ArticleScientific reports2015
Random Plant Viral Variants Attain Temporal Advantages During Systemic Infections and in Turn Resist other Variants of the Same Virus.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- CRISPR-Cas systems for plant virus management: detection, surveillance, and host resistance.Frontiers in plant science · 2026Review
- Identification of the Matrix Protein as a Conserved and Central Determinant of Superinfection Exclusion in Plant Rhabdoviruses.Molecular plant pathology · 2025Article
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- Article
- Intracellular bottlenecking permits no more than three tomato yellow leaf curl virus genomes to initiate replication in a single cell.PLoS pathogens · 2023Article
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- A Spontaneous Complementary Mutation Restores the RNA Silencing Suppression Activity of HC-Pro and the Virulence of Sugarcane Mosaic Virus.Frontiers in plant science · 2020Article
- The Matrix Protein of a Plant Rhabdovirus Mediates Superinfection Exclusion by Inhibiting Viral Transcription.Journal of virology · 2019Article
- A New Mechanistic Model for Viral Cross Protection and Superinfection Exclusion.Frontiers in plant science · 2018Review
- A self-perpetuating repressive state of a viral replication protein blocks superinfection by the same virus.PLoS pathogens · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection of plants with viruses containing multiple variants frequently leads to dominance by a few random variants in the systemically infected leaves (SLs), for which a plausible explanation is lacking. We show here that SL dominance by a given viral variant is adequately explained by its fortuitous lead in systemic spread, coupled with its resistance to superinfection by other variants. We analyzed the fate of a multi-variant turnip crinkle virus (TCV) population in Arabidopsis and N. benthamiana plants. Both wild-type and RNA silencing-defective plants displayed a similar pattern of random dominance by a few variant genotypes, thus discounting a prominent role for RNA silencing. When introduced to plants sequentially as two subpopulations, a twelve-hour head-start was sufficient for the first set to dominate. Finally, SLs of TCV-infected plants became highly resistant to secondary invasions of another TCV variant. We propose that random distribution of variant foci on inoculated leaves allows different variants to lead systemic movement in different plants. The leading variants then colonize large areas of SLs, and resist the superinfection of lagging variants in the same areas. In conclusion, superinfection resistance is the primary driver of random enrichment of viral variants in systemically infected plants.
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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.