ArticlePLoS pathogens2016
The Lymphocytic Choriomeningitis Virus Matrix Protein PPXY Late Domain Drives the Production of Defective Interfering Particles.
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 27 papers.
What it found
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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
27 citing papers in PubMed, 41 citations in OpenAlex.
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- Bioinformatics identification of copyback and multihost-adapted defective viral genomes in dengue virus.Frontiers in cellular and infection microbiology · 2026Article
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- Polyclonal B cells acquire LCMV antigens in a GP1-dependent manner.PLoS pathogens · 2025Article
- Seoul orthohantavirus evades innate immune activation by reservoir endothelial cells.PLoS pathogens · 2024Article
- Review
- S RNA Intergenic Deletions Drive Viral Interference during Arenavirus Infections.bioRxiv : the preprint server for biology · 2023Article
- Persistent Reptarenavirus and Hartmanivirus Infection in Cultured Boid Cells.Microbiology spectrum · 2022Article
- Masitinib is a broad coronavirus 3CL inhibitor that blocks replication of SARS-CoV-2.Science (New York, N.Y.) · 2021Article
- Distinct Molecular Mechanisms of Host Immune Response Modulation by Arenavirus NP and Z Proteins.Viruses · 2020Review
- Defective Interfering Particles of Negative-Strand RNA Viruses.Trends in microbiology · 2020Review
- Article
- NEDD4 family ubiquitin ligases associate with LCMV Z's PPXY domain and are required for virus budding, but not via direct ubiquitination of Z.PLoS pathogens · 2019Article
- Defective viral genomes are key drivers of the virus-host interaction.Nature microbiology · 2019Review
- The Antiviral and Antitumor Effects of Defective Interfering Particles/Genomes and Their Mechanisms.Frontiers in microbiology · 2019Review
- Hemorrhagic Fever-Causing Arenaviruses: Lethal Pathogens and Potent Immune Suppressors.Frontiers in immunology · 2019Review
- Host-Driven Phosphorylation Appears to Regulate the Budding Activity of the Lassa Virus Matrix Protein.Pathogens (Basel, Switzerland) · 2018Article
- Viridot: An automated virus plaque (immunofocus) counter for the measurement of serological neutralizing responses with application to dengue virus.PLoS neglected tropical diseases · 2018Article
- Visualization of Arenavirus RNA Species in Individual Cells by Single-Molecule FluorescenceJournal of virology · 2018Article
- Emergency Services of Viral RNAs: Repair and Remodeling.Microbiology and molecular biology reviews : MMBR · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Arenaviruses cause severe diseases in humans but establish asymptomatic, lifelong infections in rodent reservoirs. Persistently-infected rodents harbor high levels of defective interfering (DI) particles, which are thought to be important for establishing persistence and mitigating virus-induced cytopathic effect. Little is known about what drives the production of DI particles. We show that neither the PPXY late domain encoded within the lymphocytic choriomeningitis virus (LCMV) matrix protein nor a functional endosomal sorting complex transport (ESCRT) pathway is absolutely required for the generation of standard infectious virus particles. In contrast, DI particle release critically requires the PPXY late domain and is ESCRT-dependent. Additionally, the terminal tyrosine in the PPXY motif is reversibly phosphorylated and our findings indicate that this posttranslational modification may regulate DI particle formation. Thus we have uncovered a new role for the PPXY late domain and a possible mechanism for its regulation.
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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.