Linked Life Data

10890918

Source:http://linkedlifedata.com/resource/pubmed/id/10890918

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pubmed-article:10890918pubmed:abstractTextThe gamma-herpesviruses, in contrast to the alpha- and beta-herpesviruses, are not known to inhibit antigen presentation to CD8(+) cytotoxic T lymphocytes (CTLs) during lytic cycle replication. However, murine gamma-herpesvirus 68 causes a chronic lytic infection in CD4(+) T cell-deficient mice despite the persistence of a substantial CTL response, suggesting that CTL evasion occurs. Here we show that, distinct from host protein synthesis shutoff, gamma-herpesvirus 68 down-regulates surface MHC class I expression on lytically infected fibroblasts and inhibits their recognition by antigen-specific CTLs. The viral K3 gene, encoding a zinc-finger-containing protein, dramatically reduced the half-life of nascent class I molecules and the level of surface MHC class I expression and was by itself sufficient to block antigen presentation. The homologous K3 and K5 genes of the related Kaposi's sarcoma-associated virus also inhibited antigen presentation and decreased cell surface expression of HLA class I antigens. Thus it appears that an immune evasion strategy shared by at least two gamma-herpesviruses allows continued lytic infection in the face of strong CTL immunity.lld:pubmed
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pubmed-article:10890918pubmed:dateRevised2009-11-18lld:pubmed
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pubmed-article:10890918pubmed:articleTitleInhibition of MHC class I-restricted antigen presentation by gamma 2-herpesviruses.lld:pubmed
pubmed-article:10890918pubmed:affiliationDivision of Virology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, United Kingdom. pgs27@mole.bio.cam.ac.uklld:pubmed
pubmed-article:10890918pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:10890918pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
pubmed-article:10890918pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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