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1型人类免疫缺陷病毒感染的黑猩猩中缺乏T细胞功能障碍和程序性细胞死亡与缺乏嗜单核细胞变体相关。

Lack of T cell dysfunction and programmed cell death in human immunodeficiency virus type 1-infected chimpanzees correlates with absence of monocytotropic variants.

作者信息

Schuitemaker H, Meyaard L, Kootstra N A, Dubbes R, Otto S A, Tersmette M, Heeney J L, Miedema F

机构信息

Department of Clinical Viro-Immunology, Central Laboratory of The Netherlands Red Cross Blood Transfusion Service, Amsterdam.

出版信息

J Infect Dis. 1993 Nov;168(5):1140-7. doi: 10.1093/infdis/168.5.1140.

DOI:10.1093/infdis/168.5.1140
PMID:8228347
Abstract

In asymptomatic human immunodeficiency virus (HIV) infection in humans, disturbed T cell functions such as anergy and programmed cell death, thought to result from inappropriate signaling by antigen-presenting cells due to HIV infection, precede increase in virus load, decline in CD4+ T cell numbers, and subsequent disease progression. Here, in 3 long-term HIV-1-infected asymptomatic chimpanzees, antigen-presenting cell function was intact and T cells had normal proliferative capacity with no evidence of HIV-1-associated programmed cell death. Polymerase chain reaction analysis demonstrated low frequencies of cells harboring proviral DNA. Primary virus isolation from the infected animals demonstrated the absence of monocytotropic HIV-1 variants, in concordance with complete insusceptibility of chimpanzee monocytes for HIV-1 infection. Possibly, because of the incapacity of HIV-1 to infect monocytes, systemic immune dysfunction will not occur, contributing to controlled viral replication and maintenance of the asymptomatic state in HIV-infected chimpanzees.

摘要

在人类无症状性人类免疫缺陷病毒(HIV)感染中,T细胞功能紊乱,如无反应性和程序性细胞死亡,被认为是由于HIV感染导致抗原呈递细胞信号传导不当所致,这些功能紊乱先于病毒载量增加、CD4+T细胞数量下降以及随后的疾病进展。在此,在3只长期感染HIV-1的无症状黑猩猩中,抗原呈递细胞功能完好,T细胞具有正常的增殖能力,且没有HIV-1相关程序性细胞死亡的证据。聚合酶链反应分析显示,携带前病毒DNA的细胞频率较低。从受感染动物中进行的原发性病毒分离表明,不存在嗜单核细胞性HIV-1变体,这与黑猩猩单核细胞对HIV-1感染完全不敏感相一致。可能由于HIV-1无法感染单核细胞,所以不会发生全身性免疫功能障碍,这有助于控制病毒复制并维持HIV感染黑猩猩的无症状状态。

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