Claus Wilke was an invited speaker at the conference on Molecular Aspects of Virology, held in Mexico City in October 2016. During this conference, he was interviewed by Selene Zarate on why to study virus evolution. Watch the full interview here:
Wilke-lab graduate Stephanie Spielman was awarded the university’s 2016 Outstanding Dissertation Award. This award is the highest honor The University of Texas bestows upon its graduate students. Each year, three graduate students are honored, in three different areas. Stephanie won the award in Mathematics, Engineering, Physical Sciences, and Biological and Life Sciences, against steep competition from graduate students from all natural sciences and engineering.
While in the Wilke lab, Stephanie wrote and/or contributed to numerous publications, and she graduated this spring. She will be joining the Institute for Genomics and Evolutionary Medicine at Temple University later this summer.
Nature News reports an issue that caused a bit of a stir on social media this week, the long delays between acceptance of a paper and subsequent formal publication. The article prominently features a Tweet by Claus Wilke of an analysis showing that some publishers, in particular PLOS Computational Biology and PLOS Genetics, frequently take 60-80 days from acceptance to publication. The analysis was carried out by Daniel Himmelstein of UCSF, as he was waiting for the publication of his PLOS Computational Biology article. We are currently caught in the same situation as Daniel is, as we had a paper accepted by PLOS Computational Biology on June 11 and are now waiting for the official publication.
In this month’s issue of PLOS Pathogens, Wilke-lab postdoc Austin Meyer is publishing an article providing a fresh look at influenza hemagglutinin evolution. The influenza virus is one of the most rapidly evolving human viruses. Every year, it accumulates mutations that allow it to evade the host immune response of previously infected individuals. Which sites in the virus’ genome allow this immune escape is not entirely understood, but conventional wisdom states that specific “immune epitope sites” in the protein hemagglutinin are preferentially attacked by host antibodies and that these sites mutate to directly avoid host recognition; as a result, these sites are commonly targeted by vaccine development efforts. Our analysis has found, however, that the available epitope sites are poor predictors of which sites in influenza hemagglutinin evolve rapidly. Instead, we find that a simple geometrical model works best: Sites that are closest to the location where the virus binds the human receptor and are exposed to solvent are the primary drivers of hemagglutinin evolution. This result suggests that either the available epitope sites do not accurately represent the true influenza antigenic sites or that host immune bias may be less important for influenza evolution than commonly thought.