Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
The role of pyroptosis during HIV infection.
СтатьяОбзорНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Yaseen Mahmoud M, Abuharfeil Nizar M, Darmani Homa, Shatnawi Mohammed N
Аннотация
BACKGROUND: Pyroptosis, a proinflammatory form of programmed cell death, has emerged as a central driver of chronic inflammation, CD4⁺ T cell depletion, and non-AIDS comorbidities in HIV infection. This review synthesizes current evidence on the molecular mechanisms and pathological consequences of pyroptosis in HIV.
METHODS: We conducted a comprehensive analysis of the literature, examining the molecular pathways of pyroptosis triggered by abortive HIV infection, the roles of specific inflammasomes (e.g., AIM2, NLRP3, CARD8) and viral proteins, and the subsequent amplification of inflammation through cytokine release and gut barrier dysfunction.
RESULTS: Abortive infection in resting CD4⁺ T cells generates cytosolic viral DNA, activating inflammasomes (primarily AIM2/IFI16) and executing pyroptosis via GSDMD. This process initiates a vicious cycle of immune activation, mucosal damage, microbial translocation, and systemic inflammation, leading to CD4⁺ T cell loss, reservoir persistence, and end-organ damage. Therapeutic targeting of key nodes (e.g., caspase-1, NLRP3, GSDMD) shows promise in preclinical models.
CONCLUSION: Pyroptosis is a critical pathological engine in HIV, linking viral infection to chronic immunodeficiency and comorbidities. Adjunctive therapies targeting this pathway may reduce inflammation, preserve immune function, and support strategies toward a functional cure.
METHODS: We conducted a comprehensive analysis of the literature, examining the molecular pathways of pyroptosis triggered by abortive HIV infection, the roles of specific inflammasomes (e.g., AIM2, NLRP3, CARD8) and viral proteins, and the subsequent amplification of inflammation through cytokine release and gut barrier dysfunction.
RESULTS: Abortive infection in resting CD4⁺ T cells generates cytosolic viral DNA, activating inflammasomes (primarily AIM2/IFI16) and executing pyroptosis via GSDMD. This process initiates a vicious cycle of immune activation, mucosal damage, microbial translocation, and systemic inflammation, leading to CD4⁺ T cell loss, reservoir persistence, and end-organ damage. Therapeutic targeting of key nodes (e.g., caspase-1, NLRP3, GSDMD) shows promise in preclinical models.
CONCLUSION: Pyroptosis is a critical pathological engine in HIV, linking viral infection to chronic immunodeficiency and comorbidities. Adjunctive therapies targeting this pathway may reduce inflammation, preserve immune function, and support strategies toward a functional cure.