Vpr和Vpu对于1型人类免疫缺陷病毒在体外人淋巴组织中的高效复制及CD4+ T细胞耗竭至关重要。
Vpr and Vpu are important for efficient human immunodeficiency virus type 1 replication and CD4+ T-cell depletion in human lymphoid tissue ex vivo.
作者信息
Rücker Elke, Grivel Jean-Charles, Münch Jan, Kirchhoff Frank, Margolis Leonid
机构信息
National Institute of Child Health, Building 10, Room 9D58, Bethesda, MD 20892, USA.
出版信息
J Virol. 2004 Nov;78(22):12689-93. doi: 10.1128/JVI.78.22.12689-12693.2004.
Abstract
The relevance of the accessory vpr, vpu, and nef genes for human immunodeficiency virus type 1 (HIV-1) replication in human lymphoid tissue (HLT), the major site of viral replication in vivo, is largely unknown. Here, we show that an individual deletion of nef, vpr, or vpu significantly decreases HIV-1 replication and prevents CD4+ T-cell depletion in ex vivo HLT. However, only combined defects in all three accessory genes entirely disrupt the replicative capacity of HIV-1. Our results demonstrate that nef, vpr, and vpu are all essential for efficient viral spread in HLT, suggesting an important role in AIDS pathogenesis.
摘要
在体内病毒复制的主要部位——人类淋巴组织（HLT）中，辅助基因vpr、vpu和nef对于1型人类免疫缺陷病毒（HIV-1）复制的相关性在很大程度上尚不清楚。在此，我们表明，单独缺失nef、vpr或vpu会显著降低HIV-1在体外HLT中的复制，并防止CD4+ T细胞耗竭。然而，只有所有这三个辅助基因的联合缺陷才会完全破坏HIV-1的复制能力。我们的结果表明，nef、vpr和vpu对于HIV-1在HLT中的有效传播均至关重要，提示它们在艾滋病发病机制中发挥重要作用。
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