CONTRIBUTION OF OIS TO INTESTINAL DYSFUNCTION AND WASTING

这个子项目是利用由NIH/NCRR资助的中心拨款提供的资源的许多研究子项目之一。子项目和调查员(PI)可能从另一个NIH来源获得了主要资金，因此可能会出现在其他CRISE条目中。列出的机构是针对中心的，而不一定是针对调查员的机构。CD4T细胞的显著丢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之一。用SIV感染的猕猴来研究这种关系。对一组恒河猴的研究表明，感染SIV的恒河猴在其血液中的CD_4细胞数下降到500个/uL以下和病毒载量增加时，会自发获得比氏恒河猴的感染，从而建立了恒河猴感染与SIV感染的免疫状态之间的关系。使用微小隐孢子虫/SIV混合感染模型，SIV感染的猕猴在慢性SIV感染或急性SIV感染期间都会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，肠道粘膜中的CD4状态即使不比外周CD4水平更关键，也是同样关键的。相比之下，只有SIV幼稚猕猴才能诱发急性隐孢子虫病。SIV感染的猕猴在慢性SIV阶段发生慢性微孢子虫病，采用E.bieneusi/SIV混合感染模型。

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.