When all is said and done, I expect that 2021 will end with more good news and less news overall about coronaviruses than 2020 had. In the short term, we are going to have more epidemiology and virology to talk about. The topic most interesting to me is the new B.1.1.7 variant of SARS-CoV-2 (also known by several other alphanumeric identifiers). It was identified in December in the UK and has been found in samples taken there from as early as September. Since then it has be isolated from patients in numerous countries including the United States. Evidence suggests it is more contagious, making it worth knowing something about.
What is that evidence? Primarily it is epidemiological, meaning public health data about cases and contacts and such. Data from the UK show a tendency for contacts of cases with the B.1.1.7 variant to be more likely to become infected themselves than contacts of cases with other variants. Add in the speed at which the strain has spread in time and space and it looks likely this variant spreads more readily. Current estimates suggest about 50% more readily, which is significant but not paradigm changing. In terms of R, the reproductive number or average number of new cases from one infected person, we’re looking at something like a shift from 1.1 to 1.5. There are viruses with an R greater than 10, so this is not suddenly the most contagious virus we’ve ever seen. And masks and distancing and hand washing will still mitigate spread, bearing in mind that they have always offered relative reductions and not absolute protection.
There is also some clinical indication that patients with this variant have more virus in their upper airways, which may be at least part of the mechanism for increased infectivity; however, those data are not from controlled studies that could rule out other possibilities like the B.1.1.7 patients have been sampled at a different point in the infection cycle. Laboratory evidence also shows changes in binding and enzyme activity which may be related to infectivity as well.
At the same time, there is still a chance this variant happened to spread more readily because it just happened to be the version present at a superspreader event or two, giving it an opportunity to become abundant quickly without meaningful biological differences. Or it may have managed to move into a previously isolated network of human interaction with little or no immunity from prior exposure. At this stage in the pandemic, those scenarios are less likely, but not impossible.
We can also consider the variant from an evolutionary perspective. For that, we might need some more context. The B.1.1.7 variant is identified by a set of mutations relative to the reference genome for SARS-CoV-2 published last January. Now, not every virus particle floating around has the reference genome. Many if not most are likely to have some variation or another relative to it. That’s because mutations are occurring in every person infected by the virus. The frequency of those mutations has to do with the biochemistry of the virus’ genome replication process, which is not as accurate as our own. But different mutations are occurring in different cells and viral lineages, and so not all of them wind up in the particles that get passed onto the next person.
Some of those mutations materially reduce the virus’ ability to reproduce, maybe by changing its ability to get into cells or to spread from one person to another or by making it more susceptible to the immune system. If that reduction is significant enough, those mutations are unlikely to get copied in sufficient numbers to be spread widely, because other viruses without those mutations will reproduce faster and/or in greater numbers. This is known as negative or purifying selection.
Some of those mutations have little or no impact on the virus’ ability to reproduce. They will not get removed from the population by negative selection. Some of them will get passed on and some of them won’t, each with roughly equal probability. These neutral mutations can thus accumulate over time, a process known as drift. How quickly they accumulate is influenced by the relative frequency of neutral mutations and deleterious mutations. The more a genome can tolerate change, the more neutral mutations are available to try and the faster they will accumulate. The more constrained a genome is, the more mutations there are that will get eliminated by negative selection. Viruses with the same frequency of mutations from one generation to the next due to similar biochemistry of genome reproduction could still vary in how quickly mutations accumulate in the population because one genome may be more constrained than the other. The accumulation of mutations in the population thus provides a fairly regular rhythm to the evolution of a given virus population.
A notable feature of B.1.1.7 is that it appears to have evolved to a different rhythm. While the general population of SARS-CoV-2 viruses has been accumulating mutations at a pace of one or two a month, this variant showed up with at least 27 mutations. Some of those have been seen individually in other variants, but they had not been seen all together or accumulating together in this way. One possible explanation involves a third kind of mutation, mutations that materially increase the ability to reproduce. That could mean greater reproduction on a cellular level, or greater ability to spread from person to person, or both. Such mutations are more likely to get passed down and become widespread in the population, the process of positive selection. Now, all 17 mutations needn’t be individually advantageous, and it needn’t be the case that all 17 had to happen together or all at once to provide an advantage. More likely, one or a few increased reproduction and the rest just came along for the ride because they happened to be present when the advantageous one(s) occurred. In any event, this deviation from the rhythm of the virus’ evolution is also consistent with the claim that the B.1.1.7 variant is indeed more readily spread.