PHENOTYPIC AND GENOTYPIC DETERMINANTS OF SHIV PATHOGENESIS

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。 我们研究了SHIVSF162P3N(P3N)及其克隆的致病机理和传播性，该克隆是否能完全概括亲本分离株的体内复制特性。SHIVSF162P3N，(P3N)和克隆都是粘膜可传播的、优先耗尽记忆的CD4T细胞。15只动物接受直肠挑战，3只P3N+克隆动物和12只单独克隆动物。两种病毒均经直肠感染，克隆组有6/12只动物控制了病毒，而用P3N和克隆混合病毒攻击的1只动物能够控制病毒。初步结果表明，这两种病毒都是通过粘膜传播的，在病毒设定点和疾病进展方面没有显著差异。

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. We investigated pathogenesis and transmissibility of SHIVSF162P3N (P3N) and the clone, whether the clone could fully recapitulate the in vivo replicative characteristics of the parental isolate. Both SHIVSF162P3N, (P3N) and the clone were mucosally transmissible, preferentially depleted memory CD4 T cells. Fifteen (15) animals were rectally challenged, 3 animals with P3N plus clone and 12 animals with the clone alone. Both virus infected rectally, 6/12 animals controlled the virus in the clone group, whereas one animals challenged with the mixture virus ( P3N and clone) was able to control the virus. Preliminary results indicate that both virus were transmitted mucosally with no significant difference in viral set points and progression to disease.