CONTRIBUTION OF OIS TO INTESTINAL DYSFUNCTION AND WASTING

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. A significant loss of CD4+ T cells may be responsible for the development of microsporidiosis and cryptosporidiosis in AIDS patients. SIV infected macaques were used to investigate this relationship. Study on cohort group of macaques showed that spontaneous acquisition of E. bieneusi infection in SIV-infected macaques occurred when their CD4+ counts drops less than 500 cell/ul of blood and increase in viral load, establishing a relationship between E. bieneusi infection and the immune status of SIV-infected macaques. Using C.parvum/SIV co-infection models, SIV-infected macaques develop chronic cryptosporidiosis both during chronic SIV-infection or acute SIV-infection. These studies also indicate that the CD4+ status in the gut mucosa is as, if not more, critical than the peripheral CD4+ level to susceptibility to intestinal pathogens. In contrast, only acute cryptosporidiosis can be induced in SIV-naive macaques. Using E. bieneusi/SIV co-infection model, SIV-infected macaques develop chronic microsporidiosis during chronic SIV-stage.