In September of 2020 a new lineage of SARS-CoV-2, known as B.1.1.7, was discovered in the United Kingdom. This lineage was found to have developed 14 lineage-specific amino acid replacements and 3 deletions prior to its discovery. It appears that the B.1.1.7 is now evolving at a rate similar to other SARS-CoV-2 lineages which have a rate of mutation of about one to two mutations per month (Duchene et al. 2020).

One of the mutations associated with this lineage is a N501Y in the spike protein of the virus. It is believed that this mutation is able to increase the spike protein’s affinity for the host ACE2 receptor (Starr et al. 2020) and it has been associated with increased infectivity and virulence (Gu et al. 2020). B.1.1.7 viruses have also been shown to have a P681H mutation in the cleavage site of spike protein. This location is one of the residues that make up the furin cleavage site between S1 and S2 in spike. The S1/S2 furin cleavage site has been shown in animal models to promote viral entry into respiratory epithelial cells and transmission (Hoffmann et al. 2020; Peacock et al. 2020; Zhu et al. 2020). The spike proteins of this lineage has also been shown to have a deletion at amino acids 69-70. This mutation in the receptor binding domain of spike is a recurrent deletion that has been found in various lineages associated with SARS-CoV-2 (McCarthy et al. 2020; Kemp et al. 2020). Outside of spike, a Q27 stop mutation truncates the ORF8 protein of the virus, rendering the protein inactive. An ORF8 deletion at amino acid 382 has a mild effect on virus replication in human airway cells (Gamage et al. 2020). The B.1.1.7. lineage also has five synonymous mutations in ORF1ab and one synonymous mutation in the M gene.