DIFFERENTIAL APOPTOSIS IN SIV-INFECTED SOOTY MANGABEYS AND RHESUS MACAQUES

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 与致病性慢病毒感染不同，SIV在其自然宿主中的慢性感染以缺乏慢性免疫激活为特征。在最近的研究中，我们发现恒河猴感染SIV后的急性事件在存在CD4+T淋巴细胞凋亡和诱导肿瘤坏死因子受体相关的凋亡诱导配体(TRAIL)方面不同于自然宿主炭疽猴。该项目的目标是更好地确定致病性和非致病性SIV感染的早期宿主对SIV反应的差异。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. In contrast to pathogenic lentiviral infections, chronic SIV infection in its natural host is characterized by a lack of chronic immune activation. In recent studies we have shown that acute events following SIV infection in rhesus macaques differ from those occurring in the natural host sooty mangabeys with regards to the presence of CD4+ T lymphocyte apoptosis and induction of TNF-receptor associated apoptosis-inducing ligand (TRAIL). The goal of this project is to better define differences in the early host response to SIV in pathogenic and nonpathogenic SIV infection.