{"title":"Interplay between autophagy and apoptosis in human viral pathogenesis","authors":"Qingqing Shao , Tong Liu , Bin Hu , Liuqing Chen","doi":"10.1016/j.virusres.2025.199611","DOIUrl":null,"url":null,"abstract":"<div><div>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.</div></div>","PeriodicalId":23483,"journal":{"name":"Virus research","volume":"359 ","pages":"Article 199611"},"PeriodicalIF":2.7000,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Virus research","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0168170225000899","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"VIROLOGY","Score":null,"Total":0}
引用次数: 0
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.
期刊介绍:
Virus Research provides a means of fast publication for original papers on fundamental research in virology. Contributions on new developments concerning virus structure, replication, pathogenesis and evolution are encouraged. These include reports describing virus morphology, the function and antigenic analysis of virus structural components, virus genome structure and expression, analysis on virus replication processes, virus evolution in connection with antiviral interventions, effects of viruses on their host cells, particularly on the immune system, and the pathogenesis of virus infections, including oncogene activation and transduction.