ArticlePLoS pathogens2016
Viral Replication Protein Inhibits Cellular Cofilin Actin Depolymerization Factor to Regulate the Actin Network and Promote Viral Replicase Assembly.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 58 citations in OpenAlex.
- Mobilization of nuclear antiviral factors by exportin XPO1 via the actin network inhibits RNA virus replication.PLoS pathogens · 2025Article
- Screening bacterial effectors and human virus proteins in yeast to identify host factors driving tombusvirus RNA recombination: a role for autophagy and membrane phospholipid content.Journal of virology · 2025Article
- Complex changes in serum protein levels in COVID-19 convalescents.Scientific reports · 2024Article
- Manipulation of the Cellular Membrane-Cytoskeleton Network for RNA Virus Replication and Movement in Plants.Viruses · 2023Review
- A sword or a buffet: plant endomembrane system in viral infections.Frontiers in plant science · 2023Review
- Seneca Valley Virus Enters PK-15 Cells via Caveolae-Mediated Endocytosis and Macropinocytosis Dependent on Low-pH, Dynamin, Rab5, and Rab7.Journal of virology · 2022Article
- F-actin dynamics in midgut cells enables virus persistence in vector insects.Molecular plant pathology · 2022Article
- The Characterization of the Tobacco-Derived Wild Tomato Mosaic Virus by Employing Its Infectious DNA Clone.Biology · 2022Article
- Vimentin inhibits α-tubulin acetylation via enhancing α-TAT1 degradation to suppress the replication of human parainfluenza virus type 3.PLoS pathogens · 2022Article
- Patterns of Genetic Diversity among Alphasatellites InfectingPathogens (Basel, Switzerland) · 2022Article
- Race against Time between the Virus and Host: Actin-Assisted Rapid Biogenesis of Replication Organelles is Used by TBSV to Limit the Recruitment of Cellular Restriction Factors.Journal of virology · 2022Article
- Phytosterol metabolism in plant positive-strand RNA virus replication.Plant cell reports · 2022Review
- Contribution of yeast models to virus research.Applied microbiology and biotechnology · 2021Review
- Article
- Development of a Viral RdRp-Assisted Gene Silencing System and Its Application in the Identification of Host Factors of Plant (+)RNA Virus.Frontiers in microbiology · 2021Article
- Key interplay between the co-opted sorting nexin-BAR proteins and PI3P phosphoinositide in the formation of the tombusvirus replicase.PLoS pathogens · 2020Article
- Co-opted Cellular Sac1 Lipid Phosphatase and PI(4)P Phosphoinositide Are Key Host Factors during the Biogenesis of the Tombusvirus Replication Compartment.Journal of virology · 2020Article
- Review
- Interviral Recombination between Plant, Insect, and Fungal RNA Viruses: Role of the Intracellular CaJournal of virology · 2019Article
- ScreeningProceedings of the National Academy of Sciences of the United States of America · 2019Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RNA viruses exploit host cells by co-opting host factors and lipids and escaping host antiviral responses. Previous genome-wide screens with Tomato bushy stunt virus (TBSV) in the model host yeast have identified 18 cellular genes that are part of the actin network. In this paper, we show that the p33 viral replication factor interacts with the cellular cofilin (Cof1p), which is an actin depolymerization factor. Using temperature-sensitive (ts) Cof1p or actin (Act1p) mutants at a semi-permissive temperature, we find an increased level of TBSV RNA accumulation in yeast cells and elevated in vitro activity of the tombusvirus replicase. We show that the large p33 containing replication organelle-like structures are located in the close vicinity of actin patches in yeast cells or around actin cable hubs in infected plant cells. Therefore, the actin filaments could be involved in VRC assembly and the formation of large viral replication compartments containing many individual VRCs. Moreover, we show that the actin network affects the recruitment of viral and cellular components, including oxysterol binding proteins and VAP proteins to form membrane contact sites for efficient transfer of sterols to the sites of replication. Altogether, the emerging picture is that TBSV, via direct interaction between the p33 replication protein and Cof1p, controls cofilin activities to obstruct the dynamic actin network that leads to efficient subversion of cellular factors for pro-viral functions. In summary, the discovery that TBSV interacts with cellular cofilin and blocks the severing of existing filaments and the formation of new actin filaments in infected cells opens a new window to unravel the way by which viruses could subvert/co-opt cellular proteins and lipids. By regulating the functions of cofilin and the actin network, which are central nodes in cellular pathways, viruses could gain supremacy in subversion of cellular factors for pro-viral functions.
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