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We evaluated here the fate of bystander T cells activated by third party cognate antigens during acute viral infections<jats:named-content content-type=\"genus-species\">in vivo<\/jats:named-content>, using distinct models to track and specifically activate HY and P14 transgenic bystander CD8 T cells<jats:named-content content-type=\"genus-species\">in vivo<\/jats:named-content>during acute arenavirus infections of mice. Viral infections acted as stimulatory adjuvants when bystander T cells were exposed to an inflammatory milieu and cognate antigens at the beginning of infections, but bystander CD8 T cell proliferation in response to cognate antigen was inhibited 3 to 9 days after virus infection. Reduced proliferation was not dependent on Fas-FasL- or tumor necrosis factor (TNF)-induced activation-induced cell death or on deficiencies of antigen presentation. Instead, reduced proliferation was associated with a delayed onset of division that was an intrinsic defect of T cells. Inhibition of proliferation could be simulated by exposure of T cells to the Toll-like receptor agonist and type I interferon (IFN) inducer poly(I \u00b7 C). T cells lacking IFN-\u03b1\/\u03b2 receptors resisted both the suppressive effects of preexposure to poly(I \u00b7 C) and the stimulatory effects of type I IFN, indicating that the timing of exposure to IFN can have negative or positive effects on T cell proliferation. Inhibition of T cell receptor-stimulated bystander CD8 T cell proliferation during acute viral infections may reflect the reduced ability of vaccines to elicit protective immunity when administered during an acute illness.<\/jats:p>","DOI":"10.1128\/jvi.02516-10","type":"journal-article","created":{"date-parts":[[2011,4,7]],"date-time":"2011-04-07T12:45:22Z","timestamp":1302180322000},"page":"5929-5939","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":87,"title":["Virus-Induced Transient Immune Suppression and the Inhibition of T Cell Proliferation by Type I Interferon"],"prefix":"10.1128","volume":"85","author":[{"given":"Heather D.","family":"Marshall","sequence":"first","affiliation":[{"name":"Department of Pathology, Program in Immunology and Virology, University of Massachusetts Medical School, Worcester, Massachusetts 01655"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stina L.","family":"Urban","sequence":"additional","affiliation":[{"name":"Department of Pathology, Program in Immunology and Virology, University of Massachusetts Medical School, Worcester, Massachusetts 01655"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raymond M.","family":"Welsh","sequence":"additional","affiliation":[{"name":"Department of Pathology, Program in Immunology and Virology, University of Massachusetts Medical School, Worcester, Massachusetts 01655"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.178.2.427"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni724"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.clim.2006.12.001"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.174.4.2220"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2008-12-191296"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.187.5.685"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1615\/CritRevImmunol.v18.i3.10"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0005659"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.vaccine.2004.09.038"},{"key":"e_1_3_2_11_2","doi-asserted-by":"crossref","first-page":"6762","DOI":"10.4049\/jimmunol.163.12.6762","article-title":"Vaccinia virus inhibits the maturation of human dendritic cells: a novel mechanism of immune evasion","volume":"163","author":"Engelmayer J.","year":"1999","unstructured":"EngelmayerJ. . 1999. 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