首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Amino acid deletions are introduced into the V2 region of gp120 during independent pathogenic simian immunodeficiency virus/HIV chimeric virus (SHIV) infections of rhesus monkeys generating variants that are macrophage tropic
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Amino acid deletions are introduced into the V2 region of gp120 during independent pathogenic simian immunodeficiency virus/HIV chimeric virus (SHIV) infections of rhesus monkeys generating variants that are macrophage tropic

机译:在恒河猴的独立病原性猿猴免疫缺陷病毒/ HIV嵌合病毒(SHIV)感染过程中将氨基酸缺失引入gp120的V2区域

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摘要

Highly pathogenic simian immunodeficiency virus/HIV chimeric viruses (SHIVs) cause extremely rapid, irreversible, and systemic depletions of CD4+ T lymphocytes in inoculated rhesus monkeys. In the absence of this T cell subset, virus production can be sustained for several months by tissue macrophage. During independent infections of seven animals with uncloned virus stocks, SHIV variants emerged bearing amino acid deletions that affected specific residues of the gp120 V2 loop. Some of these macrophage-phase SHIVs replicated to high levels in alveolar macrophage.
机译:高致病性猿猴免疫缺陷病毒/ HIV嵌合病毒(SHIV)在接种的恒河猴中引起CD4 + T淋巴细胞的极快速,不可逆和全身性消耗。在没有这种T细胞亚群的情况下,组织巨噬细胞可将病毒生产持续数月。在用未克隆的病毒原种独立感染7只动物的过程中,出现了SHIV变异体,带有氨基酸缺失,影响了gp120 V2环的特定残基。这些巨噬细胞期SHIV中的一些在肺泡巨噬细胞中复制至高水平。

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