Human immunodeficiency virus (HIV) infection in CD4+ T lymphocytes genetically deficient in LFA-1: LFA-1 is required for HIV-mediated cell fusion but not for viral transmission.
Human immunodeficiency virus (HIV) infection in CD4+ T lymphocytes genetically deficient in LFA-1: LFA-1 is required for HIV-mediated cell fusion but not for viral transmission.
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CD4+ T淋巴细胞中的人类免疫缺陷病毒（HIV）感染在LFA-1上缺乏LFA-1：LFA-1是HIV介导的细胞融合所必需的，但对于病毒传播不足。
DOI：
10.1084/jem.173.2.511
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发表时间：
1991-02-01
影响因子：
15.3
通讯作者：
Fauci, A S
中科院分区：
文献类型：
--
作者：
Pantaleo, G;Butini, L;Graziosi, C;Poli, G;Schnittman, S M;Greenhouse, J J;Gallin, J I;Fauci, A S
在本研究中，我们证明了LFA-1分子的表达是必要的细胞融合和合胞体形成在人类免疫缺陷病毒（HIV）感染的CD 4 + T淋巴细胞。相反，LFA-1表达的缺乏不会显著影响HIV的细胞间传播。事实上，从白细胞粘附缺陷患者获得的LFA-1- T淋巴细胞在感染HIV-1或HIV-2时不能融合并形成合胞体，尽管HIV感染的效率（即，病毒进入、HIV传播和病毒复制水平）与在LFA- 1+ T淋巴细胞中观察到的相当。此外，我们提供的证据表明，LFA-1通过介导细胞融合有助于体外清除HIV感染的CD 4 + T淋巴细胞。
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.