PATHOGENICITY OF SIVMAC239 VARIANTS IN NEONATAL MACAQUES

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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.