Persister cells and the paradox of chronic infections

Microbe

Volumn 5, Issue 10, 2010, Pages 429-437

  Lewis, Kim ^a  

^a NORTHEASTERN UNIVERSITY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

EID: 79952945215     PISSN: 15587452     EISSN: 15587460     Source Type: Journal    
DOI: 10.1128/microbe.5.429.1     Document Type: Article

References (9)

1. Balaban, N. Q., J. Merrin, R. Chait, L. Kowalik, and S. Leibler. 2004. Bacterial persistence as a phenotypic switch. Science 305:1622-1665.
2. Correia, F. F., A. D'Onofrio, T. Rejtar, L. Li, B. L. Karger, K. Makarova, E. V. Koonin, and K. Lewis. 2006. Kinase activity of overexpressed HipA is required for growth arrest and multidrug tolerance in Escherichia coli. J. Bacteriol. 188:8360-8367.
3. Dorr, T., M. Vulic, and K. Lewis. 2010. Ciprofloxacin causes persister formation by inducing the TisB toxin in Escherichia coli. PLOS Biol 8:e1000317.
4. Dubnau, D., and R. Losick. 2006. Bistability in bacteria. Mol. Microbiol. 61:564-572.
5. Hansen, S., K. Lewis, and M.K. Vulic. 2008. The role of global regulators and nucleotide metabolism in antibiotic tolerance in Escherichia coli. Antimicrob. Agents Chemother. 52:2718-2726.
6. Keren, I., N. Kaldalu, A. Spoering, Y. Wang, and K. Lewis. 2004. Persister cells and tolerance to antimicrobials. FEMS Microbiol Lett 230:13-18.
7. LaFleur, M. D., Q. Qi, and K. Lewis. 2010. Patients with long-term oral carriage harbor high-persister mutants of Candida albicans. Antimicrob. Agents Chemother. 54:39-44.
8. Lewis, K. 2007. Persister cells, dormancy and infectious disease. Nature Rev. Microbiol. 5:48-56.
9. Schumacher, M. A., K. M. Piro, W. Xu, S. Hansen, K. Lewis, and R. G. Brennan. 2009. Molecular mechanisms of HipA-mediated multidrug tolerance and its neutralization by HipB. Science 323:396-401.