Structure of SARS-CoV-2 Spike protein denoting location of Q677P within a disordered loop adjacent to the polybasic (furin) cleavage site (Cited from https://www.medrxiv.org/content/10.1101/2021.02.12.21251658v2.full.pdf).
This variant was first detected in samples collected in New York City in November.
On study found a steady increase (12.3%) in the detection rate from late December to mid-February in New York.
Detection of B.1.526 variant is scattered in the Northeast of US.
The variant has L5F, T95I, D253G, E484K, D614G, and A701V mutations in the spike protein.
D253G resides in the antigenic supersite within the N-terminal domain, which is a target for neutralizing antibodies.
The impact of the E484K mutation on antibody neutralization: neutralizing activities of convalescent plasma or vaccinee sera are lower by 7.7-fold or 3.4-fold, respectively, against the E484K variant (refer to the publication below).
Evaluation of susceptibility of variants identified through global surveillance and in subjects treated with bamlanivimab is ongoing. Pseudovirus harboring the E484K substitution had reduced susceptibility to bamlanivimab. E484K reduced bamlanivimab neutralization >2000-fold.
The variant was first detected in Peru in December 2020 and currently is causing eighty percent of new cases of COVID-19 in Peru.
The variant has become a dominant variant in South America and found in more than 30 countries.
The variant has been categorized as a “variant of interest” by the World Health Organization.
The researchers found that while pseudotyped virus expressing the C.37 viral spike protein was less susceptible to vaccine-elicited neutralizing antibodies. However, the reduction in neutralization was minor.
Viral transmissibility and severity have not been well characterized yet.
The variant contains a novel deletion (S:Δ247-253, located at the N-terminal domain) and G75V, T76I, D614G, L452Q, F490S, and T859N mutations in the Spike gene.
Mutations L452Q and F490S locate in the Spike protein’s receptor-binding domain.
L452R is known to be associated with increased affinity for the ACE2 receptor.
F490S has been associated with reduced in vitro susceptibility to antibody neutralization.
The variant known as Epsilon was first detected in California, USA
It has two distinct lineages, B.1.427 and B.1.429, in clade 20C
The most recent common ancestor emerged on May 20, 2020 (95% highest posterior. The branches giving rise to the B.1.427 and B.1.429 lineages were predicted to have diverged In July and June, respectively.
Increased frequency of detection from 0% to >50% of sequenced cases from September 2020 to January.
Each lineage rising in parallel in California as well as in multiple other states.
An estimated increase in transmission rate of the B.1.427/B.1.429 variant relative to circulating non-B.1.427/B.1.429 lineages was 18.6-24.2%.
A moderate resistance to neutralization by antibodies elicited by prior infection (4.0 to 6.7-fold) or vaccination (2-fold).
One person who tested positive for CAL.20C in January of this year had previously been infected with a different SARS-CoV-2 virus, in July 2020.
B.1.429 variant is defined by 5 mutations: I4205V in ORF1a; D1183Y in ORF1b: S13I, W152C and L452R in the S protein.
B.1.427 variant is defined by L452R mutation in the S protein.
L452R mutation in the S protein locates in the receptor binding domain. L452R was first detected in minks in Denmark (March 2020).
L452R mutation may stabilize the interaction between the spike protein and its human ACE2 receptor and thereby increase infectivity.
Emergence of B.1.429 containing additional mutation (Q677H) in the spike protein.
L452R mutation resulted in reduced or abolished neutralizing activity.