ArticlePLoS pathogens2017
A self-perpetuating repressive state of a viral replication protein blocks superinfection by the same virus.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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.
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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.
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Who cites it
32 citing papers in PubMed, 55 citations in OpenAlex.
- Concepts of RNA virus evolution for the design of better antiviral countermeasures.Nature reviews. Microbiology · 2026Review
- Potyvirus HcPro Suppressor of RNA Silencing Induces PVY Superinfection Exclusion in a Strain-Specific Manner.International journal of molecular sciences · 2025Article
- Identification of the Matrix Protein as a Conserved and Central Determinant of Superinfection Exclusion in Plant Rhabdoviruses.Molecular plant pathology · 2025Article
- Article
- Natural self-attenuation of pathogenic viruses by deleting the silencing suppressor coding sequence for long-term plant-virus coexistence.PLoS pathogens · 2025Article
- Article
- Intra-Host Citrus Tristeza Virus Populations during Prolonged Infection Initiated by a Well-Defined Sequence Variant inViruses · 2024Article
- Article
- Quasispecies are constantly selected through virus-encoded intracellular reproductive population bottlenecking.Journal of virology · 2024Article
- Japanese encephalitis virus inhibits superinfection of Zika virus in cells by the NS2B protein.Journal of virology · 2024Article
- Single-cell mutation rate of turnip crinkle virus (-)-strand replication intermediates.PLoS pathogens · 2023Article
- P3 and NIa-Pro of Turnip Mosaic Virus Are Independent Elicitors of Superinfection Exclusion.Viruses · 2023Article
- Intracellular bottlenecking permits no more than three tomato yellow leaf curl virus genomes to initiate replication in a single cell.PLoS pathogens · 2023Article
- Unveil the Secret of the Bacteria and Phage Arms Race.International journal of molecular sciences · 2023Review
- Article
- Turnip crinkle virus-encoded suppressor of RNA silencing interacts with Arabidopsis SGS3 to enhance virus infection.Molecular plant pathology · 2023Article
- Developing reverse genetics systems of northern cereal mosaic virus to reveal superinfection exclusion of two cytorhabdoviruses in barley plants.Molecular plant pathology · 2022Article
- Generation of Variability inViruses · 2021Article
- Replication-Dependent Biogenesis of Turnip Crinkle Virus Long Noncoding RNAs.Journal of virology · 2021Article
- A Core35S Promoter of Cauliflower Mosaic Virus Drives More Efficient Replication of Turnip Crinkle Virus.Plants (Basel, Switzerland) · 2021Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Diverse animal and plant viruses block the re-infection of host cells by the same or highly similar viruses through superinfection exclusion (SIE), a widely observed, yet poorly understood phenomenon. Here we demonstrate that SIE of turnip crinkle virus (TCV) is exclusively determined by p28, one of the two replication proteins encoded by this virus. p28 expressed from a TCV replicon exerts strong SIE to a different TCV replicon. Transiently expressed p28, delivered simultaneously with, or ahead of, a TCV replicon, largely recapitulates this repressive activity. Interestingly, p28-mediated SIE is dramatically enhanced by C-terminally fused epitope tags or fluorescent proteins, but weakened by N-terminal modifications, and it inversely correlates with the ability of p28 to complement the replication of a p28-defective TCV replicon. Strikingly, p28 in SIE-positive cells forms large, mobile punctate inclusions that trans-aggregate a non-coalescing, SIE-defective, yet replication-competent p28 mutant. These results support a model postulating that TCV SIE is caused by the formation of multimeric p28 complexes capable of intercepting fresh p28 monomers translated from superinfector genomes, thereby abolishing superinfector replication. This model could prove to be applicable to other RNA viruses, and offer novel targets for antiviral therapy.
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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.