Title | Metabolic principles of persistence and pathogenicity in Mycobacterium tuberculosis. |
Publication Type | Journal Article |
Year of Publication | 2018 |
Authors | Ehrt S, Schnappinger D, Rhee KY |
Journal | Nat Rev Microbiol |
Volume | 16 |
Issue | 8 |
Pagination | 496-507 |
Date Published | 2018 08 |
ISSN | 1740-1534 |
Keywords | Energy Metabolism, Host-Pathogen Interactions, Humans, Mycobacterium tuberculosis, Tuberculosis, Virulence |
Abstract | Metabolism was once relegated to the supply of energy and biosynthetic precursors, but it has now become clear that it is a specific mediator of nearly all physiological processes. In the context of microbial pathogenesis, metabolism has expanded outside its canonical role in bacterial replication. Among human pathogens, this expansion has emerged perhaps nowhere more visibly than for Mycobacterium tuberculosis, the causative agent of tuberculosis. Unlike most pathogens, M. tuberculosis has evolved within humans, which are both host and reservoir. This makes unrestrained replication and perpetual quiescence equally incompatible strategies for survival as a species. In this Review, we summarize recent work that illustrates the diversity of metabolic functions that not only enable M. tuberculosis to establish and maintain a state of chronic infection within the host but also facilitate its survival in the face of drug pressure and, ultimately, completion of its life cycle. |
DOI | 10.1038/s41579-018-0013-4 |
Alternate Journal | Nat Rev Microbiol |
PubMed ID | 29691481 |
PubMed Central ID | PMC6045436 |
Grant List | R01 AI063446 / AI / NIAID NIH HHS / United States U19 AI111143 / AI / NIAID NIH HHS / United States |
Submitted by wcm_microbiolog... on October 30, 2018 - 3:28pm