Lymphocyte deficiencies increase susceptibility to friend virus-induced erythroleukemia in Fv-2 genetically resistant mice

The study of genetic resistance to retroviral diseases provides insights in to the mechanisms by which organisms overcome potentially lethal infections . Fv-2 resistance to Friend virus-induced erythroleukemia acts through noni nmunological mechanisms to prevent early virus spread, but it does not comp letely block infection. The current experiments were done to determine whet her Fv-2 alone could provide resistance or whether immunological mechanisms mere also required to bring infection under control. Fv-2-resistant mice t hat were CD4(+) T-cell deficient were able to restrict early virus replicat ion and spread as well as normal Fv-2-resistant mice, but they could not ma intain control and developed severe Friend virus-induced splenomegaly and e rythroleukemia by 6 to 8 weeks postinfection, Mice deficient in CD8(+) T ce lls and, to a lesser extent, B cells were also susceptible to late Friend v irus-induced disease. Thus, Fv-2 resistance does not independently prevent FV-induced erythroleukemia but works in concert with the immune system by l imiting early infection long enough to allow virus-specific immunity time t o develop and facilitate recovery.