Imamichi Hiromi, Igarashi Tatsuhiko, Imamichi Tomozumi, Donau Olivia K, Endo Yasuyuki, Nishimura Yoshiaki, Willey Ronald L, Suffredini Anthony F, Lane H Clifford, Martin Malcolm A
Science Applications International Corporation-Frederick, Inc., Frederick, MD 21702, USA.
Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13813-8. doi: 10.1073/pnas.212511599. Epub 2002 Oct 7.
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.
高致病性猿猴免疫缺陷病毒/艾滋病毒嵌合病毒(SHIVs)在接种的恒河猴中会导致CD4(+) T淋巴细胞极其迅速、不可逆且全身性的耗竭。在缺乏这一T细胞亚群的情况下,组织巨噬细胞可使病毒产生持续数月。在用未克隆病毒株对7只动物进行独立感染期间,出现了带有氨基酸缺失的SHIV变体,这些缺失影响了gp120 V2环的特定残基。其中一些巨噬细胞期SHIVs在肺泡巨噬细胞中大量复制。