Nakamura Taichi, Suzuki Hisako, Okamoto Takashi, Kotani Syuji, Atsuji Yoriko, Tanaka Toshio, Ito Yasuhiko
Department of Microbiology, Mie University School of Medicine, 2-171 Edobashi, Tsu, Mie 514-8507, Japan.
Virus Res. 2002 Dec;90(1-2):263-8. doi: 10.1016/s0168-1702(02)00230-7.
We have found that an HIV-1 accessory gene product Vpr enhanced HIV-1 reproduction in U1 cells chiefly by the induction of TNF, a proinflammatory cytokine, which was also known to be an activator of HIV-1 reproduction. We have generated the functional HIV-1 accessory gene product Vpr in bacterial cells. Vpr was generated in an Escherichia coli system (rVpr), purified with antibodies (Ab) to the 16 C-terminal amino acids of Vpr. The purified rVpr of 15 kDa was examined for its ability to upregulate HIV-1 reproduction in U1 cells, which is a reported function of the authentic Vpr. rVpr upregulated HIV-1 reproduction in U1 cells in a dose-dependent manner and induced the secretion of TNF. The upregulation of HIV-1 by rVpr was completely inhibited not only by anti-Vpr antibodies but also by anti-TNF antibody. These findings suggested that Vpr caused an HIV-1 reproduction in U1 cells through the induction of TNF.
我们发现,HIV-1辅助基因产物Vpr主要通过诱导促炎细胞因子TNF来增强HIV-1在U1细胞中的复制,TNF也是已知的HIV-1复制激活剂。我们已在细菌细胞中产生了具有功能的HIV-1辅助基因产物Vpr。Vpr在大肠杆菌系统(rVpr)中产生,并用针对Vpr 16个C末端氨基酸的抗体(Ab)进行纯化。对纯化后的15 kDa rVpr上调U1细胞中HIV-1复制的能力进行了检测,这是天然Vpr的一项已报道功能。rVpr以剂量依赖方式上调U1细胞中HIV-1的复制,并诱导TNF分泌。rVpr对HIV-1的上调不仅被抗Vpr抗体完全抑制,也被抗TNF抗体完全抑制。这些发现表明,Vpr通过诱导TNF导致U1细胞中的HIV-1复制。