What is a virus variant?
Back in March as the Covid-19 pandemic began, we discussed that viruses are very simple envelopes of information. The information is DNA or RNA, the same stuff that makes up genes in the human body, and the envelope is a lipid (fat) and protein shell which serves to carry and deliver the DNA or RNA message inside. Just like in the human body, the genetic information in a virus acts as an instruction manual to properly make many new entire copies of itself. It would be as if I published a book that contained instructions for making many copies of the exact same book.
While viruses have all the information they need to replicate themselves, they don’t have the tools do it. It would be like having the book mentioned before but needing to break into a printing store to steal the copy machine, extra paper, scissors, and the binding apparatus to make more of the final product. Viruses that infect your cells basically turn them into their own personal mass-replication facilities. By hijacking many of the proteins in the cell, they make copies of their genetic material (DNA or RNA) and use our cellular machinery to read out this genetic material to make the proteins required for their viral capsid. The end result is the assembly of tons of new viruses which kill your cell upon exiting like popping a balloon by poking a hole in it from the inside.
Even though viruses aren’t technically alive because they cannot reproduce on their own, they have genetic material, just like all living things do. And all genetic material, whether in a person or a virus, is subject to a constant level of background mutation caused by ultraviolet light, errors when the DNA is copied, and other background contaminants all around us. These mutations are then passed on to future generations when a cell divides or a virus replicates. This creates the genetic diversity that makes all of the individuals of the same species unique. Just as no two humans are exactly the same, no SARS-CoV-2 viruses are either; their genomes are slightly different due to random mutation.
When we have a population of slightly different individuals, things get interesting. By random chance, some virus variants will have mutations that completely ruin their integrity- perhaps by making a key part of the viral capsid no longer able to assemble or by preventing the viral genome from being read out properly. Similarly, over time, a few individual SARS-CoV-2 viruses will come along with some advantage over the others: perhaps they can spread farther through the air, better evade your immune system, or make more copies of themselves. In that case, the new variant virus will have an advantage over its differently altered counterparts and will start to make up a larger percentage of the viral population. The new viral population is now a viral variant.
How is the B.1.1.7 variant different from SARS-CoV-2?
The B126.96.36.199 variant was first identified in the UK at the end of September, but it became particularly concerning in the beginning of December, when scientists discovered nearly half of a new surge in cases were caused by this variant. Per the logic above, this indicates that the variant must have mutations that make it more successful at reproducing.
This is exactly what scientists have found. By determining the RNA sequence of the variant, we know that it has over twenty changes in its genome compared to the original SARS-CoV-2 virus. Most of the changes affect the infamous spike protein: the large key on the virus coat that allows the virus to dock onto the ACE-2 receptors in human cells to infect them. It seems that the mutations have made the spike better at binding to the ACE-2 receptor- in other words- the viral key to get into our cells fits the lock better. This seems to make it easier for the B.1.1.7 variant to infect cells, explaining why the variant seems to be much more infectious than plain-old SARS-CoV-2.
Will the Covid-19 vaccines and other treatments work against the variant?
The answer so far, seems to be yes. Although the Covid-19 vaccines train the immune system by showing it a mug shot of the SARS-CoV-2 spike protein from the original virus, the spike protein of the B.1.1.7 variant is not different enough to confuse the immune system. In other words, while the B.1.1.7 variant can make more people sick than the original SARS-CoV-2 virus, the same treatments and vaccines should work on the variant just as well as the original. B.1.1.7 is not an entirely new virus- just a new flavor of the SARS-CoV-2 virus we’ve seen since last year.
Closing thoughts: why it is important
Viral variants are incredibly common. At the moment, there are at least three SARS-CoV-2 variants making rounds in different parts of the globe. Other viruses, such as the common influenza A virus which causes the flu, exist in over 130 different varieties, with a different variant dominating each year. As a direct result, the flu vaccine is different each year to target the variants predicted to be most common.
So far, there is much less variation in the SARS-CoV-2 virus and the variants we see will be equally combatted by the current Covid-19 vaccines being produced. Unfortunately, this might not always be the case. There is currently an escalating war being waged between the SARS-CoV-2 viruses and the human species: as we are better able to prevent or treat the spread of the SARS-CoV-2 virus, any variants arising by chance that can evade these barriers will begin to make up more of the population as vulnerable viruses are eliminated. And the more virus that is circulating (aka the more people that are infected and spreading more viral copies), the higher the chance that new mutants will appear. This means that aside from the damage the SARS-CoV-2 virus can do to any individual it infects, each infection gives the virus many more opportunities to create new variants that can better combat our virus-suppression tactics. If we do not lower infection rates, a new viral strain that will be unaffected by our vaccines could easily beat us to the punch. More than ever, it’s critical we limit the continued reproduction of SARS-CoV-2 via masks, soap and water, and Covid-19 vaccines as available.
Hannah Margolis is a postbaccalaureate researcher at the National Institutes of Health with a degree in biochemistry from Dartmouth College. She can be reached at firstname.lastname@example.org.