Recently, global media has been abuzz with news and speculation about a new variant of SARS-CoV-2, the virus responsible for COVID-19.
The variant, which researchers first identified in the U.K., is called B.1.1.7, though as scientists began to express concern about it, initial U.K. government documents dubbed it VUI – 202012/01, standing for “the first variant under investigation in December 2020.”
Later government documents from December designated it as a “variant of concern,” and referred to it as VOC 202012/01.
B.1.1.7 was first spotted in the U.K. in September 2020. It began to draw attention from the scientific community and governmental authorities in early December, when the U.K. health secretary, Matt Hancock, suggested that it was spreading fast and likely contributing to the rising number of SARS-CoV-2 infections in the outh of England.
Now, at the time of this article’s publication, the new variant has been spotted in at least 33 countries.
But why is this variant of so much interest to scientists, public health organizations, and the public at large? In this Special Feature, we review what we know so far about B.1.1.7 and look into the questions that scientists are still trying to answer.
Below, we explore what viral mutations are, how they relate to the development of new viral strains, and whether the new SARS-CoV-2 variant identified in the U.K. is a cause for concern.
Also, MNT have been in touch with Pfizer and the National Institute of Allergy and Infectious Diseases (NIAID) to find out whether the COVID-19 vaccines currently available in the United States and Europe will be effective against B.1.1.7. Learn what they had to tell us.
Why do viruses mutate?
Viruses are prone to mutations. Indeed, all genetic material, including that of humans, can mutate when mistakes occur during replication.
A mutation of a virus occurs when there is a change in its genetic sequence. This creates variation and drives virus evolution.
Mutations lead to changes in the proteins that are encoded in the viral genetic code. These changes can either be advantageous, harmful, or neutral.
How many mutations does it take to produce a new strain of the virus? This is not easy to answer, in part because scientists disagree about the definition of the word “strain.”
In general, if a virus has enough mutations to make its biology significantly different, it may be a considered new strain. This means that it may respond differently to vaccines or treatments, or it may infect a different species or transmit in a different way.
But if the biology of the virus broadly remains the same, despite the mutations, the term “variant” may be more scientifically accurate.
Since the start of the pandemic, there has been much discussion about SARS-CoV-2 mutations and what implications they may have.
SARS-CoV-2, like many other coronaviruses, has an enzyme that proofreads its genetic code during replication, reducing the rate of mutations.
While the novel coronavirus has a relatively stable genome, compared with other types of virus, it does mutate sometimes, and scientists have closely monitored these changes.
One of the most widely talked about mutations has resulted in the D614G variant. This causes a change in the spike protein, which interacts with the ACE2 receptor on human cells to facilitate viral entry.
Specifically, an amino acid in the spike protein at position 614 is changed from aspartic acid to glycine.
Research by Dr. Bette Korber, from the Los Alamos National Laboratory, in New Mexico, and colleagues suggests that this change allows the variant to infect people more easily.
The D614G variant has become the predominant variant of SARS-CoV-2 worldwide, the research shows.
The team’s data indicate that people with the D614G variant of the virus may have higher levels of viral RNA than people with the original variant. But no evidence indicates that this causes more severe COVID-19.
Still, not all scientists agree with this group’s interpretation. Referring to the paper, Dr. Nathan Grubaugh, from the Yale School of Public Health, in New Haven, CT, and colleagues commented that more research is needed to support the idea that this variant is indeed more transmissible.
While researchers continue to study the differences between the D and G variants, the world has turned its focus toward B.1.1.7 and how it may shape the course of the pandemic.
B.1.1.7 and the founder effect
The B.1.1.7 variant has 23 mutations. Six cause no change in the amino acid sequence of the virus. Of the remaining 17 mutations, eight affect the spike protein.
The N501Y change, which involves a switch from asparagine to tyrosine at position 501, is located in the receptor-binding domain of the spike protein. This is a crucial section, as it interacts directly with the ACE2 receptor.
Another mutation in the RNA that encodes the spike protein allows researchers to detect this variant in polymerase chain reaction (PCR) test samples. This is because the mutation lies in one of the targeted areas that many diagnostic PCR tests use.
These tests also use other targets, usually a combination of at least two. Scientists can look for PCR tests that are negative for the spike sequence but positive for the other targets. This would indicate that the person has the B.1.1.7 variant of the SARS-CoV-2 virus.
Researchers from Public Health England used this method to track the spread of the variant in the British population and estimate how its transmissibility compared with those of earlier variants.
But studying how easily a virus transmits from one person to another is technically challenging. Epidemiological data can provide models, and laboratory investigations into the dynamics of infection can uncover more detail. Such studies are ongoing.
Some scientists have called into question whether the B.1.1.7 variant has a higher rate of transmissibility, suggesting that the high numbers of these cases of infection may result from the founder effect.
The founder effect is a term used by scientists who study evolution. It stipulates that a small group of individuals can give rise to a new population.
In the context of viruses, the founder effect could explain how B.1.1.7 has spread so rapidly. Researchers have suggested that superspreading events and a rise in rates of infection throughout England may be the reason for such large numbers of infections with the B.1.1.7 variant.
We spoke to two experts about this.
“While this was initially thought possible when the variant was first identified in September, the evidence has increasingly shown this to be unlikely and has now been largely ruled out,” Prof. Martin Hibberd, a professor of emerging infectious disease at the London School of Hygiene and Tropical Medicine (LSHTM), in the U.K., told us.
Prof. Jonathan Stoye, a group leader at The Francis Crick Institute, in London, whose lab studies virus-host interactions, echoed this sentiment. “Initially I thought this might be the case,” he noted, adding:
“Though it might make some contribution to the initial spread of the new variant, it seems unlikely to explain the greatly increased case incidence, given the simultaneous increase in the proportion of the variant in multiple settings. Rather, it would appear likely that higher levels of virus release, perhaps resulting from the infection of more cells, lead to higher rates of virus transmission.” – Prof. Jonathan Stoye