人类免疫缺陷病毒包膜糖蛋白V3区对细胞结合能力的研究

目的：研究人类免疫缺陷病毒（ＨＩＶ）不同亲嗜株包膜糖蛋白Ｖ３区结合于靶细胞的能力。方法：合成来源于不同嗜性ＨＩＶ－１Ｖ３区的生物素标记和非标记的多肽。采用流式细胞计数分析生物素化的 Ｖ３多肽对细胞的结合能力以及细胞表面的结合配体。结果：ＨＩＶ－１Ｘ４　亲嗜株ＩＩＩＢＶ３区能结合于多种细胞的表面，包括辅助受体ＣＸＣＲ４；竞争实验结果显示蛋白酶抑制剂能抑制该结合。Ｒ５亲嗜株 ＡＤＡ Ｖ３区只极微弱地结合于外周血单核细胞和表达ＣＣＲ５ 的人星形胶质细胞表面。结论：不同嗜性ＨＩＶ－１Ｖ３区结合于细胞表面的能力不同从亲嗜株Ｖ３区直接结合于细胞表面并被其自身所增强，其靶分子至少包括辅助受体 ＣＸＣＲ４和蛋白酶分子；而Ｒ５亲嗜株 ＡＤＡ Ｖ３区则不结合于 ＣＣＲ５和蛋白酶。

The binding ability of V3 region derived from diverse human immunodeficience type 1 (HIV-1) to different cells

Objective:To determine the binding ability of ~V-1 V3 loop to target cells.Methods:V3 loop peptides(V3-HBIO,V3-ADA,V3-89.6)derived from different HIV-1 strains LIIB(X4-nopic),ADA(R5-tmpic),89.6(R5X4-tropic) and the biotinylated V3-BH1O(biotin-BHIO) and V3 -ADA( biotin-ADA) were synthesized. The binding of the biotinylated V3 peptides to cells and the binding targets were analyzed using flow cytometry. Results:V3 BH10 can bind to a wide range of cell lines, while bio-ADA scarcely binds to the monocytes derived from periperal blood mononuclear cells.Antibody anti-CXCR4 binding to cells blocked by V3 -BH10 and biotin-BH1O binding was blocked by protease inhibitors. The binding of V3-BH10 could be significantly enhanced by V3-BHlO but by neither V3-89.6 nor V3-ADA.Conclusion:The binding ability of the V3 loop derived from diverse HIV- I strains are different. The V3 loop derived from HIV-1 X4-tropic strain directly binds to a wide range of cell lines, the binding targets are multiple including at least coreceptor and proteases. The V3 loop derived from R5 -tropic strain ADA does scarcely.