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人血浆可增强1型原发性人类免疫缺陷病毒分离株在外周血单核细胞和单核细胞衍生巨噬细胞中的感染性。

Human plasma enhances the infectivity of primary human immunodeficiency virus type 1 isolates in peripheral blood mononuclear cells and monocyte-derived macrophages.

作者信息

Wu S C, Spouge J L, Conley S R, Tsai W P, Merges M J, Nara P L

机构信息

National Center for Biotechnology Information, National Library of Medicine, Bethesda, Maryland 20894, USA.

出版信息

J Virol. 1995 Oct;69(10):6054-62. doi: 10.1128/JVI.69.10.6054-6062.1995.

Abstract

Physiological microenvironments such as blood, seminal plasma, mucosal secretions, or lymphatic fluids may influence the biology of the virus-host cell and immune interactions for human immunodeficiency virus type 1 (HIV-1). Relative to media, physiological levels of human plasma were found to enhance the infectivity of HIV-1 primary isolates in both phytohemagglutinin-stimulated peripheral blood mononuclear cells and monocyte-derived macrophages. Enhancement was observed only when plasma was present during the virus-cell incubation and resulted in a 3- to 30-fold increase in virus titers in all of the four primary isolates tested. Both infectivity and virion binding experiments demonstrated a slow, time-dependent process generally requiring between 1 and 10 h. Human plasma collected in anticoagulants CPDA-1 and heparin, but not EDTA, exhibited this effect at concentrations from 90 to 40%. Furthermore, heat-inactivated plasma resulted in a loss of enhancement in peripheral blood mononuclear cells but not in monocyte-derived macrophages. Physiological concentrations of human plasma appear to recruit additional infectivity, thus increasing the infectious potential of the virus inoculum.

摘要

诸如血液、精液、粘膜分泌物或淋巴液等生理微环境可能会影响人类免疫缺陷病毒1型(HIV-1)的病毒-宿主细胞生物学特性及免疫相互作用。相对于培养基而言,发现人血浆的生理水平可增强HIV-1原代分离株在植物血凝素刺激的外周血单核细胞和单核细胞衍生的巨噬细胞中的感染性。仅当在病毒-细胞孵育期间存在血浆时才观察到增强作用,并且在所测试的所有四种原代分离株中病毒滴度增加了3至30倍。感染性和病毒体结合实验均表明这是一个缓慢的、时间依赖性过程,通常需要1至10小时。用抗凝剂CPDA-1和肝素而非EDTA收集的人血浆在浓度为90%至40%时表现出这种效应。此外,热灭活血浆导致外周血单核细胞中的增强作用丧失,但在单核细胞衍生的巨噬细胞中未丧失。人血浆的生理浓度似乎可募集额外的感染性,从而增加病毒接种物的感染潜力。

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