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The T-even phages, T2, T4, and T6, were used as model systems for the study of virus multiplication.
RNA interference is a defense response against virus multiplication.
Inhibition of RdRP activity will prevent genome replication and virus multiplication.
The first successes were obtained embarking from the principle of pathogen-derived resistance (PDR) by transforming host plants with viral genes or sequences with the purpose to block a specific step during virus multiplication in the plant.
Transcripts were used to infect tobacco plants for virus multiplication.
Virus-associated cell damages were analyzed in relation with virus multiplication.
Both viral proteins prevent premature insect cell death and thereby promote virus multiplication.
Furthermore, we also analysed the relationship between virus multiplication and virulence in each accession separately.
It might be speculated that the highly host-virus specific effects of virus infection require different threshold levels of virus multiplication, so that a relationship between virus multiplication and virulence would not occur.
A positive correlation between virus multiplication and virulence was found, though, for a small number of the analysed accessions.
In these interactions characterised by unique symptoms, virus multiplication in the infected plant and virulence were unrelated.
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