人类免疫缺陷病毒免疫逃逸后嗜性的改变
Change in tropism upon immune escape by human immunodeficiency virus.
作者信息
McKnight A, Weiss R A, Shotton C, Takeuchi Y, Hoshino H, Clapham P R
机构信息
Chester Beatty Laboratories, Institute of Cancer Research, London, United Kingdom.
出版信息
J Virol. 1995 May;69(5):3167-70. doi: 10.1128/JVI.69.5.3167-3170.1995.
Abstract
The V3 loop of human immunodeficiency virus type 1 is both a determinant of viral cell tropism and a target for neutralizing antibodies. This relationship was investigated. Selection of a dual-tropic (T cells and macrophages) virus to replicate in CD4+ brain cells results in loss of macrophage tropism and of neutralization by an anti-V3 loop monoclonal antibody. Moreover, selection of the brain-selected variant to escape from V3 loop-specific neutralizing monoclonal antibodies results in the reduction or loss of brain cell tropism and the reacquisition of macrophage tropism. These data may indicate that the antigenic diversification of human immunodeficiency virus type 1 apparent after seroconversion can be selected either by immune responses or by colonization of new cell types.
摘要
人类免疫缺陷病毒1型的V3环既是病毒细胞嗜性的决定因素，也是中和抗体的作用靶点。对这种关系进行了研究。选择一种双嗜性（T细胞和巨噬细胞）病毒在CD4+脑细胞中复制，会导致巨噬细胞嗜性丧失以及抗V3环单克隆抗体的中和作用丧失。此外，选择逃避V3环特异性中和单克隆抗体的脑选变体，会导致脑细胞嗜性降低或丧失，并重新获得巨噬细胞嗜性。这些数据可能表明，血清转化后出现的人类免疫缺陷病毒1型抗原多样化，既可以通过免疫反应选择，也可以通过新细胞类型的定植选择。
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