superinfection/brassica

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A New Mechanistic Model for Viral Cross Protection and Superinfection Exclusion.

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Plants pre-infected with a mild variant of a virus frequently become protected against more severe variants of the same virus through the cross protection phenomenon first discovered in 1929. Despite its widespread use in managing important plant virus diseases, the mechanism of cross protection

Superinfection Exclusion by p28 of Turnip Crinkle Virus Is Separable from Its Replication Function.

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We recently reported that the p28 auxiliary replication protein encoded by turnip crinkle virus (TCV) is also responsible for eliciting superinfection exclusion (SIE) against superinfecting TCV. However, it remains unresolved whether the replication function of p28 could be separated from its

A self-perpetuating repressive state of a viral replication protein blocks superinfection by the same virus.

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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

Mosaic disease induced by turnip yellow mosaic Tymovirus.

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Mosaic disease is one of the most common consequences of infection of plants by viruses. Most such mosaics include islands of dark green tissue, which are normal in appearance, contain little or no virus and are resistant to superinfection at least for a period of weeks. The mosaic pattern that

The expression, localization, and effect of a human interferon in plants.

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The ORF II of Cauliflower mosaic virus (CaMV) DNA was replaced with the human IFN alpha D coding sequence to yield a stable CaMV strain designated Ca524i. Inoculation of turnip (Brassica rapa cv "Just Right") with strain Ca524i DNA excised from plasmid pCa524i resulted in the production of

Random Plant Viral Variants Attain Temporal Advantages During Systemic Infections and in Turn Resist other Variants of the Same Virus.

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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

The Multiplicity of Cellular Infection Changes Depending on the Route of Cell Infection in a Plant Virus.

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The multiplicity of cellular infection (MOI) is the number of virus genomes of a given virus species that infect individual cells. This parameter chiefly impacts the severity of within-host population bottlenecks as well as the intensity of genetic exchange, competition, and complementation among

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