van Hemel K
Rev Neurol (Paris). 1989;145(11):802-5.
Data of the literature about frequency and specificity of giant cells during AIDS encephalitis are conflicting. These discrepancies could be explained by several factors. Envelope glycoprotein Gp 120, when free, induces the formation of giant cells through the fusion of cerebral monocytes. The concentration of this protein depends on the level of its production, function of the quantity and of the maturation of the HIV, and on the rapidity of its catabolism, due to anti-Gp 120 antibodies. On the other hand, the tropism of the virus for monocytes and lymphocytes could vary; this would lead to the formation of giant cells with a different life span. The fusion capability of HIV-2 might be lower on account of the smaller size of its Gp 120. The frequency of mutations in HIV lentivirus leading to the synchronous development of several different clones of HIV-1 in the same patient and the associated infectious diseases, due to risk factors common to the diseased population, current endemic or opportunistic agents, could explain the variability of the density of giant cells according to the country where the patients live.
关于艾滋病脑炎期间巨细胞频率和特异性的文献数据相互矛盾。这些差异可由几个因素来解释。游离的包膜糖蛋白Gp 120通过脑单核细胞融合诱导巨细胞形成。该蛋白的浓度取决于其产生水平、HIV的数量和成熟功能，以及由于抗Gp 120抗体导致的其分解代谢速度。另一方面，病毒对单核细胞和淋巴细胞的嗜性可能不同；这将导致形成具有不同寿命的巨细胞。由于HIV-2的Gp 120尺寸较小，其融合能力可能较低。HIV慢病毒中的突变频率导致同一患者体内几种不同HIV-1克隆的同步发展以及相关传染病，由于患病群体共有的风险因素、当前的地方病或机会性病原体，这可以解释根据患者所在国家不同巨细胞密度的变异性。
