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人类免疫缺陷病毒1型的包膜糖蛋白可能已融合了来自人白细胞抗原DQβ1的CD4结合位点。

The envelope glycoprotein of HIV-1 may have incorporated the CD4 binding site from HLA-DQ beta 1.

作者信息

Brinkworth R I

机构信息

Graduate School of Science and Technology, Bond University, Gold Coast, Queensland, Australia.

出版信息

Life Sci. 1989;45(20):iii-ix. doi: 10.1016/0024-3205(89)90536-5.

DOI:10.1016/0024-3205(89)90536-5
PMID:2557504
Abstract

An hypothesis is presented which states that the increased binding for CD4 by the envelope glycoprotein (gp120) from HIV-1 compared with that from HIV-2 is due to the env gene from HIV-1 having at some stage incorporated exon 2 of the gene coding for the beta subunit of a class II MHC protein, possibly HLA-DQ, which contains part of the CD4 binding site. Evidence is presented from amino acid sequence analysis and consideration of putative binding residues from gp120 and HLA-DQ.

摘要

提出了一种假说,该假说指出,与HIV-2的包膜糖蛋白(gp120)相比,HIV-1的包膜糖蛋白对CD4的结合增加是由于HIV-1的env基因在某个阶段整合了编码II类MHC蛋白β亚基(可能是HLA-DQ)的基因的外显子2,该外显子包含部分CD4结合位点。从氨基酸序列分析以及对gp120和HLA-DQ的假定结合残基的考虑中提供了证据。

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