Several independent studies have recently converged upon the conclusion that the human bacterial pathogen Mycobacterium tuberculosis encounters copper during infections. At least three independently regulated pathways respond to excess copper and are required for the full virulence of M. tuberculosis in animals. In this review, I will discuss the functions of the best-characterized copper-responsive proteins in M. tuberculosis, the potential sources of copper during an infection, and remaining questions about the interface between copper and tuberculosis.
Keywords: Mycobacterium tuberculosis; bacterial pathogenesis; copper; gene regulation; infectious disease; virulence.
© 2015 by The American Society for Biochemistry and Molecular Biology, Inc.