{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T17:10:56Z","timestamp":1791047456754,"version":"4.1.0"},"reference-count":59,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2005,11,22]],"date-time":"2005-11-22T00:00:00Z","timestamp":1132617600000},"content-version":"vor","delay-in-days":6444,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[1988,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>A murine model of virally induced acquired immunodeficiency was analyzed in mice. The effect of systemic infection with various isolates of lymphocytic choriomeningitis virus (LCMV) on the capacity of mice to mount a T cell\u2010independent IgM and a T cell\u2010dependent IgG neutralizing antibody response against a subsequent infection with vesicular stomatitis virus (VSV) was analyzed. DBA\/2 mice infected with the LCMV\u2010WE isolate were impaired in their IgM and IgG responses to VSV. Immune suppression was not caused by interferons inhibiting proper VSV antigen expression, since responses to inactivated VSV were also suppressed. The higher the dose of the LCMV and the lower the dose of the challenging VSV infection the more drastic was the apparent lack of immune responsiveness and the longer it lasted. Kinetics of induction of suppression of the T cell\u2010independent IgM responses closely followed that of a normal cytotoxic T cell response to LCMV\u2010WE, starting on day 6 and reaching maximal levels by day 8 to 10. The T cell\u2010dependent IgG response to VSV was suppressed with a kinetics that was shifted by about 6 days when compared with suppression of IgM responses, <jats:italic>i.e.<\/jats:italic> LCMV infection on the same day or before (but not after) VSV infection led to suppression of IgG responses that are usually first detected by day 6\u20107 after initiation of the VSV infection. Severity and duration of immunosuppressiveness depended upon the LCMV isolate and the mouse strain used: LCMV\u2010WE and LCMV\u2010Docile were most, whereas LCMV\u2010Armstrong was in general least immunosuppressive. Antibody responses to VSV\u2010NJ seemed to be more subject to LCMV\u2010induced immune suppression than VSV\u2010IND\u2010specific responses. Mouse strains differed considerably with respect to extent of suppression, dependent upon both major histocompatibility genes (MHC) and non\u2010MHC genes. DBA and Swiss type mice were generally more susceptible than C57BL and CBA mice, and H\u20102<jats:sup>q<\/jats:sup> and H\u20102<jats:sup>k<\/jats:sup> seemed to be more susceptible than H\u20102<jats:sup>b<\/jats:sup> or H\u20102<jats:sup>d<\/jats:sup> mice.<\/jats:p><jats:p>Mice infected with LCMV\u2010WE showed signs of acquired immunodeficiency diseases since they were more susceptible to superinfection with VSV and developed paralytic disease and tended to die from VSV infection. Since LCMV is basically a noneytopathic virus, this murine model of virally induced immune suppression may serve to analyze immune pathogenesis of virus\u2010induced acquired immunodeficiency.<\/jats:p>","DOI":"10.1002\/eji.1830180404","type":"journal-article","created":{"date-parts":[[2007,3,1]],"date-time":"2007-03-01T01:14:40Z","timestamp":1172711680000},"page":"511-518","source":"Crossref","is-referenced-by-count":40,"title":["An acquired immune suppression in mice caused by infection with lymphocytic choriomeningitis virus"],"prefix":"10.1002","volume":"18","author":[{"given":"Hanspeter","family":"Roost","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shiv","family":"Charan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rita","family":"Gobet","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edith","family":"R\u00fcedi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hans","family":"Hengartner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alana Althage","family":"And","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rolf M.","family":"Zinkernagel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2005,11,22]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.83.24.9278"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198711193172101"},{"key":"e_1_2_1_4_2","volume-title":"Pathogenesis of infectious disease","author":"Mims C. 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