Pantaleo G, Butini L, Graziosi C, Poli G, Schnittman S M, Greenhouse J J, Gallin J I, Fauci A S
Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892.
J Exp Med. 1991 Feb 1;173(2):511-4. doi: 10.1084/jem.173.2.511.
In the present study, we demonstrated that expression of the LFA-1 molecule is necessary for cell fusion and syncytia formation in human immunodeficiency virus (HIV)-infected CD4+ T lymphocytes. In contrast, the lack of expression of LFA-1 does not influence significantly cell-to-cell transmission of HIV. In fact, LFA-1- T lymphocytes obtained from a leukocyte adhesion deficiency patient were unable to fuse and form syncytia when infected with HIV-1 or HIV-2, despite the fact that efficiency of HIV infection (i.e., virus entry, HIV spreading, and levels of virus replication) was comparable with that observed in LFA-1+ T lymphocytes. In addition, we provide evidence that LFA-1 by mediating cell fusion contributes to the depletion of HIV-infected CD4+ T lymphocytes in vitro.
在本研究中，我们证明淋巴细胞功能相关抗原-1（LFA-1）分子的表达对于人类免疫缺陷病毒（HIV）感染的CD4+ T淋巴细胞中的细胞融合和多核巨细胞形成是必需的。相比之下，LFA-1表达的缺失对HIV的细胞间传播没有显著影响。事实上，从白细胞黏附缺陷患者获得的LFA-1阴性T淋巴细胞在感染HIV-1或HIV-2时无法融合并形成多核巨细胞，尽管HIV感染效率（即病毒进入、HIV传播和病毒复制水平）与在LFA-1阳性T淋巴细胞中观察到的相当。此外，我们提供证据表明，LFA-1通过介导细胞融合在体外促成了HIV感染的CD4+ T淋巴细胞的耗竭。
