2016 Recipient of the Victoria J. Fraser, MD Fellowship Award
November 24, 2016
The Victoria J. Fraser, M.D. Fellowship for Graduate Studies in Infectious Diseases was established with a generous donation by the Terry and Kathy Bader Family Foundation and Harry and Barbara Schukar. This donation was made in honor of Dr. Victoria J. Fraser to establish a fellowship that can be used for pre-doctoral trainees in the Infectious Diseases Division who are pursuing additional research.
Alexander Polino, BA, pre-doctoral trainee in Dr. Daniel Golberg’s laboratory, Infectious Diseases Division, recently received the Victoria J. Fraser, M.D. Fellowship Award. Using a recently developed genetic technique, the award will assist Alex in his effort to identify targets for future drug development against the malaria causing parasite, Plasmodium falciparum.
Alex grew up outside Buffalo, NY with an interest in science. He pursued a degree in Biological Sciences from Cornell Universiy in prepartaion for medical school. However, courses in bacterial pathogenesis and medical parasitology ignited his interest in microbiological research which lead him off the medical track. He pursued his interests with two years in the lab of Dr. John Parker studying mammalian orthoreovirus evasion of cell innate immune factors. This experience convinced him that he should apply to graduate schools and was drawn to Washington University by the “breadth of infectious disease research, the collaborative environment, and of course, the St. Louis-style pizza at Imo’s”. Alex joined Dr. Daniel Goldberg’s lab to do his PhD work using new reverse-genetics tools to probe the mechanisms by which the parasite Plasmodium falciparum infects human red blood cells and causes disease. Says Polino, “So far, I have had a great time learning and growing here in the Goldberg lab, and I look forward to much more of that in the years to come”.
Abstract of Alex Polino’s research plans:
“ Malaria kills nearly 500,000 people per year, the vast majority of whom are children under the age of 5 years. The symptoms of malaria are caused by infection of red blood cells by the parasite Plasmodium falciparum. Once inside the red blood cell, the parasite sends out hundreds of proteins which radically modify the host red blood cell, transforming it into an environment in which the parasite can thrive. This ability to export proteins that remodel the host red blood cell is crucial for parasite survival. As such, our lab is interested in determining how the parasite exports its proteins into the host cell. Most export-destined proteins made in the parasite carry a small export-signal. This signal is recognized by a parasite enzyme called Plasmepsin V, which cleaves the signal, sending the protein out to the host cell.
While we know that Plasmepsin V plays this critical role in protein export, how it accomplishes this task is not known. In the six months since I joined the lab, I have used a recently- developed genetic technique to show that Plasmepsin V is essential for parasite survival. Now, using this tool, I am determining which parts of the Plasmepsin V enzyme are required for parasite survival, as well as how each piece of the enzyme functions. Since Plasmepsin V is required for parasite survival, it is a promising target for the development of new antimalarial drugs. This work could help to inform that development by indicating which parts of the enzyme might serve as good targets for future drug development.”Categories: Division Announcements