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Metabolic principles of persistence and pathogenicity in Mycobacterium tuberculosis.

TitleMetabolic principles of persistence and pathogenicity in Mycobacterium tuberculosis.
Publication TypeJournal Article
Year of Publication2018
AuthorsEhrt S, Schnappinger D, Rhee KY
JournalNat Rev Microbiol
Volume16
Issue8
Pagination496-507
Date Published2018 Aug
ISSN1740-1534
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.

DOI10.1038/s41579-018-0013-4
Alternate JournalNat. Rev. Microbiol.
PubMed ID29691481
PubMed Central IDPMC6045436
Grant ListR01 AI063446 / AI / NIAID NIH HHS / United States
U19 AI111143 / AI / NIAID NIH HHS / United States

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