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The effect of genotype (main factor) and passage number (covariable), as well as their interaction, on virulence, virus accumulation and infectivity were assessed by a model II ANOVA.
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That means high-virulence viruses do better.
In those circumstances, low-virulence viruses do best.
In terms of virulence, this virus is comparable to the H2N2 virus that caused the relatively mild pandemic of 1957 (4– 7).
Virulence of virus strains could be regulated through interaction between herd immunity, introduction of naïve individuals, and ability of virus to shed and to generate new strains [ 5].
PB1 gene encodes a polypeptide of almost 80 amino acids, with specific polymorphism and has been implicated in virulence of virus with specific polymorphism (Chen et al., 2001).
Following the previous empirical observations, the model does not consider changes in virulence and virus replicative fitness along time.
In this study, the activation of PI3K/AKT may be associated with EV71 strain virulence and virus titer.
The non-structural regions play major roles in viral replication, protein processing, virulence, and virus shedding [ 63- 66], and thus influence host immune responses [ 67].
Here, we investigated if this phenomenon was present in a plant-potyvirus system using two viruses of different virulence (Tobacco etch virus and Turnip mosaic virus).
Despite the variability in host tropism and virulence, orthopox viruses exhibit a high degree of similarity in morphology, life cycle, and structure of the assembled virus.
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