Evidence for adaptive evolution in the receptor-binding domain of seasonal coronaviruses OC43 and 229E
- University of Washington, United States
- Fred Hutchinson Cancer Research Center, United States
Abstract
Seasonal coronaviruses (OC43, 229E, NL63 and HKU1) are endemic to the human population, regularly infecting and reinfecting humans while typically causing asymptomatic to mild respiratory infections. It is not known to what extent reinfection by these viruses is due to waning immune memory or antigenic drift of the viruses. Here, we address the influence of antigenic drift on immune evasion of seasonal coronaviruses. We provide evidence that at least two of these viruses, OC43 and 229E, are undergoing adaptive evolution in regions of the viral spike protein that are exposed to human humoral immunity. This suggests that reinfection may be due, in part, to positively-selected genetic changes in these viruses that enable them to escape recognition by the immune system. It is possible that, as with seasonal influenza, these adaptive changes in antigenic regions of the virus would necessitate continual reformulation of a vaccine made against them.
Data availability
All data used in this study can be found at https://www.viprbrc.org/ or in the Github repository for this project: https://github.com/blab/seasonal-cov-adaptive-evolution.
Article and author information
Author details
Funding
National Science Foundation (Graduation Research Fellowship Program,DGE-1762114)
- Kathryn E Kistler
Pew Charitable Trusts (Pew Biomedical Scholar,NIH R35 GM119774-01)
- Trevor Bedford
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Copyright
© 2021, Kistler & Bedford
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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Evidence for adaptive evolution in the receptor-binding domain of seasonal coronaviruses OC43 and 229E
eLife 10:e64509.
https://doi.org/10.7554/eLife.64509
Further reading
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- Evolutionary Biology
The majority of highly polymorphic genes are related to immune functions and with over 100 alleles within a population, genes of the major histocompatibility complex (MHC) are the most polymorphic loci in vertebrates. How such extraordinary polymorphism arose and is maintained is controversial. One possibility is heterozygote advantage (HA), which can in principle maintain any number of alleles, but biologically explicit models based on this mechanism have so far failed to reliably predict the coexistence of significantly more than 10 alleles. We here present an eco-evolutionary model showing that evolution can result in the emergence and maintenance of more than 100 alleles under HA if the following two assumptions are fulfilled: first, pathogens are lethal in the absence of an appropriate immune defence; second, the effect of pathogens depends on host condition, with hosts in poorer condition being affected more strongly. Thus, our results show that HA can be a more potent force in explaining the extraordinary polymorphism found at MHC loci than currently recognised.
