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Minisymposium Presentation
Mutation Count Alone does not Predict the Severity of Common Variants of SARS-CoV-2
Presenter
In 2012, Daniel Janies joined the faculty of the University of North Carolina at Charlotte as The Carol Grotnes Belk Distinguished Professor of Bioinformatics and Genomics. Dr. Janies serves as the co-Director of Computational Intelligence to Predict Health and Environmental Risks (CIPHER). Dr. Janies has also served as director of the Ribarsky Center for Visual Analytics. Dr. Janies received a Bachelor of Sciences degree in Biology from the University of Michigan in 1988 and a Ph.D. in Zoology from the University of Florida in 1995. Dr. Janies worked as a postdoctoral fellow (1996 - 1999) and a principal investigator (2000-2002) at the American Museum of Natural History in New York City where he led a team that, using off-the-shelf PC components, built one of the worlds largest computing clusters in 2001. Most recently, Dr. Janies was a tenured faculty member in the College of Medicine at the Ohio State University. Dr. Janies has served as a national principal investigator in the Tree of Life program of the National Science Foundation. Dr. Janies awards include DoD sponsored work to understand the spread of pathogens. He originated the field of mapping pathogen genetic data in concert with geography and host animals. Dr. Janies has advised the White House, the Pentagon, the Interagency Risk Assessment Consortium, and testified to both Houses of Congress on emerging infectious diseases.
Description
SARS-CoV-2 Omicron variants BA.2.86 and JN.1 have mutations that have raised concerns over their health impact. Genomic surveillance of JN.1 has shown it to be the dominant variant circulating in the USA.
Empirical studies on immune evasion and transmissibility on BA.2.86 and JN.1 are contradictory. To assess immune evasion of BA.2.86 and JN.1, we performed in silico analyses of the Receptor Binding Domain (RBD) of SARS-CoV-2 variants. We calculated the relative binding affinity of neutralizing antibodies derived from vaccinated patients, infected patients, and therapy to the RBDs. To assess transmissibility, we calculated the relative binding affinity of the RBDs to the Angiotensin Converting Enzyme-2 (ACE2) host cell receptor.
We found minor changes in some binding affinity metrics for neutralizing antibodies and ACE2 to RBDs of BA.2.86 and JN.1. However, most changes are not statistically significant. We conclude that BA.2.86 and JN.1 have inconsequential changes in immune evasion or transmissibility. We caution that genomic surveillance that counts mutations and the prevalence of a variant does not reveal the functional and health impacts of the variant. In concordance with our results, there has not been a surge on hospitals in the USA with the rise in the prevalence of BA.2.86 and JN.1.