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HIV-1感染淋巴细胞需要CD4分子中不参与病毒结合或形成多核巨细胞的区域。

Regions of the CD4 molecule not involved in virus binding or syncytia formation are required for HIV-1 infection of lymphocytes.

作者信息

Hasunuma T, Tsubota H, Watanabe M, Chen Z W, Lord C I, Burkly L C, Daley J F, Letvin N L

机构信息

Harvard Medical School, New England Regional Primate Research Center, Southborough, MA 01772.

出版信息

J Immunol. 1992 Mar 15;148(6):1841-6.

PMID:1371792
Abstract

Cell surface-expressed CD4 binds to the envelope glycoprotein of HIV-1 and mediates syncytia formation through interacting with membrane expressed HIV-1 gp120. Further possible roles of the CD4 molecule in the process of cell infection by HIV-1 remain poorly understood. In our study we describe two mAb that recognize the V3/V4 domain of the CD4 molecule. Although these mAb do not inhibit gp120-CD4 binding or HIV-1-induced syncytia formation, they inhibit HIV-1 infection of human PBL. These findings suggest that discrete, definable domains of the CD4 molecule may be involved in interactions after HIV-1 envelope binding that lead to virus entry into the cell.

摘要

细胞表面表达的CD4与HIV-1的包膜糖蛋白结合,并通过与膜表达的HIV-1 gp120相互作用介导合胞体形成。CD4分子在HIV-1细胞感染过程中的其他可能作用仍知之甚少。在我们的研究中,我们描述了两种识别CD4分子V3/V4结构域的单克隆抗体。尽管这些单克隆抗体不抑制gp120-CD4结合或HIV-1诱导的合胞体形成,但它们抑制HIV-1对人外周血淋巴细胞的感染。这些发现表明,CD4分子离散的、可定义的结构域可能参与HIV-1包膜结合后导致病毒进入细胞的相互作用。

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