Tobiume Minoru, Lineberger Janet E, Lundquist Christopher A, Miller Michael D, Aiken Christopher
Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2363, USA.
J Virol. 2003 Oct;77(19):10645-50. doi: 10.1128/jvi.77.19.10645-10650.2003.
The human immunodeficiency virus type 1 (HIV-1) accessory protein Nef stimulates viral infectivity by an unknown mechanism. Recent studies have suggested that Nef may act by regulating the efficiency of virus entry into cells. Here we provide evidence to the contrary. Using a quantitative assay of HIV-1 virus-cell fusion, we observed equivalent rates and extents of fusion of wild-type and Nef-defective HIV-1 particles with MT-4 cells and CD4-expressing HeLa cells. In studies using soluble CD4 (sCD4) to inhibit infection, wild-type and Nef-defective HIV-1 escaped the sCD4 block with similar kinetics. We conclude that Nef acts at a postentry step in infection, probably by facilitating intracellular transport of the HIV-1 ribonucleoprotein complex.
1型人类免疫缺陷病毒（HIV-1）辅助蛋白Nef通过未知机制刺激病毒感染性。最近的研究表明，Nef可能通过调节病毒进入细胞的效率发挥作用。在此我们提供了相反的证据。通过对HIV-1病毒-细胞融合进行定量测定，我们观察到野生型和Nef缺陷型HIV-1颗粒与MT-4细胞和表达CD4的HeLa细胞融合的速率和程度相当。在使用可溶性CD4（sCD4）抑制感染的研究中，野生型和Nef缺陷型HIV-1以相似的动力学逃脱了sCD4阻断。我们得出结论，Nef在感染的进入后步骤发挥作用，可能是通过促进HIV-1核糖核蛋白复合物的细胞内运输。
