ArticleVirology2013
P-body components LSM1, GW182, DDX3, DDX6 and XRN1 are recruited to WNV replication sites and positively regulate viral replication.
Article in Virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 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
83 citing papers in PubMed, 143 citations in OpenAlex.
- A key role for the exoribonuclease XRN1 in regulating the hepatitis B viral transcriptome.iScience · 2026Article
- The Rice Stripe Virus p2 Interacts With Lsm1 and Disrupts the Lsm1-Lsm4 Complex to Facilitate the Viral infection.Molecular plant pathology · 2026Article
- DDX6 undergoes phase separation to modulate metabolic plasticity and chemoresistance.Nature communications · 2025Article
- Hijacking the Host Cell for Replication: Pro-Viral Host Factors Involved in EVA71 Infection.International journal of molecular sciences · 2025Review
- Herpes Simplex 2 Virus Depletes Cells of DEAD-Box Helicase 3 Protein by Packaging It into Virions.Viruses · 2025Article
- Emerging RNA-centric technologies to probe RNA-protein interactions: importance in decoding the life cycle of positive sense single strand RNA viruses and antiviral discovery.Frontiers in cellular and infection microbiology · 2025Review
- Review
- PRRSV hijacks DDX3X protein and induces ferroptosis to facilitate viral replication.Veterinary research · 2024Article
- Review
- The Dynamic Landscape of Capsid Proteins and Viral RNA Interactions in Flavivirus Genome Packaging and Virus Assembly.Pathogens (Basel, Switzerland) · 2024Review
- Restriction of Flaviviruses by an Interferon-Stimulated Gene SHFL/C19orf66.International journal of molecular sciences · 2022Review
- Review
- DEAD/H-Box Helicases in Immunity, Inflammation, Cell Differentiation, and Cell Death and Disease.Cells · 2022Review
- An integrative multi-omics analysis based on liquid-liquid phase separation delineates distinct subtypes of lower-grade glioma and identifies a prognostic signature.Journal of translational medicine · 2022Article
- The human DEAD-box helicase DDX3X as a regulator of mRNA translation.Frontiers in cell and developmental biology · 2022Review
- DDX3X structural analysis: Implications in the pharmacology and innate immunity.Current research in immunology · 2022Review
- Enterovirus 71 2A Protease Inhibits P-Body Formation To Promote Viral RNA Synthesis.Journal of virology · 2021Article
- Specific Interaction of DDX6 with an RNA Hairpin in the 3' UTR of the Dengue Virus Genome Mediates GJournal of virology · 2021Article
- Level of Murine DDX3 RNA Helicase Determines Phenotype Changes of Hepatocytes In Vitro and In Vivo.International journal of molecular sciences · 2021Article
- RNA Helicase DDX3: A Double-Edged Sword for Viral Replication and Immune Signaling.Microorganisms · 2021Review
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In mammalian cells, proteins involved in mRNA silencing and degradation localize to discrete cytoplasmic foci called processing or P-bodies. Here we show that microscopically visible P-bodies are greatly diminished following West Nile viral infection, but the component proteins are not depleted. On the other hand, many P-body components including LSM1, GW182, DDX3, DDX6 and XRN1, but not others like DCP1a and EDC4 are recruited to the viral replication sites, as evidenced by their colocalization at perinuclear region with viral NS3. Kinetic studies suggest that the component proteins are first released from P-bodies in response to WNV infection within 12 h post-infection, followed by recruitment to the viral replication sites by 24-36 h post-infection. Silencing of the recruited proteins individually with siRNA interfered with viral replication to varying extents suggesting that the recruited proteins are required for efficient viral replication. Thus, the P-body proteins might provide novel drug targets for inhibiting viral infection.
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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.