Jeffrey D. Dvorin, MD, PhD, assistant professor in the Division of Pediatric Infectious Diseases at Children’s Hospital Boston and Harvard Medical School, is one of two recipients of the 2011 Astellas Young Investigator Award. This award provides funding to young investigators who have demonstrated outstanding research in any area of infectious diseases.
After graduating with honors in physics from Brown University, Dr. Dvorin received his medical and doctoral (cellular and molecular biology) degrees from the University of Pennsylvania. He served as intern and resident in pediatrics at the Children’s Hospital in Philadelphia. He then completed a clinical fellowship in infectious diseases at Children’s Hospital Boston, and a research fellowship in parasitology at the Harvard School of Public Health. In 2010, he became part of the faculty at Children’s Hospital Boston and Harvard Medical School.
Dr. Dvorin’s colleagues at Children’s Hospital Boston describe him as an excellent researcher, noted for his impressive clinical knowledge base, his inquisitive approach to medicine, and his warm and enthusiastic manner. Dr. Dvorin’s aptitude for basic research and his strong interest in global health led him to work on the molecular pathogenesis of malaria during the research phase of his fellowship.
Dr. Dvorin’s research focuses on novel therapies that target fundamental life cycle steps of Plasmodium falciparum. Clinical malaria results from the exponential replication of the parasite in human red blood cells. The parasite requires efficient invasion into and egress out of human red blood cells during the blood stage of its life cycle. Dr. Dvorin has identified a plant-like calcium-dependent protein kinase, PfCDPK5, which is crucial for P. falciparum egress. When the level of this protein is decreased, the parasites remain trapped inside an infected red blood cell. The trapped parasites are unable to initiate a new round of replication. Dr. Dvorin hypothesizes that PfCDPK5 mediates an essential step in the parasite’s life cycle through phosphorylation of effector substrate proteins in response to a calcium-based egress trigger.
His proposal is to provide a molecular characterization of PfCDPK5 function with advanced genetic and cell biologic techniques. Because the egress life cycle step is not currently targeted by anti-malarials, the identification of the signaling pathway downstream of PfCDPK5 may identify new targets for malaria therapies.
Alexander Ploss, PhD, research assistant professor at Rockefeller University, is one of two recipients of the 2011 Astellas Young Investigator Award. The Astellas award provides funding to young investigators who have demonstrated outstanding research in any area of infectious diseases.
Dr. Ploss completed his doctorate in immunology in 2004 at Cornell University/Memorial Sloan-Kettering Cancer Center. He then went to the Center for the Study of Hepatitis C at The Rockefeller University to complete his postdoctoral fellowship in virology and immunology. Afterward, he became a research associate and in 2009, he was appointed as research assistant professor at the same institution.
His mentor says that Dr. Ploss has “all the qualities one looks for in a rising star: intelligence, incredible drive and energy, the ability to multitask without sacrificing quality, seamless interaction with others at all levels, and tight experimental plans that yield stellar data.”
Dr. Ploss’ research has focused on immune responses and pathogenesis to human infectious diseases, including hepatitis C virus (HCV), yellow fever virus, dengue virus, and malaria. His proposal builds on a recent breakthrough from his group—an engineered mouse that is permissive for HCV entry. The model, where human HCV entry factors are delivered either transiently or through germ line transgenesis, provides an in vivo model for studying inhibitors of the entry process, including virus-neutralizing antibodies. One block to a fully HCV permissive mouse is overcoming a low level of RNA replication that is likely a consequence of a mismatch between HCV (a highly adapted specific human pathogen) and the murine hepatocyte environment. Dr. Ploss proposes to use state-of-the-art in vivo mutagenesis approaches, coupled with capture of HCV-permissive infected cells, to identify mutations that facilitate HCV replication in the murine cell environment. His goal is to create a fully HCV-permissive mouse model.
Suzanne Noble, MD, PhD
Jennifer A. Phillips, MD, PhD
William J. Muller, MD, PhD
Manuela Raffatellu, MD
Adrianus W.M. van der Velden, PhD
Rebecca Pellett Maden, MD
Melanie J. Scott, MD, Phd, MRCSEd
Timothy Lahey, MD, MMSc
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