Beschreibung:
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To ensure their survival, pathogens have to adapt immediately to new environments in their hosts, for example, during the transition from the gut to the bloodstream. Here, we investigated the basis of this adaptation in a group of fungal species which are among the most common causes of hospital-acquired infections, the
<jats:italic>Candida</jats:italic>
species. On the basis of a human whole-blood infection model, we studied which genes and processes are active over the course of an infection in both the host and four different
<jats:italic>Candida</jats:italic>
pathogens. Remarkably, we found that, while the human host response during the early phase of infection is predominantly uniform, the pathogens pursue largely individual strategies and each one regulates genes involved in largely disparate processes in the blood. Our results reveal that
<jats:named-content content-type="genus-species">C. albicans</jats:named-content>
,
<jats:named-content content-type="genus-species">C. glabrata</jats:named-content>
,
<jats:named-content content-type="genus-species">C. parapsilosis</jats:named-content>
, and
<jats:named-content content-type="genus-species">C. tropicalis</jats:named-content>
all have developed individual strategies for survival in the host. This indicates that their pathogenicity in humans has evolved several times independently and that genes which are central for survival in the host for one species may be irrelevant in another.
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