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dc.contributor.authorGammon, Don B.
dc.contributor.authorDuraffour, Sophie
dc.contributor.authorRozelle, Daniel K.
dc.contributor.authorHehnly, Heidi
dc.contributor.authorSharma, Rita
dc.contributor.authorSparks, Michael E.
dc.contributor.authorWest, Cara C.
dc.contributor.authorChen, Ying
dc.contributor.authorMoresco, James J.
dc.contributor.authorAndrei, Graciela
dc.contributor.authorConnor, John H.
dc.contributor.authorConte, Darryl Jr.
dc.contributor.authorGundersen-Rindal, Dawn E.
dc.contributor.authorMarshall, William L.
dc.contributor.authorYates, John R.
dc.contributor.authorSilverman, Neal S.
dc.contributor.authorMello, Craig C.
dc.date2022-08-11T08:09:08.000
dc.date.accessioned2022-08-23T16:19:02Z
dc.date.available2022-08-23T16:19:02Z
dc.date.issued2014-06-25
dc.date.submitted2014-11-26
dc.identifier.citationElife. 2014 Jun 25;3. doi: 10.7554/eLife.02910. <a href="http://dx.doi.org/10.7554/eLife.02910">Link to article on publisher's site</a>
dc.identifier.issn2050-084X (Linking)
dc.identifier.doi10.7554/eLife.02910
dc.identifier.pmid24966209
dc.identifier.urihttp://hdl.handle.net/20.500.14038/34950
dc.description.abstractVirus-host interactions drive a remarkable diversity of immune responses and countermeasures. We found that two RNA viruses with broad host ranges, vesicular stomatitis virus (VSV) and Sindbis virus (SINV), are completely restricted in their replication after entry into Lepidopteran cells. This restriction is overcome when cells are co-infected with vaccinia virus (VACV), a vertebrate DNA virus. Using RNAi screening, we show that Lepidopteran RNAi, Nuclear Factor-kappaB, and ubiquitin-proteasome pathways restrict RNA virus infection. Surprisingly, a highly conserved, uncharacterized VACV protein, A51R, can partially overcome this virus restriction. We show that A51R is also critical for VACV replication in vertebrate cells and for pathogenesis in mice. Interestingly, A51R colocalizes with, and stabilizes, host microtubules and also associates with ubiquitin. We show that A51R promotes viral protein stability, possibly by preventing ubiquitin-dependent targeting of viral proteins for destruction. Importantly, our studies reveal exciting new opportunities to study virus-host interactions in experimentally-tractable Lepidopteran systems.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=24966209&dopt=Abstract">Link to Article in PubMed</a>
dc.rightsThis is an open-access article, free of all copyright, and may befreely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under theCreative Commons CC0 public domain dedication.
dc.subjectImmunology
dc.subjectMicrobiology and infectious disease
dc.subjectLymantria dispar
dc.subjectvaccinia virus
dc.subjectvesicular stomatitis virus
dc.subjectSindbis virus
dc.subjectmicrotubules
dc.subjectubiquitin
dc.subjectMouse Viruses
dc.subjectImmunity
dc.subjectImmunology and Infectious Disease
dc.subjectImmunology of Infectious Disease
dc.subjectInfectious Disease
dc.subjectVirology
dc.subjectViruses
dc.titleA single vertebrate DNA virus protein disarms invertebrate immunity to RNA virus infection
dc.typeJournal Article
dc.source.journaltitleeLife
dc.source.volume3
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1171&amp;context=infdis_pp&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/infdis_pp/172
dc.identifier.contextkey6399369
refterms.dateFOA2022-08-23T16:19:02Z
html.description.abstract<p>Virus-host interactions drive a remarkable diversity of immune responses and countermeasures. We found that two RNA viruses with broad host ranges, vesicular stomatitis virus (VSV) and Sindbis virus (SINV), are completely restricted in their replication after entry into Lepidopteran cells. This restriction is overcome when cells are co-infected with vaccinia virus (VACV), a vertebrate DNA virus. Using RNAi screening, we show that Lepidopteran RNAi, Nuclear Factor-kappaB, and ubiquitin-proteasome pathways restrict RNA virus infection. Surprisingly, a highly conserved, uncharacterized VACV protein, A51R, can partially overcome this virus restriction. We show that A51R is also critical for VACV replication in vertebrate cells and for pathogenesis in mice. Interestingly, A51R colocalizes with, and stabilizes, host microtubules and also associates with ubiquitin. We show that A51R promotes viral protein stability, possibly by preventing ubiquitin-dependent targeting of viral proteins for destruction. Importantly, our studies reveal exciting new opportunities to study virus-host interactions in experimentally-tractable Lepidopteran systems.</p>
dc.identifier.submissionpathinfdis_pp/172
dc.contributor.departmentRNA Therapeutics Institute
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentDepartment of Medicine, Division of Infectious Diseases and Immunology


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