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SIV REPLICATION DYNAMICS IN AFRICAN NON-HUMAN PRIMATE HOSTS

SIV REPLICATION DYNAMICS IN AFRICAN NON-HUMAN PRIMATE HOSTS
非洲非人类灵长类动物宿主中的 SIV 复制动态
批准号:
7349110
负责人:
Ivona Vasile Pandrea
金额:
$6.54万
依托单位国家:
美国
项目类别:
财政年份:
2006
资助国家:
美国
项目状态:
已结题
起止时间:
2006-05-01 至 2007-04-30

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中文摘要
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英文摘要
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.
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