IMMUNE CORRELATES OF PROTECTION AGAINST SIVE

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 尽管广泛使用高效抗逆转录病毒治疗（HAART），神经系统疾病继续大大有助于与艾滋病毒感染相关的发病率和死亡率。 免疫学相关的保护对艾滋病毒脑炎（HIVE）尚未确定，然而，这一信息是至关重要的设计艾滋病疫苗，能够安全地抑制病毒在大脑中的复制，以及在外周淋巴组织。 尽管抗病毒抗体对HIV神经发病过程的特异性作用知之甚少，但最近的报告表明，中和抗体（NAb）反应受损的患者可能会增加HIV相关性痴呆（HAD）的风险。 在这项研究计划中，我们正在使用神经毒性SIV/猕猴模型，以调查适应性宿主免疫的作用，提供保护，防止SIV脑炎（SIVE）的发展。 该项目的中心假设认为，NAb对于在具有次优细胞介导的免疫应答的动物中提供针对SIVE发展的附带保护是重要的。

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. Despite the widespread use of highly active antiretroviral therapy (HAART), neurological disorders continue to contribute significantly to the morbidity and mortality associated with HIV infection. The immunological correlates of protection against HIV encephalitis (HIVE) have not been identified; however, this information is critical for designing AIDS vaccines that are capable of safely suppressing viral replication in the brain as well as in peripheral lymphoid tissues. Although little is known about the specific effect of antiviral antibodies on the course of HIV neuropathogenesis, recent reports suggest that patients with impaired neutralizing antibody (NAb) responses may be at increased risk for the development of HIV-associated dementia (HAD). In this research program we are using a neurovirulent SIV/macaque model to investigate the role of adaptive host immunity in providing protection against the development of SIV encephalitis (SIVE). The central hypothesis of this project argues that NAb are important for providing collateral protection against the development of SIVE in animals with suboptimal cell-mediated immune responses.