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Lymphocyte deficiencies increase susceptibility to friend virus-induced erythroleukemia in Fv-2 genetically resistant mice.
Hasenkrug KJ; Laboratory of Persistent Viral Diseases, Rocky Mountain;
October 30, 1999
J Virol. 1999 Aug;73(8):6468-73. Unique Identifier : AIDSLINE

The study of genetic resistance to retroviral diseases provides insights into the mechanisms by which organisms overcome potentially lethal infections. Fv-2 resistance to Friend virus-induced erythroleukemia acts through nonimmunological mechanisms to prevent early virus spread, but it does not completely block infection. The current experiments were done to determine whether Fv-2 alone could provide resistance or whether immunological mechanisms were also required to bring infection under control. Fv-2-resistant mice that were CD4(+) T-cell deficient were able to restrict early virus replication and spread as well as normal Fv-2-resistant mice, but they could not maintain control and developed severe Friend virus-induced splenomegaly and erythroleukemia by 6 to 8 weeks postinfection. Mice deficient in CD8(+) T cells and, to a lesser extent, B cells were also susceptible to late Friend virus-induced disease. Thus, Fv-2 resistance does not independently prevent FV-induced erythroleukemia but works in concert with the immune system by limiting early infection long enough to allow virus-specific immunity time to develop and facilitate recovery.

JOURNAL ARTICLE Animal CD4-Positive T-Lymphocytes/*IMMUNOLOGY CD8-Positive T-Lymphocytes/*IMMUNOLOGY Disease Susceptibility/IMMUNOLOGY Female Friend Virus/*IMMUNOLOGY Immunity, Natural Leukemia, Erythroblastic, Acute/*IMMUNOLOGY Leukemia, Experimental/*IMMUNOLOGY Male Mice Mice, Inbred C57BL Retroviridae Infections/*IMMUNOLOGY Tumor Virus Infections/*IMMUNOLOGY