The pathogenic fungus Cryptococcus neoformans exhibits a striking propensity to cause central nervous system (CNS) disease in people with HIV/AIDS. Given that cryptococcal infections are generally initiated by pulmonary colonization, dissemination requires that the fungus withstand phagocytic killing, cross the alveolar–capillary interface in the lung, survive in the circulatory system and breach the blood–brain barrier. We know little about the molecular mechanisms underlying dissemination, but there is a rapidly growing list of mutants that fail to cause CNS disease. These mutants reveal a remarkable diversity of functions and therefore illustrate the complexity of the cryptococcal–host interaction. The challenge now is to extend the analysis of these mutants to acquire a detailed understanding of each step in dissemination.

病原菌新型隐球菌在 HIV/AIDS 患者中表现出显着的导致中枢神经系统 (CNS) 疾病的倾向。鉴于隐球菌感染通常是由肺部定植引起的，传播要求真菌能够经受住吞噬性杀伤，穿过肺中的肺泡 - 毛细血管界面，在循环系统中存活并突破血脑屏障。我们对传播的分子机制知之甚少，但是有一个快速增长的突变体列表，它们不会引起中枢神经系统疾病。这些突变体揭示了显着的功能多样性，因此说明了隐球菌-宿主相互作用的复杂性。现在的挑战是扩展对这些突变体的分析，以详细了解传播的每个步骤。