ArticleAutophagy2014
Autophagy enhances the replication of classical swine fever virus in vitro.
Article in Autophagy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 149 citations in OpenAlex.
- Article
- Article
- Poxvirus A52 protein subverts autophagy flux by blocking autophagosome-lysosome fusion to promote viral replication.PLoS pathogens · 2026Article
- Article
- Integrated Transcriptomics Reveals a SHEV ORF3-Mediated circRNA Network That Disrupts Riboflavin Metabolism and Activates the ko05212 Pathway.Veterinary sciences · 2026Article
- Review
- VPS34-mediated autophagosome-lysosome fusion facilitates classical swine fever virus replication.Journal of virology · 2025Article
- Host-Microbe Interactions: Understanding the Mechanism of Autophagy in Viral Replication and Immune Evasion.Veterinary sciences · 2025Review
- Classical swine fever virus hijacks ESCRT-III and VPS4A to promote phagophore closure for accelerating mitophagy.Autophagy · 2025Article
- Strategies of Classical Swine Fever Immune Evasion.International journal of molecular sciences · 2025Review
- LDHA-lactate axis modulates mitophagy inhibiting CSFV replication.Journal of virology · 2025Article
- Classical Swine Fever Virus Envelope Glycoproteins EBiomolecules · 2025Article
- Transcriptome analysis of 3D4/21 cells expressing CSFV NS4B.Frontiers in microbiology · 2025Article
- The roles and mechanisms of endoplasmic reticulum stress-mediated autophagy in animal viral infections.Veterinary research · 2024Review
- Article
- IDO1 promotes CSFV replication by mediating tryptophan metabolism to inhibit NF-κB signaling.Journal of virology · 2024Article
- PKM2 induces mitophagy through the AMPK-mTOR pathway promoting CSFV proliferation.Journal of virology · 2024Article
- Inhibition of porcine deltacoronavirus entry and replication by Cepharanthine.Virus research · 2024Article
- CSFV restricts necroptosis to sustain infection by inducing autophagy/mitophagy-targeted degradation of RIPK3.Microbiology spectrum · 2024Article
- CRISPR/Cas9-mediated knockout of STAT1 in porcine-derived cell lines to elucidate the role of STAT1 in autophagy following classical swine fever virus infection.Frontiers in immunology · 2024Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy plays an important role in cellular responses to pathogens. However, the impact of the autophagy machinery on classical swine fever virus (CSFV) infection is not yet confirmed. In this study, we showed that CSFV infection significantly increases the number of autophagy-like vesicles in the cytoplasm of host cells at the ultrastructural level. We also found the formation of 2 ubiquitin-like conjugation systems upon virus infection, including LC3-I/LC3-II conversion and ATG12-ATG5 conjugation, which are considered important indicators of autophagy. Meanwhile, high expression of ATG5 and BECN1 was detected in CSFV-infected cells; conversely, degradation of SQSTM1 was observed by immunoblotting, suggesting that CSFV infection triggered a complete autophagic response, most likely by the NS5A protein. Furthermore, by confocal immunofluorescence analysis, we discovered that both envelope protein E2 and nonstructural protein NS5A colocalized with LC3 and CD63 during CSFV infection. Examination by immunoelectron microscopy further confirmed the colocalization of both E2 and NS5A proteins with autophagosome-like vesicles, indicating that CSFV utilizes the membranes of these vesicles for replication. Finally, we demonstrated that alteration of cellular autophagy by autophagy regulators and shRNAs affects progeny virus production. Collectively, these findings provide strong evidence that CSFV infection needs an autophagy pathway to enhance viral replication and maturity in host cells.
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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.