Infection-Associated Genes of Candida Albicans

Abstract

Advances in the medical treatment of life-threatening disorders have increased the population of patients that are more susceptible to opportunistic microbial infections, such as those caused by the Candida species, in particular Candida albicans. This fungus normally belongs to the microbial flora but may cause a range of diseases from superficial to disseminated. What exactly causes the transition from commensalism to pathogenesis is not clear and how this fungus switches from a commensal mode of growth to a parasitic lifestyle remains unknown. Identifying the genes and factors essential for the different stages of C. albicans infections will not only help understanding of the infection process but also provide information about those fungal factors that have to be inhibited, and those parts of the immune system that have to be stimulated, in order to control or prevent infections. Furthermore, knowledge of those genes whose expression is associated with infection but not commensalism may provide valuable information to improve our diagnostic tools. A number of methodologies and models have already been used to identify infection-associated genes. In addition to genes encoding classical virulence determinants, such as those involved in interactions with the immune system and immune evasion, scientists have monitored the expression of genes involved in nutrient acquisition, metabolism, stress response, physical interaction and hyphal formation in infection models and have begun to elucidate the roles of these genes.

Keywords: :

• Candida albicans
• host–pathogen interactions
• hyphal formation
• immune evasion
• infection models
• metabolism
• microarrays
• nutrient acquisition
• physical interaction
• stress response
• transcriptional profiling

Acknowledgements

The author would like to thank Julian Naglik, King‘s College London, UK, and Abigail Mavor, Robert Koch-Institut, Berlin, Germany, for critical reading of the manuscript and S Thewes, Robert Koch-Institut, for useful discussions. The author apologizes to authors whose interesting data could not be included due to space constraints. The author‘s own investigations were supported by the Robert Koch-Institut, the Deutsche Forschungsgemeinschaft and the European commission.