The feline and human immunodeficiency viruses (FIV and HIV) target helper T cells selectively, and in doing so they induce a profound immune dysfunction. The primary determinant of HIV cell tropism is the expression pattern of the primary viral receptor CD4 and co-receptor(s), such as CXCR4 and CCR5. FIV employs a distinct strategy to target helper T cells; a high affinity interaction with CD134 (OX40) is followed by binding of the virus to its sole co-receptor, CXCR4. Recent studies have demonstrated that the way in which FIV interacts with its primary receptor, CD134, alters as infection progresses, changing the cell tropism of the virus. This review examines the contribution of the virus–receptor interaction to replication in vivo as well as the significance of these findings to the development of vaccines and therapeutics.

猫科动物和人类免疫缺陷病毒（FIV 和 HIV）选择性地靶向辅助 T 细胞，并在此过程中诱发严重的免疫功能障碍。HIV 细胞趋向性的主要决定因素是主要病毒受体 CD4 和辅助受体（如 CXCR4 和 CCR5）的表达模式。FIV 采用独特的策略来靶向辅助 T 细胞；与 CD134 (OX40) 的高亲和力相互作用之后，病毒与其唯一的共同受体 CXCR4 结合。最近的研究表明，FIV 与其主要受体 CD134 相互作用的方式会随着感染的进展而改变，从而改变病毒的细胞嗜性。本综述探讨了病毒-受体相互作用对体内复制的贡献 以及这些发现对疫苗和疗法开发的重要性。