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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Macrophage are the principal reservoir and sustain high virus loads in rhesus macaques after the depletion of CD4~+ T cells by a highly pathogenic simian immunodeficiency virus/HIV type 1 chimera (SHIV): Implications for HIV-1 infections of humans
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Macrophage are the principal reservoir and sustain high virus loads in rhesus macaques after the depletion of CD4~+ T cells by a highly pathogenic simian immunodeficiency virus/HIV type 1 chimera (SHIV): Implications for HIV-1 infections of humans

机译：高致病性猿猴免疫缺陷病毒/ HIV 1型嵌合体（SHIV）耗尽CD4〜+ T细胞后，巨噬细胞是恒河猴的主要储存库，并维持高病毒载量：对人类HIV-1感染的影响

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The highly pathogenic simian immunodeficiency virus/HIV type 1 (SHIV) chimeric virus SHIV_DH12R induces a systemic depletion of CD4~+ T lymphocytes in rhesus monkeys during the initial 3--4 weeks of infection. Nonatheless, high levels of viral RNA production continue unabated for an additional 2--5 months. In situ hybridization and immunohistochemical analyses revealed that tissue macrophage in the lymph nodes, spleen, gastrointestinal tract, liver, and kidney sustain high plasma virus loads in the absence of CD4~+ T cells. Quantitative confocal immunofluorescence analysis indicated that greater than 95/100 of the virus-producing cells in these tissues are macrophage and less than 2/100 are T lymphocytes. Interestingly, the administration of a potent reverse transcriptase inhibitor blocked virus production during the early T cell phase but not during the later macrophage phase of the SHIV_DH12R infection. When interpreted in the context of HIV-1 infections, these results implicate tissue macro- phage as an important reservoir of virus in vivo. They become infected during the acute infection, gradually increase in number over time, and can be a major contributor to total body virus burden during the symptomatic phase of the human infection.
机译：高致病性猿猴免疫缺陷病毒/ HIV 1型（SHIV）嵌合病毒SHIV_DH12R在感染的最初3--4周期间诱导了猕猴CD4〜+ T淋巴细胞的系统耗竭。尽管如此，高水平的病毒RNA产生仍会持续2--5个月。原位杂交和免疫组织化学分析表明，在没有CD4〜+ T细胞的情况下，淋巴结，脾脏，胃肠道，肝脏和肾脏中的组织巨噬细胞可维持较高的血浆病毒载量。共聚焦免疫荧光定量分析表明，这些组织中大于95/100的病毒产生细胞是巨噬细胞，小于2/100的T淋巴细胞。有趣的是，强效逆转录酶抑制剂的施用在SHIV_DH12R感染的早期T细胞阶段阻止了病毒的产生，但在后来的巨噬细胞阶段却没有阻止。当解释为HIV-1感染时，这些结果表明组织巨噬细胞是体内重要的病毒库。它们在急性感染过程中被感染，并随着时间的推移逐渐增加，并且可能在人类感染的症状阶段成为全身病毒负荷的主要贡献者。

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