What is it about?

Phylogenetic analysis showed that most B.1.1.7 spike variants can be linked to their direct predecessors at single amino acid alteration. In many cases the alteration resulted in loss of the key mutation which is associated to higher infectivity or many times B.1.1.7 SARS-CoV-2 evolved in less contagious forms. Occasionally, additional mutation was introduced to compensate for the missing one, that kept the spike protein fit. Isoleucine deletion at position 68 (∆I68) was found to compensate for the missing Valine deletion at position 70 (∆V70) in the commonly found ∆HV [69–70] deletion pair in one B.1.1.7 spike variant.

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Why is it important?

Main findings: 1. B.1.1.7 spike protein lost some of the key mutations associated to higher infectivity. 2. ∆I68 is supposed to compensate for missing ∆V70 in B.1.1.7 spike variant. 3. First report of V90T missense mutation. 4. V90T escapes 2–51 neutralizing antibody. 5. Novel formula for computing genetic distance.


As B.1.1.7 SARS-CoV-2 evolved in many other forms, B.1.1.7 spike protein lost some of the key amino acid mutations that are associated to the higher B.1.1.7 infectivity. Unreported V90T missense mutation in the N-terminal domain of SARS-CoV-2 spike protein was identified. V90T mutation showed positive affirmation towards escaping 2–51 neutralizing antibody. Novel function for computing phylogenetic distance was also proposed, that did better structural and evolutionary links predictions than Jaccard and Sorensen-Dice (Silhouette score analysis).

Ph.D Done Stojanov
Univerzitet Goce Delcev Stip

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This page is a summary of: Phylogenicity of B.1.1.7 surface glycoprotein, novel distance function and first report of V90T missense mutation in SARS-CoV-2 surface glycoprotein, Meta Gene, December 2021, Elsevier, DOI: 10.1016/j.mgene.2021.100967.
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