{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,24]],"date-time":"2026-01-24T08:05:31Z","timestamp":1769241931752,"version":"3.49.0"},"reference-count":33,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2014,5,21]],"date-time":"2014-05-21T00:00:00Z","timestamp":1400630400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Scand J Immunol"],"published-print":{"date-parts":[[2014,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Infection with murine gammaherpesvirus 68 has become an accepted model for studying the virus\/host interactions with regard to gammaherpesvirus infections. Previous studies using gene\u2010deficient mice have revealed that neither <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content><jats:italic>\u03b3<\/jats:italic> nor perforin is essential in controlling the outcome of infection or the virus load during chronic infection in C57BL\/6 mice. However, pronounced multiorgan fibrosis and splenic atrophy are observed in mice lacking <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content><jats:italic>\u03b3<\/jats:italic> or the <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content><jats:italic>\u03b3<\/jats:italic> receptor. To study the interplay between perforin and <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content><jats:italic>\u03b3<\/jats:italic> in controlling the virus\u2010induced pathology and the viral load during chronic gammaherpesvirus infection, we infected <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content><jats:italic>\u03b3<\/jats:italic>\/perforin double\u2010deficient C57BL\/6 mice and followed the course of infection. While absence of perforin prevented the splenic atrophy in <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content><jats:italic>\u03b3<\/jats:italic>\u2010deficient mice, fibrosis did not disappear. Moreover, double\u2010deficient mice developed extreme splenomegaly, were unable to control the viral load and displayed chronic immune activation. Thus, <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content><jats:italic>\u03b3<\/jats:italic> and perforin act in concert to minimize pathology and control the viral load in mice chronically infected with <jats:styled-content style=\"fixed-case\">MHV<\/jats:styled-content>68. Furthermore, while certain aspect of the virus\u2010induced pathology in <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content><jats:italic>\u03b3<\/jats:italic>\u2010deficient mice may be alleviated in double\u2010deficient mice, other aspects are exaggerated, and the normal architecture of the spleen is completely destroyed. We believe that these findings add to the understanding of the virus\/host interaction during chronic gammaherpes virus infection.<\/jats:p>","DOI":"10.1111\/sji.12176","type":"journal-article","created":{"date-parts":[[2014,3,31]],"date-time":"2014-03-31T09:08:53Z","timestamp":1396256933000},"page":"395-403","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["<scp>IFN<\/scp><i>\u03b3<\/i> and Perforin Cooperate to Control Infection and Prevent Fatal Pathology During Persistent Gammaherpesvirus Infection in Mice"],"prefix":"10.1111","volume":"79","author":[{"given":"C.","family":"Bartholdy","sequence":"first","affiliation":[{"name":"Institute of International Health Immunology and Microbiology University of Copenhagen Copenhagen Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"H\u00f8gh\u2010Petersen","sequence":"additional","affiliation":[{"name":"Institute of International Health Immunology and Microbiology University of Copenhagen Copenhagen Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P.","family":"Storm","sequence":"additional","affiliation":[{"name":"Institute of International Health Immunology and Microbiology University of Copenhagen Copenhagen Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P. 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