The UK Variant: What We Know and What We Don’t

This sidebar was fact-checked by Manolya Sag.

Viruses, with their large numbers and fast replication time, are always evolving. For the RNA virus SARS-CoV-2, mutations are constantly occurring during its replication. In fact, it has been estimated by the COVID-19 Genomics UK Consortium that approximately 4000 mutations have arisen in the virus’ spike protein alone. It is important to note, however, that most mutations are not as scary as they sound and will not end up having an effect on the virus or its function. This is because many either do not change the coded amino acid or the amino acid change does not have a major effect on protein function. With that said, sometimes mutations do have a larger effect and end up sticking around to cause trouble. To learn more about mutations, check out this sidebar

How it was discovered

The UK variant, also referred to as the B.1.1.7 variant or the 20B/501Y.V1 Variant of Concern (VOC) 202012/01, is thought to have first emerged in the United Kingdom in September of 2020. Towards the end of November, Kent, England was experiencing an increased number of cases compared to the rest of the country. No obvious link such as a workplace outbreak or super spreader event existed to explain these numbers. However, it is important to consider that the rapid rise could have been from the founder effect. For example, one person carrying the B.1.1.7 variant could have gone to small gathering and transmitted it to their friends who then went on to transmit it to even more people. On December 8, viral genome analysis found that approximately half of these cases were caused by a specific variant of SARS-CoV-2, the B.1.1.7 variant. As of the beginning of 2021, many countries including Canada, the United States, Australia, and Italy, have reported cases of the B.1.1.7 variant.

Note that “variant”, “lineage”, “strain”, and “mutant” are often used interchangeably by the media.

What is the B.1.1.7 variant?

This variant is characterized by 23 genomic mutations, in which 14 have caused amino acid changes and 3 have caused amino acid deletions. Additionally, 8 of these mutations affect the spike protein on the viral surface which is used by SARS-CoV-2 to enter human cells by binding to the Angiotensin-Converting Enzyme 2 (ACE2) found on the surface of our cells. 

Some of the key mutations found in the B.1.1.7 variant include:

  • N501Y – This shorthand notation refers to an amino acid replacement. Specifically, the replacement of the amino acid asparagine (N) with the amino acid tyrosine (Y) at position 501. The amino acid at position 501 is found in the receptor binding domain (RBD) of the spike protein. Because the RBD is what makes contact with the human ACE2 receptor, it allows the virus to bind more tightly to the human cell.
  • 69/70 deletion – Deletion of the amino acids at position 69 and 70 of SARS-CoV-2. It likely causes a change in the shape (conformational change) of the spike protein. Similarly, this may affect the ability of the virus to bind to human ACE2.
  • P681H – The replacement of the amino acid proline (P) with the amino acid histidine (H) at position 681. This mutation is in the spike protein and is near a cleavage site.  
  • ORF8 stop codon (Q27stop) – This mutation is not in the spike protein but in the open reading frame 8 (ORF8) gene. The function of this mutation is currently unknown.
  • N50Y1, 69/70 deletion, and p681H have all emerged spontaneously in other cases, while similar ORF8 mutations have also been seen. The significance of these independent events has not yet been determined, but likely points to these amino acid changes being beneficial to the virus in some fashion.

How is this variant different?

  • The New and Emerging Respiratory Virus Threats Advisory Group (NERVTAG) has reported that the B.1.1.7 variant is associated with a 71% increase in transmissibility. This was determined using epidemiological data, so it cannot tell us if something is biologically more transmissible due to amino acid changes.
  • NERVTAG also suggested that this variant may have a “selective advantage” over others as evidenced by its higher prevalence in a short amount of time. 
  • Currently, no evidence has been found to suggest that the B.1.1.7 variant has an impact on disease severity or mortality. NERVTAG found that there were 4 deaths per 1000 cases of this variant. 
  • It is still unknown if this variant has a different age distribution (i.e. affects children at a higher or lower rate) than others.
  • An interesting tidbit is the number of genomic mutations that this variant contains because SARS-CoV-2 has acquired approximately 1 or 2 mutations per month. One theory for the higher number of mutations is that the B.1.1.7 variant may have evolved rapidly while in a chronically infected patient. The accumulated mutations of this variant were then transmitted to someone else. 
  • There is limited information available on the specifics of this new variant and we will likely learn more as new studies are published.

Should we be worried?

  • accine – Vaccines are designed to mimic natural immunity. This means that vaccine-induced immunity produces antibodies that target many parts of the spike protein and virus (polyclonal antibodies). For a vaccine to become ineffective, there would need to be enough genomic mutations and amino acid changes that the immunity it produces no longer targets the variant. This is what happens with the seasonal influenza virus, which mutates quickly and requires a new flu vaccine to be created every year. There is a theoretical possibility that when a large amount of the population is vaccinated, this will act as a pressure that selects for variants that are not targeted by our antibodies (escape mutants). However, there is no evidence that the B.1.1.7 variant will become an escape mutant. Most scientists believe this would not happen due to the characteristics of SARS-CoV-2. 
  • Testing – Similarly to the vaccine, most polymerase chain reaction (PCR) tests that we use to detect the virus target multiple parts of the virus. Even if a mutation does affect the detection of a particular target, the virus should still be able to be detected. After all, genomic mutations are expected for a replicating virus and may actually be useful when it comes to contact tracing.


Kupferschmidt, K. (2021, January 1). Fast-spreading U.K. virus variant raises alarms. 

Interim: Implications of the Emerging SARS-CoV-2 Variant VOC 202012/01. 

NERVTAG meeting on SARS-CoV-2 variant under investigation VUI-202012/01.

Comment on recent spike protein changes. 

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