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The expansion of omics tools (e.g. genomics, transcriptomics, proteomics and metabolomics) allows for a better understanding of pathogenicity mechanisms and virulence levels of bacterial strains.
There are of course many modifications besides these few that we highlight here: the game could be altered to use diploid rather than haploid individuals or to test the results obtained under different virulence levels.
Therefore, adaptive evolution of TEV (i.e., associated with within-host fitness increases) may result in widely different virulence levels.
All isolates (with the exception of Human PMC2000) were used to infect mice and the lethal dose 50% (LD50) assay was performed to determine virulence levels.
Other studies have failed to demonstrate a clear association between phenotypic behavior, especially virulence levels, with the source of the isolates (human, animal and environmental) [24], [25].
Even when virulence levels are far from their optimal values (as is likely when there is an influenza emergence event), increased culling is predicted to shift selective pressures toward more virulent and transmissible strains.
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We speculated that, because R. africae had more intact genes than more virulent species, some of these genes may be involved in maintaining a low virulence level.
Selection on a dominant allele that confers resistance against influenza [1], [2] in a poultry population is modeled, as is the virulence level of influenza.
We model the virulence level of influenza and the selection on a dominant allele that confers resistance against influenza [1], [2] in a poultry population.
The virus evolved during the study period, undergoing shifts in its transmission mode, virulence level, and host range.
Thus, most tests of virulence evolution models have been relative, i.e., correlating virulence level with some environmental characteristic and determining if the correlation is in the right direction.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com