Effects of virally expressed interleukin-10 on vaccinia virus infection in mice
dc.contributor.author | Kurilla, Michael G. | |
dc.contributor.author | Swaminathan, Sankar | |
dc.contributor.author | Welsh, Raymond M. | |
dc.contributor.author | Kieff, Elliott D. | |
dc.contributor.author | Brutkiewicz, Randy R. | |
dc.date | 2022-08-11T08:09:00.000 | |
dc.date.accessioned | 2022-08-23T16:14:55Z | |
dc.date.available | 2022-08-23T16:14:55Z | |
dc.date.issued | 1993-12-01 | |
dc.date.submitted | 2008-10-15 | |
dc.identifier.citation | <p>J Virol. 1993 Dec;67(12):7623-8.</p> | |
dc.identifier.issn | 0022-538X (Print) | |
dc.identifier.pmid | 8230481 | |
dc.identifier.uri | http://hdl.handle.net/20.500.14038/33977 | |
dc.description.abstract | 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. | |
dc.language.iso | en_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.url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC238230/ | |
dc.subject | Animals; *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.subject | Life Sciences | |
dc.subject | Medicine and Health Sciences | |
dc.title | Effects of virally expressed interleukin-10 on vaccinia virus infection in mice | |
dc.type | Journal Article | |
dc.source.journaltitle | Journal of virology | |
dc.source.volume | 67 | |
dc.source.issue | 12 | |
dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/gsbs_sp/630 | |
dc.identifier.contextkey | 651100 | |
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.submissionpath | gsbs_sp/630 | |
dc.contributor.department | Department of Pathology | |
dc.contributor.department | Graduate School of Biomedical Sciences | |
dc.source.pages | 7623-8 |