UGI Seminar: Steven Fiddaman 'Using archaeological samples to track the evolution of viral virulence

Speaker:                          Steven Fiddaman (Pirbright Institute)
Date & Time:                    Wednesday, 4 December 2024, at 3pm
Venue:                               HO Schild, Anatomy Medical Sciences Building (directions)

Using archaeological samples to track the evolution of viral virulence

DNA from archaeological animal remains presents an opportunity to study the pathogens that infected the host during life, as well as the animal itself. Ancient pathogen genomes give a unique insight into host-pathogen interactions, providing reference points to understand the trajectory of evolution to modern lineages. In this talk, I will discuss the power of ancient DNA analyses to understand the evolution of Marek’s Disease Virus (MDV), a highly contagious herpesvirus of chickens. Modern MDV causes widespread visceral tumours, immunosuppression and paralysis, and the chicken industry spends billions of dollars annually to control its spread. But it wasn’t always this way. When Marek’s disease was first described in the 1900s, it was a comparatively mild disease, causing some limb paralysis with low mortality. It is widely believed that an increase in the intensity of poultry production, alongside the use of leaky vaccines since the 1970s, has selected for increased virulence of MDV. To investigate the genetic changes that underlie the virulence increase, we screened ~1000 archaeological chicken bones for traces of MDV. We recovered MDV genomes from 15 Eurasian archaeological samples from the past millennium. Using a genome-wide scan for positive selection, we identified a number of genes that were selected in the branch leading to modern MDV strains. Several of these genes have previously been associated with changes in virulence. Significantly, we found that the key driver of viral oncogenesis – Meq – had undergone adaptation between ancient and modern strains. Functional comparison between reconstructed ancient Meq and modern (virulent) Meq revealed that ancient Meq is a much weaker transcriptional regulator. These data provide strong evidence for the molecular changes that underpinned the evolution of modern hypervirulent strains of MDV.