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dc.contributor.authorBarouch, Dan H.
dc.contributor.authorKang, Hyung-joo
dc.contributor.authorLi, Wenjun
dc.date2022-08-11T08:08:20.000
dc.date.accessioned2022-08-23T15:51:26Z
dc.date.available2022-08-23T15:51:26Z
dc.date.issued2016-04-21
dc.date.submitted2017-02-17
dc.identifier.citationCell. 2016 Apr 21;165(3):656-67. doi: 10.1016/j.cell.2016.03.021. Epub 2016 Apr 13. <a href="https://doi.org/10.1016/j.cell.2016.03.021">Link to article on publisher's site</a>
dc.identifier.issn0092-8674 (Linking)
dc.identifier.doi10.1016/j.cell.2016.03.021
dc.identifier.pmid27085913
dc.identifier.urihttp://hdl.handle.net/20.500.14038/28900
dc.description<p>Full author list omitted for brevity. For full list of authors see article.</p>
dc.description.abstractThe earliest events following mucosal HIV-1 infection, prior to measurable viremia, remain poorly understood. Here, by detailed necropsy studies, we show that the virus can rapidly disseminate following mucosal SIV infection of rhesus monkeys and trigger components of the inflammasome, both at the site of inoculation and at early sites of distal virus spread. By 24 hr following inoculation, a proinflammatory signature that lacked antiviral restriction factors was observed in viral RNA-positive tissues. The early innate response included expression of NLRX1, which inhibits antiviral responses, and activation of the TGF-beta pathway, which negatively regulates adaptive immune responses. These data suggest a model in which the virus triggers specific host mechanisms that suppress the generation of antiviral innate and adaptive immune responses in the first few days of infection, thus facilitating its own replication. These findings have important implications for the development of vaccines and other strategies to prevent infection.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=27085913&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttps://doi.org/10.1016/j.cell.2016.03.021
dc.subjectImmunology and Infectious Disease
dc.titleRapid Inflammasome Activation following Mucosal SIV Infection of Rhesus Monkeys
dc.typeJournal Article
dc.source.journaltitleCell
dc.source.volume165
dc.source.issue3
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/1131
dc.identifier.contextkey9706543
html.description.abstract<p>The earliest events following mucosal HIV-1 infection, prior to measurable viremia, remain poorly understood. Here, by detailed necropsy studies, we show that the virus can rapidly disseminate following mucosal SIV infection of rhesus monkeys and trigger components of the inflammasome, both at the site of inoculation and at early sites of distal virus spread. By 24 hr following inoculation, a proinflammatory signature that lacked antiviral restriction factors was observed in viral RNA-positive tissues. The early innate response included expression of NLRX1, which inhibits antiviral responses, and activation of the TGF-beta pathway, which negatively regulates adaptive immune responses. These data suggest a model in which the virus triggers specific host mechanisms that suppress the generation of antiviral innate and adaptive immune responses in the first few days of infection, thus facilitating its own replication. These findings have important implications for the development of vaccines and other strategies to prevent infection.</p>
dc.identifier.submissionpathfaculty_pubs/1131
dc.contributor.departmentPrevention Research Center
dc.contributor.departmentDepartment of Medicine, Division of Cardiovascular Medicine
dc.contributor.departmentDepartment of Medicine, Division of Preventive and Behavioral Medicine
dc.source.pages656-67


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