nature最新的一篇综述阐述了IFNs能够控制HIV-1在体内的复制的证据，讨论IFNs在促进促进慢性HIV-1感染的病理后遗症中的有争议角色。
很久以前就已经观察到一个现象：干扰素能够抑制HIV-1在细胞培养上的复制，并且为感染HIV-1的病人使用IFNα给药治疗，但不接受抗逆转录药物的治疗，病人会有一个明显而短暂的病毒滴度下降。相反的，慢性HIV-1感染人和猴免疫缺陷病毒(英语:Simian immunodeficiency virus,简称SIV)感染动物AIDS模型中的研究表明：增加干扰素刺激基因（ISGs），以及炎症和疾病进展的生物标志物的表达，干扰素的血浆水平升高呈正相关关系。
摘要原文：[size=14.4949998855591px]The ability of interferons (IFNs) to inhibit HIV-1 replication in cell culture models has long been recognized, and the therapeutic administration of IFN[size=14.4949998855591px]α[size=14.4949998855591px] to HIV-1-infected patients who are not receiving antiretroviral therapy produces a clear but transient decrease in plasma viral load. Conversely, studies of chronic HIV-1 infection in humans and SIV-infected animal models of AIDS show positive correlations between elevated plasma levels of IFNs, increased expression of IFN-stimulated genes (ISGs), biomarkers of inflammation and disease progression. In this Review, we discuss the evidence that IFNs can control HIV-1 replication in vivo[size=14.4949998855591px] and debate the controversial role of IFNs in promoting the pathological sequelae of chronic HIV-1 infection.
Type I interferons (IFNs) bind to type I IFN receptor (IFNAR), which is composed of IFNAR1 and IFNAR2 subunits, leading to tyrosine kinase 2 (TYK2) and Janus kinase 1 (JAK1) activation.
Following HIV-1 entry into the cell, viral RNA is reverse transcribed into cDNA, which is detected by the cytoplasmic receptors cyclic GMP–AMP (cGAMP) synthase (cGAS) and interferon-γ (IFNγ)-inducible protein 16 (IFI16).
