Sentence examples for virulence would be from inspiring English sources

Complete reversion to virulence would be detected during safety testing and such lots would be eliminated, but if attenuation is enacted by the epistatic effect of multiple mutations (Burch et al. 2003), and a subset of these are lost during vaccine manufacture, then complete reversion would require fewer subsequent mutations.

A real measure of parasitoid virulence would be the number of cocoons per caterpillar per parasitoid.

A number of theories [2], [3], [4], [5], [6], [7] proposed that virulence would be maintained by natural selection and should depend on the mechanism of transmission.

In addition with selective host rotation or elimination, the effects of reducing vector population density, particularly over periods of vector migration between hosts, on virus prevalence and virulence would be enhanced.

Our results also show that the effect of vector control on virulence would be more effective in less competent hosts (Host 2), thus reducing their efficiency as reservoirs for highly competent hosts (Host 1).

If symptoms (sneezing and coughing) and transmission are coupled so the more rapid phase shifting (more virulent) bacteria are transmitted at higher rates than the more slow (benign) ones, phase shifting (virulence) would be favoured in the bacterial population.

It is logical that virulence factors would be associated with phages and related mobile elements such as genomic islands 8. Otherwise, such virulence factors would simply become extinct if the bacterium they were contained in became too virulent and killed its host.

Since campylobacterioses and reported A. butzleri-related illnesses have similar clinical outcomes [10], it might be expected that some C. jejuni virulence factors would be found in Arcobacter.

If genetic background is responsible for the increased pathogenicity towards wax moth observed in the color mutants in the B5233 background, then a different virulence pattern would be expected for color mutants in the Af293 background.

Since protein glycosylation mainly affects extracellular or surface-exposed proteins, we hypothesized that some of these virulence factors would be affected by mutations in genes affecting protein-O-mannosylation.

We hypothesised firstly that a virulence gene would be overrepresented in the hyperinvasive clonal complexes (by definition responsible for the majority of disease) and then secondly that, if the relation were causal rather than simply clonal, there would exist within the hyperinvasive complexes an association of the element with invasive disease.