Root-Bernstein R S, Hobbs S H
Department of Physiology, Michigan State University, East Lansing 48824.
J Theor Biol. 1993 Jan 21;160(2):249-64. doi: 10.1006/jtbi.1993.1017.
Coinfections of human immunodeficiency virus (HIV), EBV, and HTLV or sperm proteins act synergistically to enhance infectivity and replication and expand cellular tropism. While some aspects of these synergisms are understood, others are not. We have found that membrane or surface proteins of CMV, HTLV, EBV and sperm proteins share large regions of similarity with the CD4 protein of T-helper lymphocytes. Since HIV uses CD4 as a receptor, it may bind to CD4 homologues on CMV, HTLV, EBV or sperm proteins. HIV could then "piggyback" with these viruses into cells with which it normally has no tropism. Similarly, HIV may expand the cellular tropism of CMV, or EBV. Such a piggyback mechanism may provide insight into the formation or presentation of CD4-like antigens from CMV, HTLV, EBV and sperm proteins with class II MHC-like antigens on HIV (gp160 and Nef proteins) and may break immunological tolerance, inducing the autoimmunity observed against both CD4+ and class II MHC+ T cells in AIDS patients.
人类免疫缺陷病毒（HIV）、EB病毒、人类嗜T淋巴细胞病毒（HTLV）的合并感染或精子蛋白会协同作用，增强感染性和复制能力，并扩大细胞嗜性。虽然这些协同作用的某些方面已为人所知，但其他方面仍不清楚。我们发现，巨细胞病毒（CMV）、HTLV、EB病毒的膜蛋白或表面蛋白以及精子蛋白与辅助性T淋巴细胞的CD4蛋白有大片相似区域。由于HIV将CD4用作受体，它可能会与CMV、HTLV、EB病毒的膜蛋白或表面蛋白以及精子蛋白上的CD4同源物结合。然后，HIV可能会“搭便车”与这些病毒一起进入其通常没有嗜性的细胞。同样，HIV可能会扩大CMV或EB病毒的细胞嗜性。这种搭便车机制可能有助于深入了解CMV、HTLV、EB病毒的膜蛋白或表面蛋白以及精子蛋白中类CD4抗原与HIV上类II型主要组织相容性复合体（MHC）抗原（gp160和Nef蛋白）的形成或呈递情况，并可能打破免疫耐受，引发在艾滋病患者中观察到的针对CD4+和类II型MHC+ T细胞的自身免疫反应。
