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The Wilke lab carries out research in computational evolutionary biology, bioinformatics, and biostatistics. All our research is theoretical or computational, but we frequently collaborate with experimental groups. Much of our research focuses on molecular evolution, in particular on (i) the evolution of viruses and (ii) biophysical mechanisms of protein evolution. Other areas of interest are theoretical population genetics, epidemiology, and immunology.
04/01/2012—Matthew Tien wins NSF Graduate Research FellowshipAllan Drummond's laboratory at the University of Chicago. Matthew plans to use mass spectrometry to investigate the world of mistranslated and misfolded proteins.
04/22/2011—Contact networks shape parasite evolutionary trees
The inference of population dynamics (such as the number of infected individuals as a function of time) from molecular sequence data is becoming an important new method for the surveillance of infectious diseases. We have examined how heterogeneity in host contacts shapes the genealogies of parasitic agents. We find that contact heterogeneity can have a strong effect on how the structure of genealogies reflects epidemiologically relevant quantities such as the proportion of a population that is infected. Contact heterogeneity also can increase the number of sequence isolates required to estimate these quantities over the course of an epidemic. Our results suggest that data about contact-network structure will be required in addition to sequence data for accurate estimation of a parasitic agent's genealogy. This work is published in a special issue of the journal Perspectives on Infectious Diseases focused on network perspectives on infectious disease dynamics.
03/04/2010—Universal trend of reduced RNA stability near translation-initiation sitePLoS Computational Biology.
02/24/2010—NSF funds BEACON, a Science and Technology Center in Evolutionary Biology
01/05/2010—New York Times article on lethal mutagenesiscombating viruses with lethal mutagenesis. The article features some of the work done in the Wilke lab as well as work done by our colleagues and collaborators in the Bull lab.
09/16/2009—Novel source of HIV-1 viremia in patients on HAARTWe analyzed HIV-1 sequences isolated from resting CD4+ T cells, activated CD4+ T cells, and blood plasma using a population-genetics approach. Our analysis showed that sequences from resting and activated CD4+ T cells formed a single population, whereas some of the virus in the blood plasma seemed genetically distinct from the virus in CD4+ T cells. This result shows that circulating CD4+ T cells are not the only source of residual viremia, and it suggests that a novel cellular source may contribute significantly to ongoing virus production under HAART. This research was featured by Science Daily.
06/15/2009—Translational-accuracy selection protects buried and structurally important sitesZhou et al. that correlates the location of optimal codons with sites that are important for protein structure. The study finds that there is a tendency of optimal codons to appear at structurally important sites in a wide range of organisms. The study lends further credence to the mistranslation-induced protein-misfolding hypothesis, which argues that much of the selection pressure on coding sequences stems from the toxic effects of mistranslated and misfolded proteins.
05/20/2009—HIV viral-load dynamics under RaltegravirSedaghat et al. that discusses the possible mechanisms responsible for this accelerated decline in viral load. The study argues that the accelerated decline is likely not caused by greater antiviral efficiency of Raltegravir compared to Efavirenz. Instead, because Raltegravir acts later in the viral life cycle than Efavirenz, at the beginning of Raltegravir therapy fewer cells have progressed to a state where the drug can not inhibit virus production, and hence the viral load declines faster. The study is a follow-up to a paper published in 2008 in Proc. Natl. Acad. Sci. USA.