Bisset L R
Department of Internal Medicine, University Hospital, Zürich, Switzerland.
Med Hypotheses. 1994 Dec;43(6):388-96. doi: 10.1016/0306-9877(94)90014-0.
The immune defects characterizing infection with the human immunodeficiency virus (HIV) and culminating in the acquired immune deficiency syndrome (AIDS) are the result of a multifactorial disease process, components of which are the occurrence of autoimmune phenomena and opportunistic infection. In this discussion, the observation that both the HIV-1 gp 120 envelope and Mycoplasma genitalium adhesin proteins share an area of significant similarity with the CD4-binding site of the class II major histocompatibility complex (MHC) proteins is placed in this perspective and mechanisms by which interaction within this triad could contribute to the T-cell dysfunction, T-cell depletion, Th1-cell-->Th2-cell shift, B-cell proliferation, hyperglobulinemia and antigen-presenting cell dysfunction observed during the development of AIDS are proposed.
人类免疫缺陷病毒（HIV）感染所具有的免疫缺陷，最终导致获得性免疫缺陷综合征（AIDS），这是一个多因素疾病过程的结果，其组成部分包括自身免疫现象的出现和机会性感染。在本讨论中，从这一角度来看待HIV-1 gp 120包膜蛋白和生殖支原体粘附蛋白与II类主要组织相容性复合体（MHC）蛋白的CD4结合位点具有显著相似区域这一观察结果，并提出了在这三者之间的相互作用可能导致AIDS发展过程中所观察到的T细胞功能障碍、T细胞耗竭、Th1细胞向Th2细胞转变、B细胞增殖、高球蛋白血症和抗原呈递细胞功能障碍的机制。
