PATHOGENICITY OF SIVMAC239 VARIANTS IN NEONATAL MACAQUES

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 目的：SIV和所有慢病毒都依赖于病毒REV对含有RRE的mRNAs的核质输出和表达进行调节。我们已经产生了SIV变体，其基本的病毒调控机制被D型逆转录病毒的输出元件CTE取代，CTE利用细胞因子HTAP进行运输。被这些SIV变种感染的原代细胞产生的病毒数量更少，传染性也更低。新生儿猕猴代表了一个关键和敏感的模型系统来评估潜在减毒的SIV变异体的致病性。

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. Objective: SIV and all lentiviruses depend on the viral Rev regulation for the nucleo-cytoplasmic export and expression of the RRE-containing mRNAs. We have generated SIV variants that have the essential viral regulatory mechanism replaced by the export elements of the type D retroviruses, CTE, which utilizes a cellular factor hTAP for its transport. Primary cells infected by these SIV variants produce lower amounts of virus having reduced infectivity. The neonate macaque represents a critical and sensitive model system to evaluate the pathogenicity of potentially attenuated SIV variants.