HIV infects several cell types in the body, including CD4⁺ T cells and macrophages. Here we review the role of macrophages in HIV infection and describe complex interactions between viral proteins and host defenses in these cells. Macrophages exist in many forms throughout the body, where they play numerous roles in healthy and diseased states. They express pattern-recognition receptors (PRRs) that bind viral, bacterial, fungal, and parasitic pathogens, making them both a key player in innate immunity and a potential target of infection by pathogens, including HIV. Among these PRRs is mannose receptor, a macrophage-specific protein that binds oligosaccharides, restricts HIV replication, and is downregulated by the HIV accessory protein Vpr. Vpr significantly enhances infection in vivo, but the mechanism by which this occurs is controversial. It is well established that Vpr alters the expression of numerous host proteins by using its co-factor DCAF1, a component of the DCAF1–DDB1–CUL4 ubiquitin ligase complex. The host proteins targeted by Vpr and their role in viral replication are described in detail. We also discuss the structure and function of the viral protein Env, which is stabilized by Vpr in macrophages. Overall, this literature review provides an updated understanding of the contributions of macrophages and Vpr to HIV pathogenesis.

中文翻译：

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Vpr 是 VIP：HIV Vpr 和受感染的巨噬细胞促进病毒发病机制。

HIV 感染体内多种细胞类型，包括 CD4 ⁺ T 细胞和巨噬细胞。在这里，我们回顾了巨噬细胞在 HIV 感染中的作用，并描述了这些细胞中病毒蛋白与宿主防御之间复杂的相互作用。巨噬细胞以多种形式存在于全身，在健康和患病状态下发挥着多种作用。它们表达模式识别受体（PRR），可结合病毒、细菌、真菌和寄生病原体，使它们既是先天免疫的关键参与者，又是包括艾滋病毒在内的病原体感染的潜在目标。这些 PRR 中包括甘露糖受体，它是一种巨噬细胞特异性蛋白，可结合寡糖、限制 HIV 复制，并被 HIV 辅助蛋白 Vpr 下调。Vpr 显着增强体内感染，但其发生机制存在争议。众所周知，Vpr 通过使用其辅因子 DCAF1（DCAF1-DDB1-CUL4 泛素连接酶复合物的一个组成部分）来改变许多宿主蛋白的表达。详细描述了 Vpr 靶向的宿主蛋白及其在病毒复制中的作用。我们还讨论了病毒蛋白 Env 的结构和功能，该蛋白由巨噬细胞中的 Vpr 稳定。总体而言，这篇文献综述提供了对巨噬细胞和 Vpr 对 HIV 发病机制的贡献的最新了解。