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dc.contributor.authorKurilla, Michael G.
dc.contributor.authorSwaminathan, Sankar
dc.contributor.authorWelsh, Raymond M.
dc.contributor.authorKieff, Elliott D.
dc.contributor.authorBrutkiewicz, Randy R.
dc.date2022-08-11T08:09:00.000
dc.date.accessioned2022-08-23T16:14:55Z
dc.date.available2022-08-23T16:14:55Z
dc.date.issued1993-12-01
dc.date.submitted2008-10-15
dc.identifier.citation<p>J Virol. 1993 Dec;67(12):7623-8.</p>
dc.identifier.issn0022-538X (Print)
dc.identifier.pmid8230481
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33977
dc.description.abstractTo investigate the in vivo role of interleukin-10 (IL-10) in viral infection, we compared infections with a recombinant vaccinia virus (VV) expressing IL-10 (VV-IL10) under control of the VV P7.5 promoter and a control virus (VV-beta gal) in normal and severe combined immunodeficient mice. In normal mice, VV-IL10 infection resulted in less natural killer cell activity at 3 days postinfection and less VV-specific cytotoxic T-cell activity at 6 or 7 days postinfection than VV-beta gal infection. However, the use of dermal scarification or intraperitoneal, intranasal, or intracerebral inoculation into immunocompetent mice resulted in no difference between VV-IL10 and VV-beta gal in visible lesions, mortality, protective immunity to a 100-fold lethal VV challenge, or VV-specific antibody response. In the immunodeficient mice, VV-IL10 infection resulted in greater natural killer cell activity and lower virus replication than VV-beta gal infection. These in vivo effects were subtler and more complex than had been anticipated. From the VV-IL10 murine model, the Epstein-Barr virus-encoded homolog of human IL-10, BCRF1, may provide a selective advantage by blunting the early human natural killer cell and cytotoxic T-cell responses so that Epstein-Barr virus can establish a well-contained latent infection in B lymphocytes.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8230481&dopt=Abstract">Link to article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC238230/
dc.subjectAnimals; *Cytotoxicity, Immunologic; Drug Administration Routes; Interleukin-10; Killer Cells, Natural; Lung; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, SCID; Recombinant Proteins; Spleen; T-Lymphocytes, Cytotoxic; Vaccinia; Vaccinia virus
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleEffects of virally expressed interleukin-10 on vaccinia virus infection in mice
dc.typeJournal Article
dc.source.journaltitleJournal of virology
dc.source.volume67
dc.source.issue12
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/630
dc.identifier.contextkey651100
html.description.abstract<p>To investigate the in vivo role of interleukin-10 (IL-10) in viral infection, we compared infections with a recombinant vaccinia virus (VV) expressing IL-10 (VV-IL10) under control of the VV P7.5 promoter and a control virus (VV-beta gal) in normal and severe combined immunodeficient mice. In normal mice, VV-IL10 infection resulted in less natural killer cell activity at 3 days postinfection and less VV-specific cytotoxic T-cell activity at 6 or 7 days postinfection than VV-beta gal infection. However, the use of dermal scarification or intraperitoneal, intranasal, or intracerebral inoculation into immunocompetent mice resulted in no difference between VV-IL10 and VV-beta gal in visible lesions, mortality, protective immunity to a 100-fold lethal VV challenge, or VV-specific antibody response. In the immunodeficient mice, VV-IL10 infection resulted in greater natural killer cell activity and lower virus replication than VV-beta gal infection. These in vivo effects were subtler and more complex than had been anticipated. From the VV-IL10 murine model, the Epstein-Barr virus-encoded homolog of human IL-10, BCRF1, may provide a selective advantage by blunting the early human natural killer cell and cytotoxic T-cell responses so that Epstein-Barr virus can establish a well-contained latent infection in B lymphocytes.</p>
dc.identifier.submissionpathgsbs_sp/630
dc.contributor.departmentDepartment of Pathology
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages7623-8


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