ORAL CARRIAGE OF CANDIDA-ALBICANS IN MURINE AIDS

Oral candidiasis is a common fungal infection in patients infected wit h the human immunodeficiency virus (HIV), Although rare at the time of primary HIV infection, it is frequently found throughout the asymptom atic phase and is predictive of progressive immunodeficiency, However, the precise immune defect which results in outgrowth of commensal Can dida albicans in HIV infection has not been identified. Mice infected with the Du5H(G(6)T(2)) mixture of mouse leukemia viruses develop a sy ndrome, designated murine AIDS (MAIDS), that has many of the immune ab normalities found in HIV infection. Retrovirus-infected C57BL/6 mice w ere examined for their ability to resist the development of oral candi diasis from the carrier state established after a self-limiting acute infection and to clear a subsequent secondary inoculum of oral C. albi cans. Most of the mice orally colonized with C. albicans and then inoc ulated with the retrovirus mixture maintained a low-level oral carriag e of C. albicans, while 30% of coinfected mice developed recurring 2- to 3-week episodes of acute Candida proliferation, separated by transi ent recoveries to the carrier state. The frequencies of CD4(+) and CD8 (+) lymphocytes were, respectively, unchanged and significantly decrea sed (P < 0.05) in both cervical lymph nodes and spleens of coinfected mice compared to the corresponding frequencies in C. albicans-carrying , virus-free, age-matched control animals, Secretion of gamma interfer on by concanavalin A (ConA)-stimulated spleen cells from Candida-carry ing, retrovirus-infected mice was significantly decreased (P < 0.05) c ompared to that of C. albicans-carrying, retrovirus-free mice, in acco rdance with known abnormalities associated with MAIDS, However, produc tion of this cytokine by ConA-stimulated or unstimulated cervical lymp h node cells from coinfected mice was enhanced compared to that of vir us-free animals colonized with C. albicans, Acquired resistance to rei nfection with C. albicans was maintained in retrovirus-infected mice a nd was associated with a mucosal recruitment of CD8(+) cells not obser ved in control mice, These results suggest that alterations in mucosal immunity which occur in MAIDS differ substantially from defects obser ved at other sites and that surrogate epithelial defense mechanisms ma y function locally to limit Candida proliferation.