Inflammation, over-reacting innate immunity, and CD4⁺ T cell depletion are hallmarks of HIV-1 infection. Self-DNA is usually not considered in the context of HIV-1-associated inflammation, although self-DNA contributes to inflammation in diverse pathologies, including autoimmune diseases, cancer, multiorgan failure after trauma, and even virus infections. Cells undergoing HIV-1-associated pyroptotic bystander cell death release self-DNA and other damage-associated molecular patterns (DAMPs), including chaperones and histones. In complexes with such DAMPs or extracellular vesicles, self-DNA gains immunogenic potential and becomes accessible to intracellular DNA sensors. Therefore, we hypothesize that self-DNA can contribute to HIV-1-associated inflammation. Self-DNA might not only drive HIV-1-associated ‘inflamm-ageing’ but also provide new opportunities for ‘shock and kill’ strategies aimed at eliminating latent HIV-1.

炎症，过度反应的先天免疫和CD4 ⁺T细胞耗竭是HIV-1感染的标志。通常，在与HIV-1相关的炎症中不考虑自身DNA，尽管自身DNA会在多种病理学中导致炎症，包括自身免疫性疾病，癌症，创伤后多器官衰竭甚至病毒感染。经历过HIV-1相关的焦灼旁观者细胞死亡的细胞会释放自身DNA和其他与损伤相关的分子模式（DAMP），包括分子伴侣和组蛋白。在与此类DAMP或细胞外囊泡的复合物中，自身DNA获得了免疫原性，并变得可被细胞内DNA传感器使用。因此，我们假设自身DNA可以导致与HIV-1相关的炎症。