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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.
To see what we are currently working on, check out our recent publications.
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 HAART1] 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 sites2] 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 Raltegravir3] 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 .