Klatzmann D, Champagne E, Chamaret S, Gruest J, Guetard D, Hercend T, Gluckman J C, Montagnier L
Nature. 1984;312(5996):767-8. doi: 10.1038/312767a0.
Many viruses, including retroviruses, are characterized by their specific cell tropism. Lymphadenopathy-associated virus (LAV) is a human lymphotropic retrovirus isolated from patients with acquired immune deficiency syndrome (AIDS) or related syndromes, 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 LAV. 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). 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.
许多病毒，包括逆转录病毒，都具有特定的细胞嗜性。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出的嗜人淋巴细胞逆转录病毒，它对由相对分子质量为62000（62K）的表面糖蛋白（称为T4）表达所定义的一部分T淋巴细胞表现出选择性嗜性（参考文献6 - 8）。这种糖蛋白描绘了一个主要具有辅助/诱导功能的T淋巴细胞亚群，而相对应亚群的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。正如人类T细胞白血病病毒HTLV - I和 - II（参考文献2, 3）所描述的那样，这种嗜性可能在基因组水平上由调控序列控制。或者，也可能同时在膜水平上控制有生产性的细胞感染，这需要特定的细胞受体与病毒包膜相互作用，正如最近对爱泼斯坦 - 巴尔病毒（EBV）所证明的那样。因此，我们研究了T4分子本身是否与LAV的受体有关。我们在此报告，用三种针对T4糖蛋白的单克隆抗体对T4 + 淋巴细胞进行预孵育可阻断LAV对细胞的感染。这种阻断作用是特异性的，因为针对活化培养的T4 + 细胞上强烈表达的其他表面结构的其他单克隆抗体，如针对组织相容性位点抗原（HLA）II类的抗体或抗T细胞自然杀伤（TNK）靶点的抗体，都不能阻止LAV感染。单克隆抗体直接病毒中和作用也被排除。这些结果有力地支持了这样一种观点，即直接参与细胞功能的表面分子充当人类逆转录病毒的受体或与之相关。
