CONTRIBUTION OF OIS TO INTESTINAL DYSFUNCTION AND WASTING

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。CD4+ T细胞的显著缺失可能是艾滋病患者发生微孢子虫病和隐孢子虫病的原因。用SIV感染的猕猴来研究这种关系。恒河猴队列组研究表明，siv感染恒河猴的CD4+计数下降到500个细胞/毫升以下，病毒载量增加时，会发生自发获得性感染，建立了siv感染恒河猴与免疫状态之间的关系。利用小孢子虫/SIV共感染模型，SIV感染的猕猴在慢性SIV感染或急性SIV感染期间均发生慢性隐孢子虫病。这些研究还表明，对于肠道病原体的易感性，肠道黏膜中的CD4+状态与外周CD4+水平同样重要，甚至更重要。相比之下，只有急性隐孢子虫病可以在SIV-naive猕猴中诱导。利用布氏雌梭菌/SIV共感染模型，观察SIV感染的猕猴在慢性SIV期发生慢性微孢子虫病。

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.