In people with normally functioning immune systems, yeast infections, like those caused by Candida albicans, are often little more than an annoyance because the yeast is confined to the oxygen-rich areas of the body like the skin and the gut. In those with compromised immune systems, however, C. albicans can gain entry to cells and cause life-threatening systemic infections. Once inside cells the yeast is hard to target with drugs.
This week (Nature, Vol. 412, No. 6842, 05 Jul 2001; also see Nature Science Update), Michael Lorenz and Gerald Fink at the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts, report that they have identified the molecular mechanism that allows C. albicans and other yeasts to survive inside cells. Working with brewers’ yeast (Saccharomyces cerevisiae), a cousin of Candida, the researchers found that the yeast can survive inside cells by switching to an alternative metabolic mechanism: the glyoxylate cycle.
Mammalian cells don’t use this pathway so it may represent an ideal target for drugs treating systemic yeast infections. The glyoxylate cycle is also exploited by other pathogens, like the bacterium that causes tuberculosis, and the new work suggests the mechanism may be important in a number of microbial infections.
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