Nutritional immunity: targeting fungal zinc homeostasis

Transition metals, such as Zn(2+), are essential dietary constituents of all biological life, including mammalian hosts and the pathogens that infect them. Therefore, to thrive and cause infection, pathogens must successfully assimilate these elements from the host milieu. Consequently, mammalian immunity has evolved to actively restrict and/or pool metals to toxic concentrations in an effort to attenuate microbial pathogenicity - a process termed nutritional immunity. Despite host-induced Zn(2+) nutritional immunity, pathogens such as Candida albicans, are still capable of causing disease and thus must be equipped with robust Zn(2+) sensory, uptake and detoxification machinery. This review will discuss the strategies employed by mammalian hosts to limit Zn(2+) during infection, and the subsequent fungal interventions that counteract Zn(2+) nutritional immunity.