Mycobacterium tuberculosis in the face of host-imposed nutrient limitation

Interactions of bacteria with the human host are, in the vast majority of cases, beneficial for both partners (1). In fact, humans are dependent on their microbial associates for nutrition, defense, and development (1). However, a minority of bacteria use the human organism as a vessel to proliferate and spread and, as a consequence, leave behind collateral damage of varying degrees. These so-called pathogens have typically evolved to inhabit niches in the human body with little competition from their commensal counterparts (2). Many of these human pathogens are intracellular bacteria, meaning that their preferred niche of proliferation and persistence is within human cells. Intracellular pathogens invade phagocytic or nonphagocytic host cells, where they replicate in specialized phagosomal compartments or in the cytosol. After having made their way into their preferred niche, they try to benefit from host nutrients and other metabolites to satisfy their bioenergetic and biosynthetic requirements (3). The dynamic metabolic interplay between pathogen and host is essential for virulence, disease progression, and infection control.