SIV REPLICATION DYNAMICS IN AFRICAN NON-HUMAN PRIMATE HOSTS

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 为了确定不同自然感染宿主物种中SIV感染的潜在共同特征，我们比较了31只非洲绿色猴（10只沙猴，15只长尾猴和7只加勒比海AGM），14只山鸡和3只白眉猴（SM）的病毒复制动态，这些猴实验感染了它们的物种特异性病毒。感染后，这些SIV迅速复制，在感染后第9-14天达到10^5-10^9拷贝/ml血浆的病毒载量（VL）。在感染后第42至60天之间建立设定点病毒血症，在SM和扁桃体中的水平约为105-106拷贝/ml，在AGM中的水平较低（10^3-10^5拷贝/ml）。慢性期的VL与病毒基因组结构无关：SIVmnd-2（一种含Vpx的病毒）和SIVmnd-1（不含Vpu或Vpx）在山鸡中复制到相似的水平。VL取决于病毒株：感染3种不同病毒株的长尾小蜂表现出不同的病毒复制模式。同时使用CCR 5和CXCR 4共受体的SIVagm.sab的病毒复制模式与其他病毒相似。 我们的研究结果显示了一个共同的模式SIV复制自然和实验感染的主机。这与在猕猴的致病性SIV感染中观察到的总体相似。这一结果表明，致病性和非致病性感染之间的临床结果差异依赖于宿主反应，而不是病毒本身的特征。

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. To define potential common features of SIV infections in different naturally-infected host species, we compared the dynamics of viral replication in 31 African green monkeys (10 sabeus, 15 vervets and 7 Caribbean AGMs), 14 mandrills and 3 sooty mangabeys (SMs) that were experimentally infected with their species-specific viruses. After infection, these SIVs replicated rapidly reaching viral loads (VLs) of 10^5-10^9 copies/ml of plasma between days 9-14 p.i. Set point viremia was established between days 42 to 60 p.i., with levels of approximately 105-106 copies/ml in SM and mandrills, and lower levels (10^3-10^5 copies/ml) in AGMs. VL during the chronic phase did not correlate with viral genome structure: SIVmnd-2 (a vpx-containing virus) and SIVmnd-1 (which does not contain vpu or vpx) replicated to similar levels in mandrills. VL was dependent on virus strain: vervets infected with 3 different viral strains showed different patterns of viral replication. The pattern of viral replication of SIVagm.sab, which uses both CCR5 and CXCR4 co-receptors was similar to those of the other viruses. Our results show a common pattern of SIV replication in naturally and experimentally infected hosts. This is similar overall to that observed in pathogenic SIV infection of macaques. This result indicates that differences in clinical outcome between pathogenic and non-pathogenic infections rely on host responses rather than the characteristics of the virus itself.