A new coronavirus variant B.1.1.7 is found in UK. The mutations of this strain is complex. This variant is considered an alarming one, as it might be more contagious than other variants, but there are also some uncertainties. So, this post is to explain the 23 mutations of this new variant of the COVID-19 virus for better understandings. The relation between the new COVID Vaccines and the mutation of the virus is a critical research area.
A mutation is a change in an organism’s genetic material. When a virus makes millions of copies of itself and moves from host to host, not every copy is identical. These small mutations accumulate as the virus is passed on – and copied again and again. As the virus travels within and between countries, it mutates — a reaction to evolutionary pressure from the population it “invades”. There are several ethical issues for the covid vaccines.
At present, this new variant of coronavirus is referred to as B.1.1.7 or “SARS-CoV-2 VOC 202012/01” (i.e., the first variant of concern from 2020, December). Evidence mounts: this variant is more transmissible. It has showed up with at least 23 mutations. The press often uses the terms “variant,” “strain,” “lineage,” and “mutant” interchangeably. The terms like the “UK variant”, “South African variant”, “Brazil variant”, and the original “China variant” are often used in the press to name the virus mutations.
The New COVID Variants
The UK B.1.1.7 variant, South Africa 501.v2 variant, and the Brazil E484K variants may make the vaccines ineffective but they may be less life threatening than original covid 19. The B.1.1.248 covid lineage in Brazil spreading first. The new mutant belongs to the B.1.1.248 strain has 12 mutations in the spike protein. The antibodies people develop from previous COVID-19 infections and some of the antibody drugs, don’t seem to be as effective against all these new strains. However, further studies are required. Although viruses mutate, they mutate at varying rates. One important factor, and one that is clearly an issue here, is the wider the spread, the more opportunities for mutation. Hence, the key strategy is to control the spread.
The B.1.1.7 variant
The B.1.1.7 didn’t evolve through the normal pattern of slowly incorporating mutations into its genome as it copied itself as it spread. Several mutations of this variant affect the “crown” of the corona virus – the spike proteins that are needed to penetrate the host cell. This new variant has 14 non-synonymous amino acid (AA altering) mutations, 6 synonymous (non-AA altering), and 3 deletions. Viral dynamics knowledge is essential for formulating strategies for treatment, management and epidemiological control.
Life cycle of Coronavirus COVID-19 SARS-COV-2
The B 1.1.7 Coronavirus Mutations and Genome Sequence
The coronavirus genomes are the largest of the known RNA viruses (26 to 32 kb) and are polycistronic, generating a nested set of subgenomic RNAs with common 5′ and 3′ sequences. The 5′ two-thirds of the genome consists of two large replicase open reading frames (ORFs), ORF1a and ORF1b. More than two third of the SARS-CoV-2 genome encoded by ORF1ab gene of 21,290 nucleotides at the 5’ end and in addition 6 other ORF genes including ORF3a, ORF6, ORF7a, ORF7b, and ORF8 genes and N gene at the near 3’ end.
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The S, N, M, E form the structural proteins that play a vital role in the life cycle of the viral particles. The S protein is shaped like a clove with two subunits S1 and S2 which promotes receptor binding and membrane fusion respectively. The N protein enhances viral entry and performs post-fusion cellular processes necessary for viral survival and growth in the host. The E protein promotes virion formation and viral pathogenicity while M protein forms ribonucleoproteins and mediates inflammatory responses in hosts.
The 23 Mutations of the New B.1.1.7 Coronavirus
The details of the 23 mutations of the B.1.1.7 are shown in the figure below. This new variant has 14 non-synonymous amino acid (AA altering) mutations, 6 synonymous (non-AA altering), and 3 deletions.
A mutation in the 501st position of Aspargine (N) being replaced by Tyrosine (Y) at the Receptor binding domain where the spike protein binds to the ACE receptors in the human body has increased the affinity of the spike protein to the ACE receptors. This variant has a mutation in the receptor binding domain (RBD) of the spike protein at position 501, where amino acid asparagine (N) has been replaced with tyrosine (Y). The shorthand for this mutation is N501Y, sometimes noted as S:N501Y to specify that it is in the spike protein. This variant carries many other mutations, including a double deletion (positions 69 and 70).
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Another mutation- P681H, occurs near S1/S2 cleavage site which activates the protein and makes it easier for the virus to enter into respiratory epithelial cells. Both these mutations are of utmost importance as this is the first time that both the mutations have occurred in combination.
The full significance of the mutations is yet to be determined, the main concern is the rapid rise in infections alongside this distinct variant. Mutations such as the N501Y, P681H, and the HV 69 – 70 deletion in the spike protein are most prominent for the new coronavirus variant B.1.1.7. This novel lineage requires urgent medicine and control strategies. The recent Viral evolution may favor reinfections, and the recently described spike mutations, particularly in the receptor binding domain (RBD) in SARS-CoV-2 lineages (B.1.1.7, E484K, 501.v2, D614G, N501Y, and B.1.1.248) circulating in the UK, South Africa, and most recently in Brazil, have raised concern on their potential impact in infectivity and immune escape.