SIV REPLICATION DYNAMICS IN AFRICAN NON-HUMAN PRIMATE HOSTS

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。为了确定SIV感染在不同自然感染宿主物种中的潜在共同特征，我们比较了31只非洲绿猴（10只长尾猴、15只黑尾猴和7只加勒比绿尾猴）、14只山魈和3只黑白眉猴（SMs）的病毒复制动态。感染后，这些siv在9-14天内迅速复制，达到10^5-10^9拷贝/ml血浆的病毒载量（VLs）。设定点病毒血症在42 - 60天之间建立，SM和山猫的水平约为105-106拷贝/ml， agm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）在山魈体内的复制水平相似。VL依赖于病毒株：3种不同病毒株感染的马尾鼠表现出不同的病毒复制模式。SIVagm的病毒复制模式。sab同时使用CCR5和CXCR4共受体，与其他病毒相似。我们的结果显示了SIV在自然和实验感染宿主中复制的共同模式。这与在猕猴致病性SIV感染中观察到的总体情况相似。这一结果表明，致病性和非致病性感染之间临床结果的差异取决于宿主反应，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.