Reduction of infection by inhibiting mTOR pathway is associated with reversed repression of type I interferon by porcine reproductive and respiratory syndrome virus.
Identifieur interne : 000755 ( Main/Exploration ); précédent : 000754; suivant : 000756Reduction of infection by inhibiting mTOR pathway is associated with reversed repression of type I interferon by porcine reproductive and respiratory syndrome virus.
Auteurs : Qinfang Liu [États-Unis] ; Laura C. Miller [États-Unis] ; Frank Blecha [États-Unis] ; Yongming Sang [États-Unis]Source :
- The Journal of general virology [ 1465-2099 ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Cellules cultivées (MeSH), Cellules épithéliales (immunologie), Cellules épithéliales (virologie), Interactions hôte-pathogène (MeSH), Interféron de type I (métabolisme), Macrophages alvéolaires (immunologie), Macrophages alvéolaires (virologie), Suidae (MeSH), Sérine-thréonine kinases TOR (antagonistes et inhibiteurs), Transduction du signal (MeSH), Virus du syndrome respiratoire et reproducteur porcin (physiologie).
- MESH :
- antagonistes et inhibiteurs : Sérine-thréonine kinases TOR.
- immunologie : Cellules épithéliales, Macrophages alvéolaires.
- métabolisme : Interféron de type I.
- physiologie : Virus du syndrome respiratoire et reproducteur porcin.
- virologie : Cellules épithéliales, Macrophages alvéolaires.
- Animaux, Cellules cultivées, Interactions hôte-pathogène, Suidae, Transduction du signal.
English descriptors
- KwdEn :
- Animals (MeSH), Cells, Cultured (MeSH), Epithelial Cells (immunology), Epithelial Cells (virology), Host-Pathogen Interactions (MeSH), Interferon Type I (metabolism), Macrophages, Alveolar (immunology), Macrophages, Alveolar (virology), Porcine respiratory and reproductive syndrome virus (physiology), Signal Transduction (MeSH), Swine (MeSH), TOR Serine-Threonine Kinases (antagonists & inhibitors).
- MESH :
- chemical , antagonists & inhibitors : TOR Serine-Threonine Kinases.
- chemical , metabolism : Interferon Type I.
- immunology : Epithelial Cells, Macrophages, Alveolar.
- physiology : Porcine respiratory and reproductive syndrome virus.
- virology : Epithelial Cells, Macrophages, Alveolar.
- Animals, Cells, Cultured, Host-Pathogen Interactions, Signal Transduction, Swine.
Abstract
Type I interferons (IFNs) are critical in animal antiviral regulation. IFN-mediated signalling regulates hundreds of genes that are directly associated with antiviral, immune and other physiological responses. The signalling pathway mediated by mechanistic target of rapamycin (mTOR), a serine/threonine kinase regulated by IFNs, is key in regulation of cellular metabolism and was recently implicated in host antiviral responses. However, little is known about how animal type I IFN signalling coordinates immunometabolic reactions during antiviral defence. Here, using porcine reproductive and respiratory syndrome virus (PRRSV), we found that the genes in the mTOR signalling pathway were differently regulated in PRRSV-infected porcine alveolar macrophages at different activation statuses. Moreover, mTOR signalling regulated PRRSV infection in MARC-145 and primary porcine cells, in part, through modulating the production and signalling of type I IFNs. Taken together, we determined that the mTOR signalling pathway involves PRRSV infection and regulates expression and signalling of type I IFNs against viral infection. These findings suggest that the mTOR signalling pathway has a bi-directional loop with the type I IFN system and imply that some components in the mTOR signalling pathway can be utilized as targets for studying antiviral immunity and for designing therapeutic reagents.
