ArticlePLoS pathogens2019
Recruitment of Vps34 PI3K and enrichment of PI3P phosphoinositide in the viral replication compartment is crucial for replication of a positive-strand RNA virus.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
36 citing papers in PubMed.
- Plant viruses tap into lipid droplet biology.The New phytologist · 2026Article
- Phosphoinositides in membrane remodeling during infections and cellular stresses.FEBS letters · 2026Review
- VPS34 inhibition as a host-targeting anti-coronaviral strategy: Rational design of YBM with optimized pharmacokinetic parameters.Acta pharmaceutica Sinica. B · 2026Article
- The MNV-1 protease-polymerase precursor cleaves a novel site in the NS1-2 protein.The Journal of general virology · 2026Article
- The diverse roles of host membranes in plant-microbe interactions.PLoS pathogens · 2026Article
- Mango pangenome reveals dramatic impacts of reference bias on population genomic analyses.Horticulture research · 2025Article
- Plant negative-strand RNA virus phosphoprotein condensates exploit host trafficking and lipid synthesis for viral factory assembly.Science advances · 2025Article
- 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
- The class III phosphatidylinositol 3-kinase VPS34 supports EV71 replication by promoting viral replication organelle formation.Journal of virology · 2024Article
- Proviral role of ATG2 autophagy related protein in tomato bushy stunt virus replication through bulk phospholipid transfer into the viral replication organelle.Molecular biology of the cell · 2024Article
- Genome-wide CRISPR/Cas9 screen identifies SLC39A9 and PIK3C3 as crucial entry factors for Ebola virus infection.PLoS pathogens · 2024Article
- The C4 photosynthesis bifunctional enzymes, PDRPs, of maize are co-opted to cytoplasmic viral replication complexes to promote infection of a prevalent potyvirus sugarcane mosaic virus.Plant biotechnology journal · 2024Article
- Subversion of selective autophagy for the biogenesis of tombusvirus replication organelles inhibits autophagy.PLoS pathogens · 2024Article
- Article
- Phosphoinositides in plant-pathogen interaction: trends and perspectives.Stress biology · 2023Review
- 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
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tombusviruses depend on subversions of multiple host factors and retarget cellular pathways to support viral replication. In this work, we demonstrate that tomato bushy stunt virus (TBSV) and the closely-related carnation Italian ringspot virus (CIRV) recruit the cellular Vps34 phosphatidylinositol 3-kinase (PI3K) into the large viral replication compartment. The kinase function of Vps34 is critical for TBSV replication, suggesting that PI(3)P phosphoinositide is utilized by TBSV for building of the replication compartment. We also observed increased expression of Vps34 and the higher abundance of PI(3)P in the presence of the tombusviral replication proteins, which likely leads to more efficient tombusvirus replication. Accordingly, overexpression of PI(3)P phosphatase in yeast or plants inhibited TBSV replication on the peroxisomal membranes and CIRV replication on the mitochondrial membranes. Moreover, the purified PI(3)P phosphatase reduced TBSV replicase assembly in a cell-free system. Detection of PI(3)P with antibody or a bioprobe revealed the enrichment of PI(3)P in the replication compartment. Vps34 is directly recruited into the replication compartment through interaction with p33 replication protein. Gene deletion analysis in surrogate yeast host unraveled that TBSV replication requires the vesicle transport function of Vps34. In the absence of Vps34, TBSV cannot efficiently recruit the Rab5-positive early endosomes, which provide PE-rich membranes for membrane biogenesis of the TBSV replication compartment. We found that Vps34 and PI(3)P needed for the stability of the p33 replication protein, which is degraded by the 26S proteasome when PI(3)P abundance was decreased by an inhibitor of Vps34. In summary, Vps34 and PI(3)P are needed for providing the optimal microenvironment for the replication of the peroxisomal TBSV and the mitochondrial CIRV.
Indexed as
Identifiers
What OpenQuestion holds
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.