This week we profile a recent publication in the Journal of Infectious Disease from Dr. Alexander Greninger
and Amanda Casto (pictured) at the University of Washington Department of Laboratory Medicine.
The Greninger lab is interested in genomic and proteomic informed approaches to infectious diseases. That means we need some viral genomes to understand what we’re dealing with, i.e., diversity, evolution, recombination, etc, before moving on to making sure the genes are in the right place before we can get to more fun functional studies. For the last 3 years, we’ve focused on HSV-1, HSV-2, HHV-6, and the human parainfluenzaviruses and coronaviruses because these were relatively undersequenced and honestly understudied relative to their burden. This story is straight out of the genomic surveillance of HSV-1 and HSV-2. It’s been recently recognized that most circulating HSV-2 bears genomic scars of ancient recombination with HSV-1 as HSV-2 adapted to the human lineage from a zoonotic jump a little over a million years ago. This study significantly expands the range of HSV-1 and HSV-2 and, most importantly, shows that it is still occurring today. This is important because of the changing ecology of HSV — there’s significantly relatively more genital HSV-1 today, giving a higher chance for them to occupy the same niche and then recombine — and because of efforts to make attenuated HSV-2 vaccines or use attenuates HSV in oncolytic virus therapy — similar to poliovirus where the attenuated vaccine strain can recombine to make a less attenuated virus.
The next steps are to understand how this recombination affects HSV-2 biology, both in a culture dish and in in vivo models. This work was supported by the Department of Laboratory Medicine at the University of Washington.
