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Mechanisms of SARS-CoV-2 evolition revealing vaccine-resistant mutations…
Mechanisms of SARS-CoV-2 evolition revealing vaccine-resistant mutations in Europe and America
Wang R, Chen J, Wei G-W. 2021. Mechanisms of SARS-CoV-2 Evolution Revealing Vaccine-Resistant Mutations in Europe and America. J Phys Chem Lett. 12(49):11850–11857. doi:10.1021/acs.jpclett.1c03380.
The primary method used to identify SARS-CoV-2 (COV2) has been the spike (S) protein, coded for by the S gene.
Rapid antibody tests and vaccines rely on the S protein.
As viruses are want to do, COV2 mutated into varients.
The Y449S and N501Y varients have mutated their S gene.
They are less virulent, but they are also blind to preconceived defenses and screening.
Imparting issues on monoclonal antibody tests and vaccines.
Among ~29 genes.
By interacting with host cell transmembrane proteases to bind the S protein to angiotensin converting ezyme 2 (ACE2) on the host cells.
Which is why we build antibodies against the S protein, with or without vaccination.
The specific target on S protein, the receptor-binding domain (RBD) is a key to forming this bond.
The better this RBD and ACE2 bind, the stronger the infectivity.
Building the imperitive for the increased understanding of understandings behind the evolution of COV 2.
This is our indicator of infectivity, transmission, and future variants.
Conversely, the worse the interaction between RBD and antibodies, the more resistant the strain would be considered.
The more prevalent forms of COV2 tend to have a mutation at at least the 452 or 501 residues of S RBD.
Not only did we predict these residues, but we predicted the majority of the 100 most common variants.
The chance that all these variants evolving to increase their infectivity in this way convergently is astronomically low.
Which supports that infectivity in new variants is under natural selection.
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The drivers of mutation behind these varients has been broken down into three categories.
Molecular Scale Processes
The major contributors include: viral recombination, insertsion, deletion, transcriptional or translational errors, viral proofreading, and viral recombination.
The complexity of elucidating viral evolution and transmission is compounded by these, and more, processes of mutagenesis.
Population Scale Processes
Viruses, despite not technically meeting the requirements to be "alive," are still subject to the effects of natural selection.
Organism Scale Processes
Most likely contributions are induced by adaptive immune processes in the host and host-virus recombination.