Here are some of the common mutations present in the
spike protein of lineage B.1.617. Not all sublineages of B.1.617 share the same mutations: •
L452R. The substitution at position 452, a
leucine-to-
arginine substitution, confer stronger affinity of the spike protein for the
ACE2 receptor and decreased recognition capability of the immune system. These mutations, when taken individually, are not unique to the variant; rather, their simultaneous occurrence is. This mutation is present in all three sublineages of B.1.617. • T478K. The substitution at position 478, a
threonine-to-
lysine substitution, is only found in lineage B.1.617.2. •
E484Q. The substitution at position 484, a
glutamic acid-to-
glutamine substitution, confers lineage B.1.617 stronger binding potential to the human
ACE2 receptor, as well as better ability to evade hosts' immune systems in comparison to other variants. This mutation is not present in the B.1.617.2 genome. •
D614G. The substitution at position 614, an
aspartic acid-to-
glycine substitution, is shared with other highly transmissible lineages like
B.1.1.7,
B.1.351 and
P.1. •
P681R. The substitution at position 681, a
proline-to-
arginine substitution, which, according to
William A. Haseltine, may boost cell-level infectivity of the variant "by facilitating cleavage of the S precursor protein to the active S1/S2 configuration". This mutation is present in all three sublineages of B.1.617. == History ==