Wilke: Difference between revisions

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<b><font size="2" color=#ffffff>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 [[Wilke:Publications|publications]]. Interested in joining? [[Wilke:Positions|Click here.]]</font></b>  

= Recent News =

The spectrum of anti-HIV drugs was recently extended by a new class of drugs, the integrase inhibitors. The first drug of this class that received FDA approval is Raltegravir. Clinical data show that when previously untreated patients start treatment on Raltegravir, their viral load declines more rapidly than it does in patients who take instead the reverse-transcriptase inhibitor Efavirenz. This spring, Antiviral Therapy published a modeling study by [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2980788/ 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 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2290747 Proc. Natl. Acad. Sci. USA].

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