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1型人类免疫缺陷病毒(NC)在未感染及先前已感染的黑猩猩中诱导的CD4(+) T细胞快速丧失

Rapid CD4(+) T-cell loss induced by human immunodeficiency virus type 1(NC) in uninfected and previously infected chimpanzees.

作者信息

Novembre F J, de Rosayro J, Nidtha S, O'Neil S P, Gibson T R, Evans-Strickfaden T, Hart C E, McClure H M

机构信息

Divisions of Microbiology and Immunology, Yerkes Regional Primate Research Center, Atlanta, Georgia 30322, USA.

出版信息

J Virol. 2001 Feb;75(3):1533-9. doi: 10.1128/JVI.75.3.1533-1539.2001.

Abstract

To investigate the pathogenicity of a virus originating in a chimpanzee with AIDS (C499), two chimpanzees were inoculated with a plasma-derived isolate termed human immunodeficiency virus type 1(NC) (HIV-1(NC)). A previously uninfected chimpanzee, C534, experienced rapid peripheral CD4(+) T-cell loss to fewer than 26 cells/microl by 14 weeks after infection. CD4(+) T-cell depletion was associated with high plasma HIV-1 loads but a low virus burden in the peripheral lymph node. The second chimpanzee, C459, infected 13 years previously with HIV-1(LAV), experienced a more protracted course of peripheral CD4(+) T-cell loss after HIV-1(NC) inoculation, resulting in fewer than 200 cells/microl by 96 weeks postinoculation. The quantities of viral RNA in the plasma and peripheral lymph node from C459 were below the lower limits of detection prior to inoculation with HIV-1(NC) but were significantly and persistently increased after superinfection, with HIV-1(NC) representing the predominant viral genotype. These results show that viruses derived from C499 are more pathogenic for chimpanzees than any other HIV-1 isolates described to date.

摘要

为研究源自一只患艾滋病黑猩猩(C499)的病毒的致病性,给两只黑猩猩接种了一种源自血浆的分离株,即1型人类免疫缺陷病毒(NC)(HIV-1(NC))。一只先前未感染的黑猩猩C534在感染后14周时外周血CD4(+) T细胞迅速减少至每微升少于26个细胞。CD4(+) T细胞耗竭与血浆中高HIV-1载量相关,但外周淋巴结中的病毒负荷较低。第二只黑猩猩C459在13年前感染了HIV-1(LAV),在接种HIV-1(NC)后经历了更为漫长的外周血CD4(+) T细胞减少过程,在接种后96周时降至每微升少于200个细胞。C459血浆和外周淋巴结中的病毒RNA量在接种HIV-1(NC)之前低于检测下限,但在重叠感染后显著且持续增加,HIV-1(NC)为主要病毒基因型。这些结果表明,源自C499的病毒对黑猩猩的致病性比迄今描述的任何其他HIV-1分离株都更强。

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