Sentence examples for models of virulence from inspiring English sources

Most models of virulence evolution assume that virulence is an unavoidable consequence of within-host multiplication of parasites, resulting in trade-offs between within-host multiplication and between-host transmission fitness components.

Virus multiplication and virulence significantly varied according to the isolate x accession interaction, in agreement with the concept that phenotypes of host-parasite interactions depend on both the host and the parasite's genotypes, a concept often overlooked in models of virulence evolution [22], [23].

Although theoretical models of virulence evolution usually employ a simplified measurement of virulence, defined as the increase in host mortality due to parasite infection [5], CMV, like most plant viruses is not lethal, and its virulence cannot be quantified as the instantaneous mortality rate.

Typically, the models of virulence management are evolutionary.

Most theoretical models of virulence evolution assume that virulence arises as a direct consequence of host exploitation, the process whereby parasites convert host resources into transmission opportunities.

Therefore, genome-wide ML models of virulence have mostly been "bottom-up," blind to mechanistic knowledge, and oriented toward even smaller-genome pathogens with considerable genomic surveillance data.

In this article, Geoghegan and Holmes discuss how largely disparate research fields — theoretical modelling of virulence evolution and experimental dissection of genetic virulence determinants in laboratory model systems — can be bridged by considering real genomic data of viral evolution in a phylogenetic context.

Of the two ferric permeases, only Ftr1 is expressed when iron is limited, and FTR1 is essential in a murine bloodstream infection model of virulence [ 69].

Recognising this, several authors have argued that immunopathology is a major complication for the parasite-centric trade-off model of virulence evolution (e.g., [ 7, 18, 19]), and the implications of excessive immune responses for standard models of the evolution of virulence are now beginning to be subject to theoretical investigation (e.g., [ 20, 21]).

An additional strain (Capmr1Δ) that was severely attenuated in a mouse model of virulence was included as a control for low pathogenicity: Capmr1Δ has a weakened cell wall due to defects in O- and N-glycosylation (Bates et al., 2005).

The authors postulate that some K. pneumoniae may originate from food-animal or retail meat sources; the authors examine this link using phylogenomic methods and an animal model of virulence.