A virtual infection model quantifies innate effector mechanisms and Candida albicans immune escape in human blood.

ABSTRACT: Candida albicans bloodstream infection is increasingly frequent and can result in disseminated candidiasis associated with high mortality rates. To analyze the innate immune response against C. albicans, fungal cells were added to human whole-blood samples. After inoculation, C. albicans started to filament and predominantly associate with neutrophils, whereas only a minority of fungal cells became attached to monocytes. While many parameters of host-pathogen interaction were accessible to direct experimental quantification in the whole-blood infection assay, others were not. To overcome these limitations, we generated a virtual infection model that allowed detailed and quantitative predictions on the dynamics of host-pathogen interaction. Experimental time-resolved data were simulated usi

SUBMITTER: Hunniger K 

PROVIDER: S-EPMC3930496 | biostudies-literature | 2014 Feb

REPOSITORIES: biostudies-literature