A waxy path: Lipid dynamics during tuberculosis.

Infectious pathogens must adapt to the metabolic landscapes of their hosts, often exploiting host-derived nutrients while mitigating the stresses these resources impose. Among these challenges, host lipids are both a rich energy source and a potential liability, requiring tight regulation during infection. Mycobacterium tuberculosis, the causative agent of tuberculosis and the leading cause of death from a single infectious agent, exemplifies an extreme adaptation to lipid-rich environments. Recent studies have uncovered coordinated host and bacterial pathways that mediate fatty acid transfer, uptake, buffering, and detoxification to support intracellular survival while avoiding lipotoxicity. Concurrently, M. tuberculosis exports complex lipids that shape local immune responses and those in bystander cells. This minireview synthesizes recent advances in understanding the dynamic, bidirectional lipid interactions that define tuberculosis pathogenesis.