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首页> 美国卫生研究院文献>Journal of Virology >Transmission of Simian Immunodeficiency Virus SIVcpz and the Evolution of Infection in the Presence and Absence of Concurrent Human Immunodeficiency Virus Type 1 Infection in Chimpanzees
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Transmission of Simian Immunodeficiency Virus SIVcpz and the Evolution of Infection in the Presence and Absence of Concurrent Human Immunodeficiency Virus Type 1 Infection in Chimpanzees

机译：猿猴免疫缺陷病毒SIVcpz的传播以及黑猩猩同时存在和不存在人类免疫缺陷病毒1型感染的感染演变

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Current data suggest that the human immunodeficiency virus type 1 (HIV-1) epidemic arose by transmission of simian immunodeficiency virus (SIV) SIVcpz from a subspecies of common chimpanzees (Pan troglodytes troglodytes) to humans. SIVcpz of chimpanzees is itself a molecular chimera of SIVs from two or more different monkey species, suggesting that recombination was made possible by coinfection of one individual animal with different lentiviruses. However, very little is known about SIVcpz transmission and the susceptibility to lentivirus coinfection of its natural host, the chimpanzee. Here, it is revealed that either infected plasma or peripheral blood mononuclear cells readily confer infection when exposure occurs by the intravenous or mucosal route. Importantly, the presence of preexisting HIV-1 infection did not modify the kinetics of SIVcpz infection once it was established by different routes. Although humoral responses appeared as early as 4 weeks postinfection, neutralization to SIVcpz-ANT varied markedly between animals. Analysis of the SIVcpz env sequence over time revealed the emergence of genetic viral variants and persistent SIVcpz RNA levels of between 104 and 105 copies/ml plasma regardless of the presence or absence of concurrent HIV-1 infection. These unique data provide important insight into possible routes of transmission, the kinetics of acute SIVcpz infection, and how readily coinfection with SIVcpz and other lentiviruses may be established as necessary preconditions for potential recombination.
机译：当前数据表明，人类免疫缺陷病毒1型（HIV-1）流行是通过将猿猴免疫缺陷病毒（SIV）SIVcpz从普通黑猩猩（Pan troglodytes troglodytes）亚种传播给人类引起的。黑猩猩的SIVcpz本身就是来自两个或更多不同猴子物种的SIV的分子嵌合体，这表明重组是通过将一只单独的动物与不同的慢病毒共同感染而实现的。但是，关于SIVcpz的传播及其自然宿主黑猩猩对慢病毒共感染的敏感性了解甚少。在这里，揭示了当通过静脉内或粘膜途径发生暴露时，被感染的血浆或外周血单核细胞都容易引起感染。重要的是，一旦通过不同途径建立，先前存在的HIV-1感染并不会改变SIVcpz感染的动力学。尽管体液反应最早在感染后4周就出现了，但在动物之间对SIVcpz-ANT的中和作用却明显不同。随时间推移对SIVcpz env序列的分析显示，出现了遗传病毒变异体和持续SIVcpz RNA水平在10 4 和10 5 拷贝/毫升血浆之间，无论是否存在没有并发HIV-1感染。这些独特的数据为可能的传播途径，急性SIVcpz感染的动力学以及如何将SIVcpz和其他慢病毒共感染建立为潜在重组的必要前提条件提供了重要的见识。

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