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众所周知,获得性免疫缺陷综合征(AIDS)的病因是淋巴结病相关病毒(LAV)或称人类淋巴细胞病毒Ⅲ(HTLV-Ⅲ)感染并杀死了OKT4~+细胞。本文作者认为:LAV/HTLV-Ⅲ的转作用蛋白通过诱导细胞产生淋巴毒素而杀伤细胞,异常高浓度的淋巴毒素导致淋巴细胞的自毁,患者的淋巴毒素浓度达到血浆可检水平,从而诱发免疫抑制并使机体对机会致病性感染因子(例如卡氏肺囊虫)易感。肿瘤免疫缺陷也可能起因于OKT4~+细胞的耗竭。当LAV/HTLV-Ⅲ在体外感染OKT4~+细胞后,细胞功能受到明显抑制。临床研究表明:AIDS病人的辅助T细胞极度减少致使免疫功能低下。但T细胞耗竭的机理尚不清楚。AIDS病毒的基因组顺序已搞清并大
It is well known that the cause of Acquired Immune Deficiency Syndrome (AIDS) is infection of lymphopathogenic virus (LAV) or human lymphocytic virus III (HTLV-III) and killing of OKT4 ~ + cells. The authors conclude that transfection of LAV / HTLV-III transports proteins to kill cells by inducing lymphotoxin production in cells. High levels of lymphotoxin lead to self-destruction of lymphocytes. The patient’s lymphotoxin concentration reaches a detectable level in the plasma, thereby inducing immunity Inhibit and make the body susceptible to opportunistic pathogenic infectious agents (such as Pneumocystis carinii). Tumor immune deficiency may also result from the depletion of OKT4 ~ + cells. When LAV / HTLV-Ⅲ infected OKT4 ~ + cells in vitro, the cell function was significantly inhibited. Clinical studies have shown that AIDS patients with extremely reduced helper T cells resulting in immune dysfunction. However, the mechanism of T cell depletion is unclear. The genome sequence of the AIDS virus has been clarified and large