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自噬与凋亡在人类病毒致病机制中的相互作用。

Interplay between autophagy and apoptosis in human viral pathogenesis.

作者信息

Shao Qingqing, Liu Tong, Hu Bin, Chen Liuqing

机构信息

Department of Dermatology, Wuhan No. 1 Hospital, Wuhan, China; Department of Dermatology, Traditional Chinese and Western Medicine Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Department of Dermatology, Wuhan No. 1 Hospital, Wuhan, China; Hubei Province & Key Laboratory of Skin Infection and Immunity, Wuhan, China.

出版信息

Virus Res. 2025 Jul 30;359:199611. doi: 10.1016/j.virusres.2025.199611.

DOI:10.1016/j.virusres.2025.199611
PMID:40749962
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12345325/
Abstract

Autophagy and apoptosis are two pivotal programmed cell death pathways that regulate vital physiological processes, ranging from cellular development to intracellular homeostasis. These pathways also act as key battlegrounds in host-pathogen interactions during viral infection. This comprehensive review explores the dual regulatory mechanisms controlling autophagy and apoptosis triggered by clinically significant human viruses. These include DNA viruses-such as herpes simplex virus (HSV), Epstein-Barr virus (EBV), hepatitis viruses, human papillomavirus (HPV), and human bocavirus (HBoV)-and RNA viruses, including human immunodeficiency virus type 1 (HIV-1), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), enterovirus 71 (EV71), influenza viruses, respiratory syncytial virus (RSV), Coxsackievirus B (CVB), rabies virus (RABV), and dengue virus serotype 2 (DENV2). We specifically highlight the dynamic crosstalk between autophagic and apoptotic pathways during viral pathogenesis, analyzing how viruses strategically co-opt both cellular processes to facilitate infection. By systematically elucidating these viral manipulation strategies, this review aims to provide a reference for developing targeted antiviral strategies and identifying novel therapeutic interventions.

摘要

自噬和凋亡是两种关键的程序性细胞死亡途径,它们调节着从细胞发育到细胞内稳态等重要的生理过程。在病毒感染期间,这些途径也是宿主与病原体相互作用的关键战场。这篇综述探讨了由临床上重要的人类病毒引发的自噬和凋亡的双重调控机制。这些病毒包括DNA病毒,如单纯疱疹病毒(HSV)、爱泼斯坦-巴尔病毒(EBV)、肝炎病毒、人乳头瘤病毒(HPV)和人博卡病毒(HBoV),以及RNA病毒,包括1型人类免疫缺陷病毒(HIV-1)、严重急性呼吸综合征冠状病毒2(SARS-CoV-2)、肠道病毒71型(EV71)、流感病毒、呼吸道合胞病毒(RSV)、柯萨奇病毒B(CVB)、狂犬病病毒(RABV)和登革热病毒2型(DENV2)。我们特别强调了病毒发病机制中自噬和凋亡途径之间的动态相互作用,分析了病毒如何策略性地利用这两种细胞过程来促进感染。通过系统地阐明这些病毒操纵策略,本综述旨在为制定针对性的抗病毒策略和确定新的治疗干预措施提供参考。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa23/12345325/488561bee7ce/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa23/12345325/6d9297f5bfdc/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa23/12345325/488561bee7ce/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa23/12345325/6d9297f5bfdc/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa23/12345325/488561bee7ce/gr2.jpg

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本文引用的文献

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TRIM23 mediates cGAS-induced autophagy in anti-HSV defense.TRIM23在抗单纯疱疹病毒防御中介导cGAS诱导的自噬。
Nat Commun. 2025 May 13;16(1):4418. doi: 10.1038/s41467-025-59338-5.
2
Porcine cGAS-STING signalling induced apoptosis negatively regulates STING downstream IFN response and autophagy via different mechanisms.猪cGAS-STING信号诱导的细胞凋亡通过不同机制对STING下游的IFN反应和自噬进行负调控。
Virulence. 2025 Dec;16(1):2496436. doi: 10.1080/21505594.2025.2496436. Epub 2025 May 1.
3
Autophagy and Programmed Cell Death Modalities Interplay in HIV Pathogenesis.
自噬与程序性细胞死亡方式在HIV发病机制中的相互作用。
Cells. 2025 Feb 28;14(5):351. doi: 10.3390/cells14050351.
4
The Role of Tumor Suppressor p53 Protein in HIV-Host Cell Interactions.肿瘤抑制因子 p53 蛋白在 HIV-宿主细胞相互作用中的作用。
Cells. 2024 Sep 10;13(18):1512. doi: 10.3390/cells13181512.
5
IL-37 attenuated HPV induced inflammation and growth of oral epithelial cells via regulating autophagy.白细胞介素-37通过调节自噬减轻人乳头瘤病毒诱导的口腔上皮细胞炎症和生长。
Heliyon. 2024 Jul 24;10(15):e35131. doi: 10.1016/j.heliyon.2024.e35131. eCollection 2024 Aug 15.
6
Human Papillomavirus and Associated Cancers: A Review.人乳头瘤病毒及相关癌症:综述。
Viruses. 2024 Apr 26;16(5):680. doi: 10.3390/v16050680.
7
Friends and Foes: The Ambivalent Role of Autophagy in HIV-1 Infection.朋友与敌人:自噬在HIV-1感染中的矛盾作用
Viruses. 2024 Mar 25;16(4):500. doi: 10.3390/v16040500.
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Loss of TRIM29 mitigates viral myocarditis by attenuating PERK-driven ER stress response in male mice.在雄性小鼠中,TRIM29缺失通过减弱PERK驱动的内质网应激反应减轻病毒性心肌炎。
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J Biomed Sci. 2023 Jan 18;30(1):5. doi: 10.1186/s12929-023-00899-2.