ArticleScientific reports2020
Coxsackievirus infection induces a non-canonical autophagy independent of the ULK and PI3K complexes.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 27 citations in OpenAlex.
- ATG9A is an essential host factor for parechovirus RNA replication.Journal of virology · 2026Article
- Viral-host interactions mediated by the mTOR signaling pathway.Cell insight · 2026Review
- A Focus on Natural Autophagy Modulators as Potential Host-Directed Weapons Against Emerging and Re-Emerging Viruses.Medicinal research reviews · 2025Review
- Developing a Personalized Cancer Nanovaccine Using Coxsackievirus-Reprogrammed Cancer Cell Membranes for Enhanced Anti-Tumor Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cellular protein quality control in viral myocarditis: molecular mechanisms and therapeutic implication.Microbiology and molecular biology reviews : MMBR · 2025Review
- Autophagy-independent role of ATG9A vesicles as carriers for galectin-9 secretion.Nature communications · 2025Article
- Sequences and Structures of Viral Proteins Linked to the Genomes (VPg) of RNA Viruses.Viruses · 2025Review
- Mitochondrial injury and complement dysregulation are drivers of pathological inflammation in viral myocarditis.Journal of virology · 2025Article
- Article
- Identification of the proteolytic signature in CVB3-infected cells.Journal of virology · 2024Article
- Double-Edged Sword: Exploring the Mitochondria-Complement Bidirectional Connection in Cellular Response and Disease.Biology · 2024Review
- Biologic activity and treatment resistance to gastrointestinal cancer: the role of circular RNA in autophagy regulation.Frontiers in oncology · 2024Review
- Astrovirus replication is dependent on induction of double-membrane vesicles through a PI3K-dependent, LC3-independent pathway.Journal of virology · 2023Article
- Mitochondria Dysfunction at the Heart of Viral Myocarditis: Mechanistic Insights and Therapeutic Implications.Viruses · 2023Review
- Control of infection by LC3-associated phagocytosis, CASM, and detection of raised vacuolar pH by the V-ATPase-ATG16L1 axis.Science advances · 2022Review
- Many roads lead to CASM: Diverse stimuli of noncanonical autophagy share a unifying molecular mechanism.Science advances · 2022Review
- Viral proteases activate the CARD8 inflammasome in the human cardiovascular system.The Journal of experimental medicine · 2022Article
- Article
- Synergetic Contributions of Viral VP1, VP3, and 3C to Activation of the AKT-AMPK-MAPK-MTOR Signaling Pathway for Seneca Valley Virus-Induced Autophagy.Journal of virology · 2022Article
- CRISPR/Cas9-Mediated Knockout of theFrontiers in cellular and infection microbiology · 2022Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Coxsackievirus B3 (CVB3) is a single-stranded positive RNA virus that usurps cellular machinery, including the evolutionarily anti-viral autophagy pathway, for productive infections. Despite the emergence of double-membraned autophagosome-like vesicles during CVB3 infection, very little is known about the mechanism of autophagy initiation. In this study, we investigated the role of established autophagy factors in the initiation of CVB3-induced autophagy. Using siRNA-mediated gene-silencing and CRISPR-Cas9-based gene-editing in culture cells, we discovered that CVB3 bypasses the ULK1/2 and PI3K complexes to trigger autophagy. Moreover, we found that CVB3-induced LC3 lipidation occurred independent of WIPI2 and the transmembrane protein ATG9 but required components of the late-stage ubiquitin-like ATG conjugation system including ATG5 and ATG16L1. Remarkably, we showed the canonical autophagy factor ULK1 was cleaved through the catalytic activity of the viral proteinase 3C. Mutagenesis experiments identified the cleavage site of ULK1 after Q524, which separates its N-terminal kinase domain from C-terminal substrate binding domain. Finally, we uncovered PI4KIIIβ (a PI4P kinase), but not PI3P or PI5P kinases as requisites for CVB3-induced LC3 lipidation. Taken together, our studies reveal that CVB3 initiates a non-canonical form of autophagy that bypasses ULK1/2 and PI3K signaling pathways to ultimately converge on PI4KIIIβ- and ATG5-ATG12-ATG16L1 machinery.
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