The F456L mutation of Omicron EG.5.1 : insight of the molecular mechanism

Abstract

The E.G.5.1 sub-variant, named "Eris", from the already redoubtable Omicron, has made its way into several nations, creating a new wave of uncertainty. Although its destructive potential has yet to be fully assessed by the World Health Organization (WHO), this strain may have a high potential for transmission following its appearance in 51 countries. The entry point for sarscov2 is via the angiotensin receptor, so in our study we tried to clarify the mutation that raises many questions about its impact. We used computational approaches to try and get as close as possible to an adequate answer. We found that the mutation at position 456 allowed the L456 residue to become more flexible than the F456 residue; we found that there is a 60% gain in flexibility for this variant compared to the ancestral strain. This led to a new π-σ interaction between RBD-ACE2, thus promoting affinity. This linkage advantage may explain the exponential increase in Eris transmission, but the pathogenicity remains to be assessed over the coming months. What makes this mutation unique is that it is the first time it is been seen in this position, which raises uncertainties about vaccine efficacy and viral transmissibility.