Clavel F, Charneau P
Département SIDA et Rétrovirus, Institut Pasteur, Paris, France.
J Virol. 1994 Feb;68(2):1179-85. doi: 10.1128/JVI.68.2.1179-1185.1994.
Fusion from without is the process through which particles of some enveloped viruses can direct fusion of target cells in the absence of viral replication. We demonstrate here that human immunodeficiency virus (HIV) particles can efficiently promote fusion from without. Using HeLa-CD4 cells carrying a Tat-inducible lacZ gene, we observed syncytia as early as 6 h after exposure to HIV particles, before HIV gene expression could be detected. Efficient syncytium formation could be obtained when cells were treated with zidovudine, which prevented HIV replication and expression but not cell-cell fusion. Fusion was also observed when cells were exposed to particles of a replication-defective HIV integrase mutant. Fusion from without by HIV particles could be blocked by a monoclonal antibody specific for the V3 loop of the HIV-1 envelope glycoprotein and by soluble CD4. This mechanism of cytopathicity, which can involve cells that do not actively replicate HIV and can be directed by replication-defective particles, could participate in the pathogenicity of the CD4 cell depletion that characterizes HIV infection.
来自外部的融合是一些包膜病毒的粒子在没有病毒复制的情况下能够直接诱导靶细胞融合的过程。我们在此证明，人类免疫缺陷病毒（HIV）粒子能够有效地促进来自外部的融合。使用携带Tat诱导型lacZ基因的HeLa-CD4细胞，我们早在暴露于HIV粒子后6小时就观察到了多核巨细胞，而此时还检测不到HIV基因表达。当用齐多夫定处理细胞时，可以有效地形成多核巨细胞，齐多夫定可阻止HIV复制和表达，但不影响细胞间融合。当细胞暴露于复制缺陷型HIV整合酶突变体的粒子时，也观察到了融合。HIV粒子引起的来自外部的融合可被针对HIV-1包膜糖蛋白V3环的单克隆抗体和可溶性CD4阻断。这种细胞病变机制可涉及不主动复制HIV的细胞，并可由复制缺陷型粒子介导，可能参与了以HIV感染为特征的CD4细胞耗竭的致病性。
