5 years ago

WELCOME TO THE 2011 - Harvard Initiative for Global Health ...

WELCOME TO THE 2011 - Harvard Initiative for Global Health ...

College, London) and new

College, London) and new TB drugs with colleagues in Portugal, the U.S, Canada, and Japan. He is currently the sectional-editor for tuberculosis for the journal Thorax. Dr. Khisimuzi Mdluli Developing novel regimens with reduced treatment durations for drug-sensitive and drug-resistant tuberculosis Biography: Dr. Mdluli is a Microbiologist/Molecular Biologist with pharmaceutical industry experience in antibiotic development, and anti-TB drug development in particular. He has extensive experience in early drug discovery and development with skills ranging from as early in the development pipeline as target discovery, target validation, and assay development, all the way through lead optimization to pre-clinical drug development. Dr. Mdluli has been instrumental in defining the mechanism of action for both clinically important anti-TB drugs and novel antibiotics. He has a keen interest in defining the contribution of individual drugs in clinical TB regimens. As the Director of Biology at the TB Alliance, Dr. Mdluli manages various drug development projects, including collaborations with academic scientists, pharmaceutical partners, and contract research organizations. He has successfully managed the TB Alliance- JHU Pre-Clinical Drug Combination Testing project that forms the basis for all Combination Clinical Trial regimens. Through this project, the TB Alliance has identified various novel drug combinations, some of which have achieved lasting cure in mice in less than 2 months of therapy compared to the 6 months required for the standard of care, RHZE. Some of the combinations are completely devoid of any first-line agents, making them applicable to both drug-sensitive and drug-resistant disease. Dr. Scott Podolsky The politicization of antibiotic resistance, 1948-2012 Biography: Dr. Podolsky is an assistant professor in the Department of Social Medicine and a primary care physician at Massachusetts General Hospital. Since 2006, he has served as the Director of the Center for the History of Medicine based at the Countway Medical Library. He has co-authored Generation of Diversity: Clonal Selection Theory and the Rise of Molecular Immunology (1997), authored Pneumonia before Antibiotics: Therapeutic Evolution and Evaluation in Twentieth-Century America (2006), and co-edited Oliver Wendell Holmes: Physician and Man of Letters (2009). His current research, concerning the history of antibiotics over the past half-century, looks at evolving interactions among physicians, patients, pharmaceutical companies, governmental agencies, and therapeutic reformers throughout this period. 5

LOCAL SPEAKER ABSTRACTS AND BIOGRAPHIES 1) Super-bugs? Strain-based differences in the evolution of drug resistance Christopher B. Ford, Rupal R. Shah, Michael M. Chase, Marc Lipsitch, Sarah M. Fortune Harvard School of Public Health, Biological Sciences in Public Health, Department of Immunology and Infectious Diseases Abstract: Prior to the advent of antibiotic therapy, tuberculosis was the leading cause of adult death in many parts of the world and spread was controlled by quarantine. The recent emergence of highly drug-resistant strains of Mycobacterium tuberculosis (Mtb) raises the threat of a return to the prechemotherapeutic era of TB control. Certain strains of Mtb are more commonly associated with drug resistance than others, suggesting that the physiology of the bacterium is an important determinant in the evolution of drug resistance. We demonstrate that Mtb strains from the East Asian lineage acquire drug resistances in vitro at an accelerated rate. This is due to an increased basal level of mutation as opposed to differences in target size or the ability of the organism to acquire resistance after exposure to antibiotic. Using a stochasticmutation model of drug resistance, we show that the observed difference in mutation rate can lead to a significant increase in the predicted probability of MDR arising in patients infected with East Asian strains. Our results suggest that early diagnosis is critical to restricting the evolution of drug resistance. Biography: Chris is a fifth-year graduate student in Sarah Fortune’s lab at the Harvard School of Public Health. He is applying both well-established techniques (such as fluctuation analysis) and new technologies (such as whole genome sequencing) to understand the rate at which Mtb acquires genetic mutation and the molecular mechanisms that underlie that process. 2) Translation machinery phosphorylation and alternative ribosomal proteins in Mycobacterium tuberculosis Sladjana Prisic and Robert Husson Infectious Diseases, Children’s Hospital, Boston, MA Abstract: Protein synthesis is a tightly regulated process in every living organism and is likely to be a point of control in Mycobacterium tuberculosis (Mtb) during the course of infection. Intriguingly, in our recent phosphoproteomic study, we identified phosphorylation of several ribosomal proteins in vivo. One of these proteins, the small subunit ribosomal protein S18-1, has a paralog or “alternative” ribosomal protein S18-2. The function of the four alternative ribosomal proteins and of ribosomal protein phosphorylation in mycobacteria is not known, but we predict that they play a role in controlling ribosome activity. Therefore we chose the S18-1/S18-2 pair as a model system to investigate these two putative modes of protein synthesis regulation. To begin investigating specific activities of S18 proteins, we concentrated our efforts on their role in building ribosomes. According to the Escherichia coli ribosome assembly map, S18 forms a dimer with another ribosomal protein, S6, before entering the ribosome. We hypothesized that both Mtb S18-1 and S18-2 proteins interact with S6 and possibly compete for the same binding site. Indeed, we found that S6 interacts with either S18 protein, but S18-2 showed better binding than S18-1. However, we also found that S18-1 binds zinc ions, which increases its affinity to S6 to levels comparable to the affinity of S18-2. These data suggest a model in which S18-1 is able to bind S6 in high zinc conditions, but that it may be replaced by S18-2 when zinc is deficient. In agreement with this model, we found that expression of alternative proteins in Mtb is decreased in the setting of increased zinc concentration, while S18-1 expression was stable under a wide range of conditions. Possibly helping the exchange 6

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