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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.
09/12/2012—A structural perspective on protein sequence evolutionThe first, published in BMC Evol. Biol., looks at broad evolutionary trends in yeast. This study shows that evolutionary rate varies linearly with relative solvent accessibility of residues (RSA, a measure for how close to the surface or the core of the protein a residue is located). Hence, more exposed residues evolve faster than more buried residues. The second study, published in Mol. Biol. Evol., uses the insight gained from the first to identify individual sites in viral protein that evolve more rapidly or more slowly than expected given their RSA. When applied to two proteins of the influenza virus, hemagglutinin and neuraminidase, this method identified sites involved in cell entry, antibody binding, and drug resistance.
06/28/2012—Bringing Molecules Back into Molecular Evolutionreviews the growing trend in the field of molecular evolution to incorporate molecular structure and function into computational work. This review is part of the popular Editor's Outlook series of the journal, where PLoS Computational Biology editors take stock of what computational biology has achieved to date and what it can hope to achieve in the near future.
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 treesnetwork 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.
Sedaghat 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.