Burroughs Wellcome supports Dunham's research on bacterial persistence

Woodruff Health Sciences Center | June 13, 2016

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Quinn Eastman
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qeastma@emory.edu

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The Burroughs Wellcome Fund is supporting Emory biochemist Christine Dunham's research on bacterial persistence.

The Burroughs Wellcome Fund has awarded Emory biochemist Christine Dunham, PhD, $500,000 over five years to investigate how some bacteria withstand antibiotic treatment.

Her research aims to dissect the functions of bacterial proteins that regulate "persistence," a non-replicating antibiotic-tolerant state that may cause unexplained treatment failures in the clinic.

The grant is part of the competitive Investigators in the Pathogenesis of Infectious Disease program, which was awarded to ten early-career scientists this year (in previous years, twelve).

"The Burroughs Wellcome Fund created this award to give innovative investigators the freedom and flexibility to pursue out-of-the-box approaches in understanding infectious diseases," says the Fund’s president, John E. Burris, PhD.

The Fund was founded in 1955 as the corporate foundation of the pharmaceutical firm Burroughs Wellcome. In 1993, a gift from the UK-based Wellcome Trust enabled the Fund to become fully independent from the company, now part of GlaxoSmithKline.

Dunham is assistant professor of biochemistry at Emory University School of Medicine and part of the Emory Antibiotic Resistance Center. She says the award will allow her laboratory to pursue areas of research opened up by her and her colleagues’ work on toxin-antitoxin pairs, which regulate persistence and have the potential to be antimicrobial targets.

Trained in X-ray crystallography, she is planning physiological studies to expand scientists’ understanding of how bacterial persistence is controlled and maintained.

"As an example, many toxins degrade messenger RNA, but we think that they don’t do so indiscriminately," she says. "By studying what mRNAs toxins leave intact, we can get a better understanding of how persister cells alter their resistance profiles without the need for resistance mutations, and how persister cell formation can be targeted."