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Fungal virulence

Stuck on you

Nature Reviews Microbiology volume 1, page 91 (2003)Cite this article

Candida is responsible for 8% of serious nosocomial infections in the United States. In common with other Candida species, C. glabrata usually populates mucosal surfaces, but can breach the mucosal barrier when host defences are lowered and cause life threatening systemic infections. Unlike the diploid opportunistic pathogen Candida albicans, C. glabrata is haploid, which makes genetic manipulations far more straightforward. Previous work identified an adhesin protein — Epa1 — which enables C. glabrata to stick to epithelial cells. Epa1 is a member of a large class of cell wall proteins that are found in many fungi, including Saccharomyces and Aspergillus species.

When the EPA1 gene was deleted from the chromosome, the resulting mutant lost virtually all ability to attach to epithelial cells in the lab. So, EPA1 was an excellent candidate for a virulence gene. However, when the same mutant was tested for pathogenicity in mouse models of candidiasis it was still virulent. Pathogens like C. albicans, Trypansoma brucei and Plasmodium species commonly encode families of virulence genes. So, one possible solution to this conundrum was that C. glabrata might have a family of adhesins. The hunt was on for EPA1 homologues and now De Las Peñas et al. report the characterisation of 5 homologues of EPA1 in C. glabrata.

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ORIGINAL RESEARCH PAPER

  1. De Las Peñas, A. et al. Virulence-related surface glycoproteins in the yeast pathogen Candida glabrata are encoded in subtelomeric clusters and subject to RAP1- and SIR-dependent transcriptional silencing. Genes Dev. 17, 2245–2258 (2003)

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  1. Susan Jones
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Jones, S. Stuck on you. Nat Rev Microbiol 1, 91 (2003). https://doi.org/10.1038/nrmicro762

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  • DOI: https://doi.org/10.1038/nrmicro762

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