CELLULAR IMMUNE RESPONSES IN SIV-INFECTED SOOTY MANGABEYS

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。 这项研究利用耶尔克斯的SIV感染和群体出生的SIV阴性的煤色曼加比，通过多种不同的方式来研究细胞免疫反应在维持非致病性SIV感染中的作用。此前已有研究表明，自然感染SIV的黑尾猴能够产生与感染SIV的恒河猴相当的Th1型SIV特异性细胞免疫反应。随后，比较了感染SIV的恒河猴和煤烟猕猴在初次感染时对SIV的早期宿主反应。虽然在这两个物种中都有强大的SIV特异性细胞免疫反应，但恒河猴在急性感染时表现出更大和更长时间的非病毒特异性免疫激活。此外，CD_4~+T淋巴细胞的凋亡和肿瘤坏死因子相关的凋亡诱导配体的增加仅见于猕猴。这一数据表明，在早期的先天免疫反应中存在物种特异性差异；这似乎有助于SIV感染的自然宿主和非自然宿主的差异免疫激活。

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. The study utilizes both SIV-infected and colony born SIV negative sooty mangabeys housed at Yerkes to investigate the role of cellular immune responses in maintaining nonpathogenic SIV infection in a number of different ways. It has been previously shown that naturally SIV-infected sooty mangabeys were able to mount a substantial Th1-type SIV-specific cellular immune response comparable in magnitude to SIV-infected rhesus macaques. Subsequently, the early host response to SIV in primary infection was compared in SIV-infected rhesus macaques and sooty mangabeys. While a robust SIV-specific cellular immune response was mounted in both species, rhesus macaques displayer greater and longer non-virus-specific immune activation in acute infection. Moreover, CD4+ T lymphocyte apoptosis and increased TNF-related apoptosis inducing ligand were seen only in macaques. This data points to the presence of species-specific differences in the early innate immune response; it appears that this could contribute to differential immune activation in natural and non-natural hosts of SIV infection.