Lymphocyte deficiencies increase susceptibility to friend virus-induced erythroleukemia in Fv-2 genetically resistant mice
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1Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840, USA. khasenkrug@nih.gov
Abstract:
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.
Insights
Genetic resistance (Fv-2) to Friend virus (FV) limits early infection but requires immune responses to prevent erythroleukemia. This study shows Fv-2 works with the immune system for full retroviral disease control.
Area of Science:
- Immunology
- Virology
- Genetics
Background:
- Retroviral diseases pose significant threats, necessitating understanding of host resistance mechanisms.
- Genetic resistance, like Fv-2, offers insights into overcoming infections.
- Fv-2 resistance to Friend virus-induced erythroleukemia acts non-immunologically but doesn't fully block infection.
Purpose of the Study:
- To determine if Fv-2 resistance alone is sufficient for protection against Friend virus.
- To investigate the necessity of immunological mechanisms in conjunction with Fv-2 for controlling retroviral infections.
Main Methods:
- Experiments utilized Fv-2 resistant mice with deficiencies in CD4(+) T cells, CD8(+) T cells, and B cells.
- Assessed the impact of these immune deficiencies on Friend virus replication, spread, and disease progression.
Main Results:
- Fv-2 resistant mice lacking CD4(+) T cells initially restricted viral spread but failed to maintain control, developing severe disease.
- Mice deficient in CD8(+) T cells and B cells also showed increased susceptibility to late-stage Friend virus disease.
- Fv-2 mediated resistance is insufficient on its own to prevent disease.
Conclusions:
- Fv-2 resistance is not an independent protective mechanism against Friend virus-induced erythroleukemia.
- Fv-2 functions by limiting early viral infection, allowing time for the development of virus-specific immune responses for ultimate control and recovery.
