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dc.contributor.authorReinert, Line S.
dc.contributor.authorLopusna, Katarina
dc.contributor.authorWinther, Henriette
dc.contributor.authorSun, Chenglong
dc.contributor.authorThomsen, Martin K.
dc.contributor.authorNandakumar, Ramya
dc.contributor.authorMogensen, Trine H.
dc.contributor.authorMeyer, Morten
dc.contributor.authorVaegter, Christian
dc.contributor.authorNyengaard, Jens R.
dc.contributor.authorFitzgerald, Katherine A.
dc.contributor.authorPaludan, Soren R.
dc.date2022-08-11T08:09:46.000
dc.date.accessioned2022-08-23T16:42:58Z
dc.date.available2022-08-23T16:42:58Z
dc.date.issued2016-11-10
dc.date.submitted2017-04-14
dc.identifier.citationNat Commun. 2016 Nov 10;7:13348. doi: 10.1038/ncomms13348. <a href="https://doi.org/10.1038/ncomms13348">Link to article on publisher's site</a>
dc.identifier.issn2041-1723 (Linking)
dc.identifier.doi10.1038/ncomms13348
dc.identifier.pmid27830700
dc.identifier.urihttp://hdl.handle.net/20.500.14038/40197
dc.description.abstractHerpes simplex encephalitis (HSE) is the most common form of acute viral encephalitis in industrialized countries. Type I interferon (IFN) is important for control of herpes simplex virus (HSV-1) in the central nervous system (CNS). Here we show that microglia are the main source of HSV-induced type I IFN expression in CNS cells and these cytokines are induced in a cGAS-STING-dependent manner. Consistently, mice defective in cGAS or STING are highly susceptible to acute HSE. Although STING is redundant for cell-autonomous antiviral resistance in astrocytes and neurons, viral replication is strongly increased in neurons in STING-deficient mice. Interestingly, HSV-infected microglia confer STING-dependent antiviral activities in neurons and prime type I IFN production in astrocytes through the TLR3 pathway. Thus, sensing of HSV-1 infection in the CNS by microglia through the cGAS-STING pathway orchestrates an antiviral program that includes type I IFNs and immune-priming of other cell types.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=27830700&dopt=Abstract">Link to Article in PubMed</a>
dc.rightsCopyright © 2016, The Author(s).
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectGlial biology
dc.subjectInfectious diseases
dc.subjectInterferons
dc.subjectViral host response
dc.subjectImmunology and Infectious Disease
dc.subjectNervous System Diseases
dc.subjectVirus Diseases
dc.titleSensing of HSV-1 by the cGAS-STING pathway in microglia orchestrates antiviral defence in the CNS
dc.typeJournal Article
dc.source.journaltitleNature communications
dc.source.volume7
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=4000&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/2995
dc.identifier.contextkey10021734
refterms.dateFOA2022-08-23T16:42:58Z
html.description.abstract<p>Herpes simplex encephalitis (HSE) is the most common form of acute viral encephalitis in industrialized countries. Type I interferon (IFN) is important for control of herpes simplex virus (HSV-1) in the central nervous system (CNS). Here we show that microglia are the main source of HSV-induced type I IFN expression in CNS cells and these cytokines are induced in a cGAS-STING-dependent manner. Consistently, mice defective in cGAS or STING are highly susceptible to acute HSE. Although STING is redundant for cell-autonomous antiviral resistance in astrocytes and neurons, viral replication is strongly increased in neurons in STING-deficient mice. Interestingly, HSV-infected microglia confer STING-dependent antiviral activities in neurons and prime type I IFN production in astrocytes through the TLR3 pathway. Thus, sensing of HSV-1 infection in the CNS by microglia through the cGAS-STING pathway orchestrates an antiviral program that includes type I IFNs and immune-priming of other cell types.</p>
dc.identifier.submissionpathoapubs/2995
dc.contributor.departmentDivision of Infectious Diseases and Immunology, Department of Medicine
dc.source.pages13348


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Copyright © 2016, The Author(s).
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