Chagas disease is a neglected tropical disease caused by Trypanosoma cruzi parasites. During mammalian infection, T. cruzi alternates between an intracellular stage and extracellular stage. T. cruzi adapts its metabolism to this lifestyle, while also reshaping host metabolic pathways. Such host metabolic adaptations compensate for parasite-induced stress, but may promote parasite survival and proliferation. Recent work has demonstrated that metabolism controls parasite tropism and location of Chagas disease symptoms, and regulates whether infection is mild or severe. Such findings have important translational applications with regards to treatment and diagnostic test development, though further research is needed with regards to in vivo parasite metabolic gene expression, relationship between magnitude of local metabolic perturbation, parasite strain and disease location, and host-parasite-microbiota co-metabolism.

恰加斯病是一种被忽视的热带疾病，由克氏锥虫寄生虫引起。在哺乳动物感染期间，克氏锥虫在细胞内阶段和细胞外阶段之间交替。克氏锥虫使其新陈代谢适应这种生活方式，同时也重塑宿主的代谢途径。这种宿主代谢适应可以补偿寄生虫引起的应激，但可能促进寄生虫的存活和增殖。最近的研究表明，新陈代谢控制着寄生虫的趋向性和恰加斯病症状的位置，并调节感染是轻微还是严重。这些发现在治疗和诊断测试开发方面具有重要的转化应用，尽管还需要进一步研究体内寄生虫代谢基因表达、局部代谢扰动幅度、寄生虫菌株和疾病位置以及宿主-寄生虫-微生物群之间的关系共同代谢。