated that the ORF4b-encoded accessory protein (p4b) of MERS-CoV, BtCoV-HKU4 and BtCoV-HKU5 may indeed facilitate innate immune evasion by inhibiting the type I IFN and NF-κB signalling pathways. We also analysed the subcellular localization of p4b from MERS-CoV, BtCoV-HKU4 and BtCoV-HKU5 and demonstrated that all are localized to the nucleus. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24443473</PMID><DateCompleted><Year>2014</Year><Month>05</Month><Day>16</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1465-2099</ISSN><JournalIssue CitedMedium="Internet"><Volume>95</Volume><Issue>Pt 4</Issue><PubDate><Year>2014</Year><Month>Apr</Month></PubDate></JournalIssue><Title>The Journal of general virology</Title><ISOAbbreviation>J. Gen. Virol.</ISOAbbreviation></Journal><ArticleTitle>The ORF4b-encoded accessory proteins of Middle East respiratory syndrome coronavirus and two related bat coronaviruses localize to the nucleus and inhibit innate immune signalling.</ArticleTitle><Pagination><MedlinePgn>874-882</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1099/vir.0.062059-0</ELocationID><Abstract><AbstractText>The recently emerged Middle East respiratory syndrome coronavirus (MERS-CoV), a betacoronavirus, is associated with severe pneumonia and renal failure. The environmental origin of MERS-CoV is as yet unknown; however, its genome sequence is closely related to those of two bat coronaviruses, named BtCoV-HKU4 and BtCoV-HKU5, which were derived from Chinese bat samples. A hallmark of highly pathogenic respiratory viruses is their ability to evade the innate immune response of the host. CoV accessory proteins, for example those from severe acute respiratory syndrome CoV (SARS-CoV), have been shown to block innate antiviral signalling pathways. MERS-CoV, similar to SARS-CoV, has been shown to inhibit type I IFN induction in a variety of cell types in vitro. We therefore hypothesized that MERS-CoV and the phylogenetically related BtCoV-HKU4 and BtCoV-HKU5 may encode proteins with similar capabilities. In this study, we have demonstrated that the ORF4b-encoded accessory protein (p4b) of MERS-CoV, BtCoV-HKU4 and BtCoV-HKU5 may indeed facilitate innate immune evasion by inhibiting the type I IFN and NF-κB signalling pathways. We also analysed the subcellular localization of p4b from MERS-CoV, BtCoV-HKU4 and BtCoV-HKU5 and demonstrated that all are localized to the nucleus. </AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Matthews</LastName><ForeName>Krystal L</ForeName><Initials>KL</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Maryland at Baltimore, 685 West Baltimore St, Room 380, Baltimore, MD 21201, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Coleman</LastName><ForeName>Christopher M</ForeName><Initials>CM</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Maryland at Baltimore, 685 West Baltimore St, Room 380, Baltimore, MD 21201, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>van der Meer</LastName><ForeName>Yvonne</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Molecular Virology Laboratory, Department of Medical Microbiology, Leiden University Medical Center, PO Box 9600, 2300RC Leiden, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Snijder</LastName><ForeName>Eric J</ForeName><Initials>EJ</Initials><AffiliationInfo><Affiliation>Molecular Virology Laboratory, Department of Medical Microbiology, Leiden University Medical Center, PO Box 9600, 2300RC Leiden, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Frieman</LastName><ForeName>Matthew B</ForeName><Initials>MB</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Maryland at Baltimore, 685 West Baltimore St, Room 380, Baltimore, MD 21201, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 AI095569</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI095569-01</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>2014</Year><Month>01</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Gen Virol</MedlineTA><NlmUniqueID>0077340</NlmUniqueID><ISSNLinking>0022-1317</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007370">Interferon Type I</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054334">Viral Regulatory and Accessory 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Evasion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007370" MajorTopicYN="N">Interferon Type I</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054334" MajorTopicYN="N">Viral Regulatory and Accessory Proteins</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>1</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>1</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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|texte= The ORF4b-encoded accessory proteins of Middle East respiratory syndrome coronavirus and two related bat coronaviruses localize to the nucleus and inhibit innate immune signalling.
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