Carter Carol A, Ehrlich Lorna S
Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York 11794, USA.
Annu Rev Microbiol. 2008;62:425-43. doi: 10.1146/annurev.micro.62.081307.162758.
HIV infection of macrophages is a critically important component of viral pathogenesis and progression to AIDS. Although the virus follows the same life cycle in macrophages and T lymphocytes, several aspects of the virus-host relationship are unique to macrophage infection. Examples of these are the long-term persistence of productive infection, sustained by the absence of cell death, and the ability of progeny virus to bud into and accumulate in endocytic compartments designated multivesicular bodies (MVBs). Recently, the hypothesis that viral exploitation of the macrophage endocytic machinery is responsible for perpetuating the chronic state of infection unique to this cell type has been challenged in several independent studies employing a variety of experimental strategies. This review examines the evidence supporting and refuting the canonical hypothesis and highlights recently identified cellular factors that may contribute to the unique aspects of the HIV-macrophage interaction.
巨噬细胞的HIV感染是病毒发病机制及发展为艾滋病的一个至关重要的组成部分。尽管该病毒在巨噬细胞和T淋巴细胞中遵循相同的生命周期,但病毒与宿主关系的几个方面在巨噬细胞感染中是独特的。其中包括由细胞死亡缺失维持的 productive感染的长期持续存在,以及子代病毒出芽进入并积聚在称为多泡体(MVBs)的内吞小室中的能力。最近,在几项采用各种实验策略的独立研究中,病毒利用巨噬细胞内吞机制导致这种细胞类型特有的慢性感染状态持续存在这一假说受到了挑战。本综述审视了支持和反驳经典假说的证据,并强调了最近发现的可能有助于HIV与巨噬细胞相互作用独特方面的细胞因子。