DOI: 10.1099/jgv.0.000802
PubMed: 28613152
PubMed Central: PMC5962895
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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IFN-mediated signalling regulates hundreds of genes that are directly associated with antiviral, immune and other physiological responses. The signalling pathway mediated by mechanistic target of rapamycin (mTOR), a serine/threonine kinase regulated by IFNs, is key in regulation of cellular metabolism and was recently implicated in host antiviral responses. However, little is known about how animal type I IFN signalling coordinates immunometabolic reactions during antiviral defence. Here, using porcine reproductive and respiratory syndrome virus (PRRSV), we found that the genes in the mTOR signalling pathway were differently regulated in PRRSV-infected porcine alveolar macrophages at different activation statuses. Moreover, mTOR signalling regulated PRRSV infection in MARC-145 and primary porcine cells, in part, through modulating the production and signalling of type I IFNs. Taken together, we determined that the mTOR signalling pathway involves PRRSV infection and regulates expression and signalling of type I IFNs against viral infection. These findings suggest that the mTOR signalling pathway has a bi-directional loop with the type I IFN system and imply that some components in the mTOR signalling pathway can be utilized as targets for studying antiviral immunity and for designing therapeutic reagents.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28613152</PMID><DateCompleted><Year>2017</Year><Month>07</Month><Day>17</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1465-2099</ISSN><JournalIssue CitedMedium="Internet"><Volume>98</Volume><Issue>6</Issue><PubDate><Year>2017</Year><Month>Jun</Month></PubDate></JournalIssue><Title>The Journal of general virology</Title><ISOAbbreviation>J Gen Virol</ISOAbbreviation></Journal><ArticleTitle>Reduction of infection by inhibiting mTOR pathway is associated with reversed repression of type I interferon by porcine reproductive and respiratory syndrome virus.</ArticleTitle><Pagination><MedlinePgn>1316-1328</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1099/jgv.0.000802</ELocationID><Abstract><AbstractText>Type I interferons (IFNs) are critical in animal antiviral regulation. IFN-mediated signalling regulates hundreds of genes that are directly associated with antiviral, immune and other physiological responses. The signalling pathway mediated by mechanistic target of rapamycin (mTOR), a serine/threonine kinase regulated by IFNs, is key in regulation of cellular metabolism and was recently implicated in host antiviral responses. However, little is known about how animal type I IFN signalling coordinates immunometabolic reactions during antiviral defence. Here, using porcine reproductive and respiratory syndrome virus (PRRSV), we found that the genes in the mTOR signalling pathway were differently regulated in PRRSV-infected porcine alveolar macrophages at different activation statuses. Moreover, mTOR signalling regulated PRRSV infection in MARC-145 and primary porcine cells, in part, through modulating the production and signalling of type I IFNs. Taken together, we determined that the mTOR signalling pathway involves PRRSV infection and regulates expression and signalling of type I IFNs against viral infection. These findings suggest that the mTOR signalling pathway has a bi-directional loop with the type I IFN system and imply that some components in the mTOR signalling pathway can be utilized as targets for studying antiviral immunity and for designing therapeutic reagents.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Qinfang</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Departments of Anatomy and Physiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Miller</LastName><ForeName>Laura C</ForeName><Initials>LC</Initials><AffiliationInfo><Affiliation>USDA, Agricultural Research Service, National Animal Disease Center, Virus and Prion Research Unit, 1920 Dayton Avenue, Ames, IA 50010, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Blecha</LastName><ForeName>Frank</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Departments of Anatomy and Physiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sang</LastName><ForeName>Yongming</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Present address: Department of Agricultural and Environmental Sciences, College of Agriculture, Human and Natural Sciences, Tennessee State University, 3500 John A. Merritt Boulevard, Nashville, TN, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Departments of Anatomy and Physiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P20 RR017686</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>06</Month><Day>14</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>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054884" MajorTopicYN="Y">Host-Pathogen Interactions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007370" MajorTopicYN="N">Interferon Type I</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016676" MajorTopicYN="N">Macrophages, Alveolar</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019316" MajorTopicYN="N">Porcine respiratory and reproductive syndrome virus</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013552" MajorTopicYN="N">Swine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate 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IdType="pubmed">8392613</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Iowa</li><li>Kansas</li><li>Tennessee</li></region></list><tree><country name="États-Unis"><region name="Kansas"><name sortKey="Liu, Qinfang" sort="Liu, Qinfang" uniqKey="Liu Q" first="Qinfang" last="Liu">Qinfang Liu</name></region><name sortKey="Blecha, Frank" sort="Blecha, Frank" uniqKey="Blecha F" first="Frank" last="Blecha">Frank Blecha</name><name sortKey="Miller, Laura C" sort="Miller, Laura C" uniqKey="Miller L" first="Laura C" last="Miller">Laura C. Miller</name><name sortKey="Sang, Yongming" sort="Sang, Yongming" uniqKey="Sang Y" first="Yongming" last="Sang">Yongming Sang</name><name sortKey="Sang, Yongming" sort="Sang, Yongming" uniqKey="Sang Y" first="Yongming" last="Sang">Yongming Sang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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