Ziegler J L, Stites D P
Clin Immunol Immunopathol. 1986 Dec;41(3):305-13. doi: 10.1016/0090-1229(86)90001-2.
By attaching to the CD4 (T4) molecule of the helper-inducer lymphocyte, the human immunodeficiency virus (HIV) envelope imitates the normal ligand for this receptor, namely, an invariant component of the class II major histocompatibility antigen (MHC). Depending on the degree of antigen mimicry, the normal immune response to retrovirus envelope would be expected to recognize and cross-react to self-MHC. By disguising as "self" the virus then provokes an autoimmune attack of class-II-bearing cells and an anti-idiotypic response to the CD4 antigen. As a consequence of this immune response to virus infection, communication between CD4 lymphocytes and antigen-processing cells becomes blocked, resulting in progressive disruption of antigen recognition, immunodysregulation, and dysfunctional responses of catastrophic proportion. If this hypothesis gains support, then there are profound implications for prevention and treatment.
人类免疫缺陷病毒（HIV）包膜通过附着于辅助诱导淋巴细胞的CD4（T4）分子，模仿该受体的正常配体，即II类主要组织相容性抗原（MHC）的一个恒定成分。根据抗原模拟的程度，对逆转录病毒包膜的正常免疫反应预计会识别自身MHC并与之发生交叉反应。通过伪装成“自身”，病毒随后引发对携带II类分子细胞的自身免疫攻击以及对CD4抗原的抗独特型反应。作为对病毒感染这种免疫反应的结果，CD4淋巴细胞与抗原处理细胞之间的通讯被阻断，导致抗原识别逐渐遭到破坏、免疫调节异常以及出现灾难性比例的功能失调反应。如果这一假说得到证实，那么对预防和治疗将具有深远意义。
