The ACS Infectious Diseases Young Investigator Award recognizes outstanding young investigators in the field of infectious diseases. The award is given by ACS Infectious Diseases and the ACS Division of Biological Chemistry. The 2018 ACS Infectious Diseases Young Investigator Award goes to Anushree Chatterjee, Principal Investigator, University of Colorado; Ting Lu, Associate Professor, University of […]

The ACS Infectious DiseasesYoung Investigator Award recognizes outstanding young investigators in the field of infectious diseases. The award is given by ACS Infectious Diseases and the ACS Division of Biological Chemistry. The 2018 ACS Infectious Diseases Young Investigator Award goes to Anushree Chatterjee, Principal Investigator, University of Colorado; Ting Lu, Associate Professor, University of Illinois; and Emily Derbyshire, Assistant Professor, Duke University.

As winners of the 2018 ACS Infectious Diseases Young Investigator Awards, Chatterjee, Lu, and Derbyshire will each receive a plaque, an award of $1,000, and up to $500 in travel reimbursement to attend the 256th ACS National Meeting & Exposition in Boston, and present at an ACS Division of Biological Chemistry symposium in their honor. The journal and the Division encourage you to attend the ACS Infectious Diseases Young Investigator Awards Symposium August 21, 2018, from 1:30-4:00 P.M. during the National Meeting in Room 153 B at the Boston Convention & Exhibition Center.

I got the chance to chat with award winners Anushree Chatterjee and Ting Lu, read on to find out more about them:

Anushree Chatterjee:

How did you get into your field of study?

I completed my Ph.D. in chemical engineering at the University of Minnesota, working with Prof. Wei-Shou Hu and Prof. Gary Dunny on understanding molecular mechanisms of antibiotic resistance transfer in the clinical superbug Enterococcus faecalis using mathematical modeling and experimentation. Before joining the Department of Chemical and Biological Engineering at the University of Colorado Boulder, I was a postdoctoral research fellow with Dr. Alan S. Perelson at the Theoretical Biology and Biophysics group at Los Alamos National Laboratory where I performed both mathematical modeling and experiments to study gene regulation and evolution of drug-resistance in Hepatitis C virus. I was and continue to be fascinated by living systems, and how dynamic they are. With more systems biology-based understanding we are now learning that infectious diseases are very dynamic and heterogeneous, whereas our therapies are slow and more static in nature. It was during my Ph.D. research working on bacteria and postdoc research working on viruses that I deeply understood the global impact of antimicrobial resistance and how underprepared we are as a human race to face this challenge. Therefore I decided to commit my career towards solving the problem of antimicrobial resistance.

What’s the most exciting discovery you’ve made in your career so far?

There have been a few; I would say three to be exact. Our lab is building a new therapeutic platform called Facile Accelerated Specific Therapeutic (FAST) for the development of novel antibiotics against multi-drug resistant (MDR) bacterial clinical isolates as well as evolving pathogens in a time scale of days. The FAST platform uses interdisciplinary approaches including synthetic biology, systems biology, synthetic chemistry, and host-pathogen infection biology to engineer exogenously delivered artificial nucleic acid-based antisense therapeutics that can target any desired gene in a pathogen-specific manner for targeted inhibition without the need for any molecular cloning. This therapeutic is very potent and kills a wide range of clinical isolates of MDR bacteria. I am also excited about another highly promising new approach invented in our lab involving the development of a unique semiconductor material-based quantum dot-antibiotic (QD ABx). The QD ABx uses stimuli such as visible light-activation to produce reactive oxygen species to kill MDR clinical bacterial isolates including methicillin-resistant Staphylococcus aureus, Klebsiella pneumoniae, and Salmonella typhimurium, and carbapenem-resistant Escherichia coli. Finally, using principles of evolutionary biology, systems biology, and synthetic biology our lab has developed an approach called “Controlled Hindrance of Adaptation of OrganismS” or “CHAOS” that can slow the evolution of antibiotic resistance by interfering with processes involved in adaptive resistance. I think all three platforms offer promise, and we now need to translate these.

What are you looking forward to most about your research?

I am looking forward towards building therapeutic platforms that can significantly accelerate drug development so that we can overcome outbreaks of infectious diseases, hopefully in “real-time” in the future. We need to understand how organisms adapt to therapies and also develop therapeutic platforms that can accelerate drug development, intelligently target these microbes to eliminate them as well as reduce the emergence of resistance, and in case there is the emergence of resistance the designed therapies should be adaptable enough to keep up with evolution. In this effort, the next steps in our lab include translating FAST and QD Abx platforms by performing pre-clinical research and working with experts to make these therapies reach the clinic. We are focusing on how can we make our therapies more effective in terms of activity, transport, and bioavailability. Our lab understands that we need to do this urgently because the antimicrobial resistance crisis is “happening now” and will only get worse. We as a human race need to catch up quickly to these smart evolving pathogens.

Ting Lu

How did you get into your field of study?

I am a physicist by training but always fascinated by biology. In my graduate study at UCSD, I was very fortunate to join the laboratories of Professor Jeff Hasty and Professor Peter Wolynes, who together brought me to bacterial, synthetic biology—the modeling, design, and construction of bacterial gene networks for functional programming. Under the guidance of Professor James Collins (Wyss Institute) and Professor Ron Weiss (MIT) as a postdoc, I advanced my research interest and further identified the focus on therapeutic applications of synthetic biology. This led me to the study on the treatment and prevention of infectious diseases.

What is the most exciting discovery you have made in your career so far?

One major focus of my research is to advance the engineering methodologies for lactic acid bacteria (LAB) and to utilize them to create designer strains for controlling infectious diseases. Recently, we developed a versatile pathway-engineering platform for LAB, which offers a systematic strategy to construct and optimize complex LAB biosynthetic pathways. With the platform, we have successfully overproduced nisin, a potent antimicrobial agent, and constructed probiotic biofilm formers that can potentially outcompete pathogens like listeria and staphylococcus species.

What are you looking forward to most about your research?

I hope to advance our current research from in vitro validation to in vivo test in animal models. I am also very keen to push the boundary of designer probiotics in general.

Editor in Chief of ACS Infectious Diseases Courtney Aldrich on Emily Derbyshire:

“Dr. Emily Derbyshire is an Assistant Professor in the Department of Chemistry at Duke University. She received her Ph.D. from Berkeley with Michael Marietta then completed a postdoc with Jon Clardy at Harvard Medical School. Dr. Derbyshire studies the fundamental biology of the liver stage of malaria infection and also develops small molecule antimalarials through innovative target- and phenotypic-based approaches.”

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