Kozlowski M R, Sandler P, Lin P F, Watson A
Department of Screening and Biochemical Research, Bristol-Myers Squibb Research Institute, Wallingford, CT 06492-7660.
Brain Res. 1991 Jul 12;553(2):300-4. doi: 10.1016/0006-8993(91)90838-m.
Infection with the human immunodeficiency virus (HIV-1) often produces a set of neuropsychiatric dysfunctions which have been termed the AIDS dementia complex. This complex appears due to the infection of brain cells by HIV-1. If so, brain cells might be expected to contain a binding site for the same viral envelope glycoprotein that enables HIV-1 to bind to other cells (e.g. CD4+ T-cells), gp120. The present study shows that the cells of the brain-derived U-138MG, U-373MG, SK-N-MC and SK-N-SH cell lines bind gp120 in an inhibitable fashion. Binding of gp120 to these cells is inhibited by the dyes Aurintricarboxylic acid (ATA) and Evans blue (EB), which are known to inhibit specific gp120 and HIV-1 binding, and block HIV-1 infection, in CD4-expressing cells. Binding is not inhibited by Aurin, a dye related to ATA but lacking its anti-HIV effects. As expected, anti-CD4 antibodies are ineffective in blocking gp120 binding to brain-derived cells. These results suggest that human brain-derived cells possess a specific binding site for gp120 that is not the CD4 antigen.
人类免疫缺陷病毒（HIV-1）感染常常会引发一系列神经精神功能障碍，这些障碍被称为艾滋病痴呆综合征。这种综合征的出现是由于HIV-1感染了脑细胞。如果是这样，那么脑细胞可能预期会含有与使HIV-1能够结合其他细胞（如CD4+T细胞）的相同病毒包膜糖蛋白的结合位点，即gp120。本研究表明，源自脑的U-138MG、U-373MG、SK-N-MC和SK-N-SH细胞系的细胞以可被抑制的方式结合gp120。gp120与这些细胞的结合被金精三羧酸（ATA）和伊文思蓝（EB）染料抑制，已知这两种染料在表达CD4的细胞中可抑制特定的gp120和HIV-1结合，并阻断HIV-1感染。与ATA相关但缺乏其抗HIV作用的染料金精不能抑制结合。正如预期的那样，抗CD4抗体在阻断gp120与源自脑的细胞的结合方面无效。这些结果表明，源自人脑的细胞拥有一个针对gp120的特异性结合位点，该位点不是CD4抗原。
