Fungal pathogens now account for an unprecedented burden on human health. Like all microorganisms, these fungi must successfully forage for essential micronutrients such as zinc in order to proliferate. However, pathogenic microbes face an additional hurdle in securing zinc from their environment: the action of host nutritional immunity which strictly manipulates microbial access to this essential, but also potentially toxic trace metal. This review introduces the relevant pathogenic species and goes on to cover the molecular mechanisms of zinc uptake by human fungal pathogens. Fungi scavenge zinc from their environment via two basic mechanisms: via a family of cellular zinc importers—the ZIP transporters; and via a unique secreted zinc binding protein—the zincophore. However the genetic requirement of these systems for fungal virulence is highly species-specific. As well as zinc scarcity, potential intoxification with this heavy metal can occur and, unlike bacteria, fungi deal with environmental insult this via intraorganellar compartmentalization. Zinc availability also modulates the morphogenic behavior of a subset of pathogenic yeast species. This chapter will cover these different aspects of zinc availability on the physiology of human fungal pathogens with emphasis on the major pathogenic species Candida albicans.

真菌病原体现在对人类健康造成了前所未有的负担。像所有微生物一样，这些真菌必须成功地觅食锌等必需的微量营养素才能繁殖。然而，病原微生物在从环境中保护锌方面面临另一个障碍：宿主营养免疫的作用，它严格控制微生物获取这种必需的但也可能有毒的微量金属。这篇综述介绍了相关的病原菌种类，并继续介绍了人类真菌病原体吸收锌的分子机制。真菌通过两种基本机制从环境中清除锌：通过一系列细胞锌输入物 - ZIP 转运蛋白；并通过一种独特的分泌锌结合蛋白——锌载体。然而，这些系统对真菌毒力的遗传要求具有高度的物种特异性。除了锌缺乏外，这种重金属还可能引起潜在的中毒，并且与细菌不同，真菌通过细胞内分隔来处理环境污染。锌的可用性还调节一部分致病酵母物种的形态发生行为。本章将涵盖人类真菌病原体生理学中锌可用性的这些不同方面，重点是主要的病原体物种白色念珠菌。