LYMPHOCYTE-T T4 MOLECULE BEHAVES AS THE RECEPTOR FOR HUMAN RETROVIRUS LAV
LYMPHOCYTE-T T4 MOLECULE BEHAVES AS THE RECEPTOR FOR HUMAN RETROVIRUS LAV
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DOI：
10.1038/312767a0
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发表时间：
1984-01-01
期刊：
影响因子：
64.8
通讯作者：
MONTAGNIER, L
中科院分区：
文献类型：
--
作者：
KLATZMANN, D;CHAMPAGNE, E;MONTAGNIER, L
许多病毒，包括逆转录病毒，其特征在于其特异性细胞向性1 -3。淋巴结病相关病毒（LAV）是一种从获得性免疫缺陷综合征（AIDS）或相关综合征患者中分离的人类嗜淋巴细胞逆转录病毒4，5，对一个T淋巴细胞亚群显示选择性嗜性，该亚群通过表达相对分子量为62，000（62 K）的表面糖蛋白（称为T4）来定义（参考文献6-8）。这种糖蛋白描述了一个T淋巴细胞亚群，主要具有辅助/诱导功能，而相互亚群的T淋巴细胞表达一种称为T8的糖蛋白，主要具有细胞毒性/抑制活性，并且不能复制LAV 7，9。这种嗜性可以在基因组水平上由调节序列控制，如对人T细胞白血病病毒HTLV-I和HTLV-II所述（参考文献2，3）。可替代地或同时地，生产性细胞感染可以在膜水平上控制，需要特异性细胞受体与病毒包膜的相互作用，如最近对EB病毒（EBV）1所证明的。因此，我们研究了T4分子本身是否与LAV受体相关。我们在这里报告，预孵育的T4+淋巴细胞与三个单独的单克隆抗体针对T4糖蛋白阻断细胞感染LAV。这种阻断作用是特异性的，因为其他单克隆抗体，如组织相容性位点抗原（HLA）II类抗体或抗T细胞自然杀伤细胞（TNK）靶向其他表面结构，在活化培养的T4+细胞上强烈表达，不能阻止LAV感染。也排除了单克隆抗体的直接病毒中和。这些结果有力地支持了这样的观点，即直接参与细胞功能的表面分子作为人逆转录病毒的受体，或与人逆转录病毒的受体相关。
Many viruses, including retroviruses, are characterized by their specific cell tropism1–3. Lymphadenopathy-associated virus (LAV) is a human lymphotropic retrovirus isolated from patients with acquired immune deficiency syndrome (AIDS) or related syndromes4,5, that displays selective tropism for a subset of T lymphocytes defined by the expression of a surface glycoprotein of relative molecular mass 62,000 (62K) termed T4 (refs 6–8). This glycoprotein delineates a subset of T lymphocytes with mainly helper/inducer functions, while T lymphocytes of the reciprocal subset express a glycoprotein termed T8, have mainly cytotoxic/suppressor activities, and are unable to replicate LAV7,9. Such a tropism may be controlled at the genomic level by regulatory sequences, as described for the human T-cell leukaemia viruses HTLV-I and -II (refs 2,3). Alternatively or concomitantly, productive cell infection may be controlled at the membrane level, requiring the interaction of a specific cellular receptor with the virus envelope, as demonstrated recently for Epstein–Barr virus (EBV)1. Therefore, we have investigated whether the T4 molecule itself is related to the receptor for LAV. We report here that preincubation of T4+lymphocytes with three individual monoclonal antibodies directed at the T4 glycoprotein blocked cell infection by LAV. This blocking effect was specific, as other monoclonal antibodies—such as antibody to histocompatibility locus antigen (HLA) class II or anti-T-cell natural killer (TNK) target—directed at other surface structures strongly expressed on activated cultured T4+cells, did not prevent LAV infection. Direct virus neutralization by monoclonal antibodies was also ruled out. These results strongly support the view that a surface molecule directly involved in cellular functions acts as, or is related to, the receptor for a human retrovirus.