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Journal of Virology, August 1999, p. 6468-6473, Vol. 73, No. 8
0022-538X/99/$04.00+0

Lymphocyte Deficiencies Increase Susceptibility to Friend Virus-Induced Erythroleukemia in Fv-2 Genetically Resistant Mice

Kim J. Hasenkrug*

Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840

Received 17 February 1999/Accepted 4 May 1999

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.

* Mailing address: Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, 903 S. 4th St., Hamilton, MT 59840. Phone: (406) 363-9310. Fax: (406) 363-9286. E-mail: khasenkrug{at}nih.gov.

Journal of Virology, August 1999, p. 6468-6473, Vol. 73, No. 8
0022-538X/99/$04.00+0


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