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Date:6/7/2012

Washington, DCJune 6, 2012 Anthony R. Richardson, Ph.D., Assistant Professor, Department of Microbiology & Immunology, University of North Carolina Hill School of Medicine, has been honored with one of two 2012 Merck Irving S. Sigal Memorial Awards. These awards, given annually to two young scientists to recognize and award excellence in basic research in medical microbiology and infectious diseases, are presented in memory of Irving S. Sigal, an instrumental figure in the early discovery of therapies to treat HIV/AIDS. "Richardson is a remarkably imaginative scientist whose work bridges microbial physiology, metabolism, and pathogenesis," states his nominator, William Goldman from the University of North Carolina. "His approach is interdisciplinary and mechanistic, and his work has profound implications for understanding the evolution and emergence of highly virulent pathogens."

Richardson received his B.S. in genetic and bioengineering from Purdue University, and his Ph.D. in microbiology and molecular genetics from Emory University. He completed his postdoctoral fellowship in bacterial physiology and pathogenesis at the University of Washington, where he worked in the laboratory of Ferric Fang, who described Richardson as "extremely curious, interactive, and remarkably well readan exceedingly bright and creative scientist who is poised to make major contributions to the field of bacterial pathogenesis."

Richardson's research has always been focused on the role of basic bacterial physiology in the virulence of important human pathogens. As a graduate student, he investigated the role of DNA repair in modulating immune avoidance in epidemic meningococcal meningitis. His findings showed that the rapid host-to-host spread of Neisseria meningitidis in sub-Saharan Africa during seasonal epidemics selected for strains lacking certain aspects of DNA repair. Given the nature of N. menigitidis, this resulted in bacterial populations with extremely diversified surface immunogenicity facilitating rapid adaptation to new hosts.

As a postdoctoral fellow, Dr. Richardson continued studying bacterial metabolism in the context of its interaction with host innate immunity. He showed that host-production of nitric oxide (NO), a broad-spectrum immune effector, targeted multiple metabolic enzymes inhibiting the growth of pathogenic bacteria. In contrast, he found that the human pathogen Staphylococcus aureus, unlike all other tested bacteria including coagulase negative staphylococci, was able to resist the cytotoxic effects of host NO and thrive in its presence. S. aureus NO-resistance was shown to be essential for full virulence and hinged on the ability of the bacterium to evoke a metabolic state inherently resistant to the effects of this immune radical.

In 2008, Dr. Richardson established his laboratory at the University of North Carolina at Chapel Hill, focusing on the metabolic adaptations of S. aureus to host immunitywork that was soon featured as a Science cover article. Richardson's research studies how the availability of host arginine affects the outcomes of S. aureus infections. While the host converts free arginine to NO in response to inflammatory stimuli, arginine can also be converted to a class of compounds known as polyamines under similar conditions. S. aureus can resist the effects of NO, but for unknown reasons certain species of polyamines are lethal to the pathogen. Dr. Richardson's laboratory studies the battle between the host and S. aureus over the fate of free arginine. Mark Smeltzer, University of Arkansas for Medical Sciences, calls his work "both insightful and scientifically compelling, without exception."

Richardson's late graduate mentor, Igor Stojilijkovic, summarized Richardson to Fang: "He has a big brain, but his heart is even bigger. He is one of those rare individuals who you know will make it in any endeavor he chooses to follow."


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Contact: Garth Hogan
ghogan@asmusa.org
American Society for Microbiology
Source:Eurekalert

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