With new variants appearing regularly in headlines, and many countries easing restrictions as vaccination rates rise, lead author Dr. Emma Hodcroft at the University of Bern, says the study highlights the importance of not underestimating the impact of human behavior. “20E (EU1) did not need to be more transmissible to spread rapidly across Europe, but took advantage of loosening restrictions and increasing travel,” she explains, “It’s a timely reminder that not all rises in variant frequencies are due entirely to changes in the virus.”
The study, which was coordinated across the Universities of Basel, Bern, and ETH Zürich in Switzerland, used SARS-CoV-2 sequences to trace how 20E (EU1) expanded initially in Spain, before arriving in multiple introductions with travelers to countries across Europe and spreading onward. Both laboratory work and computational modelling suggest that the mutation associated with the variant, a change in the Spike protein at position 222, does not significantly increase transmission or change antibody binding. “The transient rise in transmission rate we see with 20E (EU1) in our models is more readily explained by travel-associated behavior and demographics than an intrinsic change in the virus,” explains Professor Tanja Stadler of ETH Zürich, one of the study’s principal investigators.
Key to the study’s success was the ability to work closely with collaborators in Spain, where 20E (EU1) first expanded, rising to make up 50% of all Spanish sequences in just a few weeks last June. Professors Iñaki Comas and Fernando González Candelas, both co-authors on the paper, helped investigate the origins and initial spread of 20E (EU1) with the SeqCOVID-SPAIN consortium, responsible for generating the sequences in Spain that allowed the variant’s transmission to be mapped.
