ArticlePLoS pathogens2015
HCV induces the expression of Rubicon and UVRAG to temporally regulate the maturation of autophagosomes and viral replication.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.
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Who cites it
88 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Interplay between Cellular Autophagy and Hepatitis B Virus Replication: A Systematic Review.Cells · 2020Pooled it
- Ubiquitination and autophagy in host-pathogen interactions: from immune surveillance to therapeutic targeting.Nature reviews. Immunology · 2026Review
- Role of Rubicon in platelets: a promoter of thrombosis but not an autophagy repressor.Blood advances · 2026Article
- The molecular mechanisms of autophagy-virus interactions: from antiviral defense to viral counterstrategies.FEMS microbiology reviews · 2026Review
- Autophagy machinery as exploited by viruses.Autophagy reports · 2025Article
- The monkeypox virus suppresses autophagy by modulating Rubicon expression.Cell death discovery · 2025Article
- The oncolytic avian reovirus p17 protein triggers chaperone-mediated autophagy by modulating Hsp90 and the T-complex protein-1 ring complex chaperones and co-chaperones to activate the IKK/NF-κB signaling.Journal of virology · 2025Article
- Mammalian innate antiviral defenses: beyond interferon.Journal of virology · 2025Review
- A Focus on Natural Autophagy Modulators as Potential Host-Directed Weapons Against Emerging and Re-Emerging Viruses.Medicinal research reviews · 2025Review
- Shaping Viral Infection Outcomes via Organelle Remodeling.Annual review of virology · 2025Review
- Unlocking the secrets of Feline calicivirus: advances in structural and nonstructural proteins and its role as a key model for other Caliciviruses.Virology journal · 2025Review
- Human adenovirus type 7 (HAdV-7) infection induces pulmonary vascular endothelial injury through the activation of endothelial autophagy.Respiratory research · 2024Article
- Extracellular Vesicles in Viral Liver Diseases.Viruses · 2024Review
- Functional Role of Hepatitis C Virus NS5A in the Regulation of Autophagy.Pathogens (Basel, Switzerland) · 2024Review
- PRRSV non-structural protein 5 inhibits antiviral innate immunity by degrading multiple proteins of RLR signaling pathway through FAM134B-mediated ER-phagy.Journal of virology · 2024Article
- Viruses and autophagy: bend, but don't break.Nature reviews. Microbiology · 2024Review
- Regulation of Autophagosome-Lysosome Fusion by Human Viral Infections.Pathogens (Basel, Switzerland) · 2024Review
- Review
- The relationship between autophagy and respiratory viruses.Archives of microbiology · 2024Review
- Host Subcellular Organelles: Targets of Viral Manipulation.International journal of molecular sciences · 2024Review
28 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Hepatitis C virus (HCV) induces autophagy to enhance its replication. However, how HCV regulates the autophagic pathway remains largely unclear. In this report, we demonstrated that HCV infection could induce the expression of Rubicon and UVRAG, which inhibited and stimulated the maturation of autophagosomes, respectively. The induction of Rubicon by HCV was prompt whereas the induction of UVRAG was delayed, resulting in the accumulation of autophagosomes in the early time points of viral infection. The role of Rubicon in inhibiting the maturation of autophagosomes in HCV-infected cells was confirmed by siRNA knockdown and the over-expression of Rubicon, which enhanced and suppressed the maturation of autophagosomes, respectively. Rubicon played a positive role in HCV replication, as the suppression of its expression reduced HCV replication and its over-expression enhanced HCV replication. In contrast, the over-expression of UVRAG facilitated the maturation of autophagosomes and suppressed HCV replication. The HCV subgenomic RNA replicon, which expressed only the nonstructural proteins, could also induce the expression of Rubicon and the accumulation of autophagosomes. Further analysis indicated that the HCV NS4B protein was sufficient to induce Rubicon and autophagosomes. Our results thus indicated that HCV, by differentially inducing the expression of Rubicon and UVRAG, temporally regulated the autophagic flux to enhance its replication.
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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.