Co-infection with Mycobacterium tuberculosis is the leading cause of death in individuals infected with HIV-1. It has long been known that HIV-1 infection alters the course of M. tuberculosis infection and substantially increases the risk of active tuberculosis (TB). It has also become clear that TB increases levels of HIV-1 replication, propagation and genetic diversity. Therefore, co-infection provides reciprocal advantages to both pathogens. In this Review, we describe the epidemiological associations between the two pathogens, selected interactions of each pathogen with the host and our current understanding of how they affect the pathogenesis of TB and HIV-1/AIDS in individuals with co-infections. We evaluate the mechanisms and consequences of HIV-1 depletion of T cells on immune responses to M. tuberculosis. We also discuss the effect of HIV-1 infection on the control of M. tuberculosis by macrophages through phagocytosis, autophagy and cell death, and we propose models by which dysregulated inflammatory responses drive the pathogenesis of TB and HIV-1/AIDS.

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HIV-1与结核分枝杆菌共感染的发病机理

与结核分枝杆菌的共同感染是感染HIV-1的个体死亡的主要原因。早就知道，HIV-1感染会改变结核分枝杆菌的病程感染并大大增加了活动性肺结核（TB）的风险。同样清楚的是，结核病增加了HIV-1复制，繁殖和遗传多样性的水平。因此，共同感染为两种病原体提供了互惠的优势。在这篇综述中，我们描述了两种病原体之间的流行病学关联，每种病原体与宿主之间的选定相互作用以及我们目前对它们如何影响合并感染个体中TB和HIV-1 / AIDS发病机理的理解。我们评估了T细胞HIV-1耗竭对结核分枝杆菌免疫反应的机制和后果。我们还讨论了HIV-1感染对结核分枝杆菌控制的影响 通过巨噬细胞通过吞噬作用，自噬和细胞死亡，我们提出了炎症反应失调驱动结核病和HIV-1 / AIDS发病机理的模型。