All bacterial populations harbor a small fraction of transiently antibiotic-tolerant cells called persisters. These phenotypic variants compromise successful antibiotic treatment because they are held responsible for the relapse of many chronic infections. In addition, studies employing experimental evolution have demonstrated that persistence contributes to the development of antibiotic resistance. Persisters are typically described as dormant cells. However, recent findings indicate a role for active mechanisms in the formation and maintenance of the persister phenotype. This review summarizes novel insights into the molecular mechanisms of persister formation and awakening, focusing on changes in cell physiology mediated by persistence effectors.
Keywords: dormancy; molecular mechanisms; persistence.
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