IL-10 and Suppression/ Susceptibility in MAIDS Model
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Individuals infected with the Human Immunodeficiency Virus (HIV) typically progress to Acquired Immune Deficiency Syndrome (AIDS). AIDS is characterized by an increase in opportunistic infections like tuberculosis, as well as the development of certain cancers, like Kaposi’s sarcoma. The debilitation of the immune system in AIDS patients usually presents a bleak prognosis of death. However, there exist a select few of HIV-positive individuals who do not progress to AIDS. These individuals, known as ‘long-term nonprogressors’ or LTNPs, remain an important area for scientific study because the activity of their immune system may provide important insight to the inhibition of AIDS. Several animal models of AIDS have been developed over the years. One such model involves the induction of AIDS-like symptoms in mice via infection with the Murine Leukemia virus (MuLV). This model is termed Murine Acquired Immunodeficiency Syndrome (MAIDS). The MAIDS model is appropriate for studying AIDS because, like humans, some mice (e.g. BALB/c) present like LTNPs while others such as the C57BL/6, present like ‘rapid progressors’. We hypothesized that in mice, a potential contribution to this phenomenon may lie in the expression of the immunosuppressant IL-10 such that the more susceptible C57BL/6 mice produce increased levels of IL-10 relative to their less susceptible BALB/c counterparts. We tested this hypothesis via Enzyme-Linked Immunosorbent Assays (ELISA). Results suggest that prior to infection, both mice express relatively equal levels of IL-10. At three days post MuLV infection however, C57BL/6 susceptible mice begin to express close to three times as much IL-10 compared to BALB/c resistant mice. This suggests that the eventual development of MAIDS in C57BL/6 mice post MuLV infection may be driven by an early over expression of the immunosuppressant IL-10. This finding is of importance because it provides insight to the potential role of immunosuppresants like IL-10 not only in MAIDS models, but also in AIDS development in humans post HIV infection.