ArticleAutophagy2015
Coxsackievirus can exploit LC3 in both autophagy-dependent and -independent manners in vivo.
Article in Autophagy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- LncRNA SNHG15: A new budding star in human cancers.Cell proliferation · 2020Pooled it
- Does Coxsackievirus B3 Require Autophagosome Formation for Replication? Evidence for an Autophagosome-Independent Mechanism: Insights into Its Limited Potential as a Therapeutic Target.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Deleterious variants in the autophagy-related gene RB1CC1/FIP200 impair immunity to SARS-CoV-2.Nature communications · 2025Article
- Influenza A virus subverts the LC3-pericentrin dynein adaptor complex for host cytoplasm entry.Science advances · 2025Article
- Modulation of Autophagy-Lysosome Axis by African Swine Fever Virus and Its Encoded Protein pEP153R.Current issues in molecular biology · 2024Article
- Host Subcellular Organelles: Targets of Viral Manipulation.International journal of molecular sciences · 2024Review
- The role of autophagy in viral infections.Journal of biomedical science · 2023Review
- Nrf2 Pathway and Autophagy Crosstalk: New Insights into Therapeutic Strategies for Ischemic Cerebral Vascular Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- The DHAV-1 protein VP1 interacts with PI3KC3 to induce autophagy through the PI3KC3 complex.Veterinary research · 2022Article
- The encephalomyocarditis virus Leader promotes the release of virions inside extracellular vesicles via the induction of secretory autophagy.Nature communications · 2022Article
- LC3B is an RNA-binding protein to trigger rapid mRNA degradation during autophagy.Nature communications · 2022Article
- Autophagy Modulators in Coronavirus Diseases: A Double Strike in Viral Burden and Inflammation.Frontiers in cellular and infection microbiology · 2022Review
- The interplay between pathogens and Atg8 family proteins: thousand-faced interactions.FEBS open bio · 2021Review
- Article
- A food-responsive switch modulates TFEB and autophagy, and determines susceptibility to coxsackievirus infection and pancreatitis.Autophagy · 2021Article
- The Roles and Mechanisms of lncRNAs in Liver Fibrosis.Frontiers in pharmacology · 2021Review
- Autophagy in Viral Development and Progression of Cancer.Frontiers in oncology · 2021Review
- Autophagy Activation by Hypoxia Regulates Angiogenesis and Apoptosis in Oxidized Low-Density Lipoprotein-Induced Preeclampsia.Frontiers in molecular biosciences · 2021Article
- The interplay of autophagy and enterovirus.Seminars in cell & developmental biology · 2020Review
- Manipulation of autophagy by (+) RNA viruses.Seminars in cell & developmental biology · 2020Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
RNA viruses modify intracellular membranes to produce replication scaffolds. In pancreatic cells, coxsackievirus B3 (CVB3) hijacks membranes from the autophagy pathway, and in vivo disruption of acinar cell autophagy dramatically delays CVB3 replication. This is reversed by expression of GFP-LC3, indicating that CVB3 may acquire membranes from an alternative, autophagy-independent, source(s). Herein, using 3 recombinant CVB3s (rCVB3s) encoding different proteins (proLC3, proLC3(G120A), or ATG4B(C74A)), we show that CVB3 is, indeed, flexible in its utilization of cellular membranes. When compared with a control rCVB3, all 3 viruses replicated to high titers in vivo, and caused severe pancreatitis. Most importantly, each virus appeared to subvert membranes in a unique manner. The proLC3 virus produced a large quantity of LC3-I which binds to phosphatidylethanolamine (PE), affording access to the autophagy pathway. The proLC3(G120A) protein cannot attach to PE, and instead binds to the ER-resident protein SEL1L, potentially providing an autophagy-independent source of membranes. Finally, the ATG4B(C74A) protein sequestered host cell LC3-I, causing accumulation of immature phagophores, and massive membrane rearrangement. Taken together, our data indicate that some RNA viruses can exploit a variety of different intracellular membranes, potentially maximizing their replication in each of the diverse cell types that they infect in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.