A variant of the pandemic coronavirus, SARS-CoV-2, is now dominating headlines and inspiring precautionary travel bans worldwide. But scientists are still trying to get a grip on what the variant can actually do differently and what it might mean for the nearly year-old pandemic.
Researchers in the United Kingdom—where the variant was identified and is now rapidly circulating—suggested it may be up to 70 percent more transmissible than other SARS-CoV-2 strains, stoking fear of surges-upon-surges of disease on the eve of year-end holidays. But other researchers are now rapidly working to collect data on the variant’s interactions with human cells and immune responses to see if those interactions differ from those seen by other SARS-CoV-2 strains.
What we know
While much remains to be known about the variant, dubbed B.1.1.7, there are some reassuring aspects. For one thing, it’s normal for viruses to accumulate the small genetic changes, such as those that created the new UK variant (more on that below). Many other variants have been identified throughout the pandemic, and none has spawned any nightmare scenarios.
So far, there’s no reason to think things will change much with the new one. There is no evidence so far that B.1.1.7 causes different or more severe COVID-19 disease; it does not appear to render COVID-19 treatments less effective, either. UK officials also suspect that the newly authorized vaccines will work just as well against the new variant, though researchers are working hurriedly to confirm that.
Together, the information at hand suggests B.1.1.7 should change little about recommended strategies to try to stamp out the pandemic, regardless of which variant is whirling through a population. “The bottom line is that we need to suppress transmission of all SARS-CoV-2 viruses as quickly as we can,” World Health Organization Director-General Tedros Adhanom Ghebreyesus said in a press briefing Monday.
It’s also important to put the increase in transmissibility in perspective. While the “up to 70 percent” figure does indeed seem alarming, the actual bump in the transmission rate is modest. In the UK, the presence of B.1.1.7 bumped the virus’ reproduction number by just 0.4—from 1.1 to 1.5, according to Maria Van Kerkhove, the WHO’s technical lead on the COVID-19 pandemic. That small increase means that the number of people each infected person goes on to infect went from an average of just over 1 person to 1.5 people. It’s unclear if this increase is due to something inherent about the virus, the behavior of people infected, or a combination of both.
A rise of 0.4 is not good news, but it is also not dramatically bad, noted Dr. Mike Ryan, executive director of the WHO’s emergencies program. A reproduction number of 1.5 can be controlled, he noted, and the reproduction number of the virus during this pandemic has been much higher at several other times.
“[This] just put the bar up a little bit,” Ryan said. “We’re not talking about a reproductive number like measles, which is somewhere between 12 and 18, or mumps and chickenpox, 10 to 12. We’re talking about 1.5. The virus may have become slightly more efficient at transmission—that can have a big impact on numbers when we have so many people being infected. But it means the virus can be contained, the virus can be suppressed [using] exactly the same interventions, exactly the same behaviors” as before.
Emphasizing the last point, Van Kerkhove elaborated that there’s no reason to think that the slight bump in transmission is because the virus has changed how spreads from one person to another—such as if it can now move farther in the air or spread more easily on surfaces. “It’s a respiratory pathogen, so it spreads between me and you through these particles in the air,” Van Kerkhove explained. “Mainly what is happening is that the virus spreads between people who are in close contact with one another. That’s still the same.”
While the WHO emphasized the similarity between B.1.1.7 and other strains of SARS-CoV-2, the UK government has been focusing on what’s new. It’s here where the strain was first identified, and most people infected with it are in the UK.
Details on the new strain became apparent because of ongoing surveillance work within the UK, where researchers randomly sequence the genomes of dozens of virus samples every month. Over the course of the pandemic, circulating strains of SARS-CoV-2 have typically picked up an average of one or two mutations a month, so this level of surveillance has been sufficient to follow the origin and spread of new strains. But B.1.1.7, first spotted in samples obtained in late September, had nothing like the sort of gradual accumulation of changes we’ve seen before. There were 17 differences between it and the most closely related known strain, giving B.1.1.7 a branch way off on its own on the coronavirus family tree.
That on its own is a curiosity, rather than a concern. What grabbed people’s attention was a correlation. In response to the winter wave of infections throughout Europe, the UK had restarted a set of social restrictions intended to bring infection levels back down. And, in most of the country, they were working as intended. But not in the southeast and east of the UK. And it was precisely that region where levels of the B.1.1.7 strain were highest; in one county, it accounted for over 20 percent of all new infections by mid-December, and that number has gone up since.
That’s not decisive evidence that the B.1.1.7 strain has any sort of advantage. The COVID-19 pandemic has been marked by many “superspreader” events, and social groups that flout public health measures. This combination can cause the rapid expansion of strains that happen to be circulating within these groups at opportune moments. But, by this weekend, B.1.1.7 was accounting for about 60 percent of the new cases in London, causing government officials there to claim that the strain can spread more rapidly.
To know this for sure, however, we’ll have to engineer the mutations found in B.1.1.7 into a lab strain, and then test its infectivity. In the mean time, scientists have looked over the mutations present in the new viral strain, and speculated on which ones could potentially be providing it with enhanced infectivity, or alter the course of infections.
Old, but in a new combination
While B.1.1.7 represents a new strain of the coronavirus, we know a fair amount about coronavirus biology, allowing us to determine when mutations alter a critical region. And, in some cases, the mutations have been found individually in different strains that we’ve characterized previously. So, it’s possible to infer some things about the behavior of B.1.1.7.
Several of them occur in the spike protein that resides on the surface of coronaviruses, and helps them latch on to a protein on the surface of cells. One of the mutations found in B.1.1.7 specifically alters part of spike that participates in this process, and has been found to increase the affinity between the viral and human proteins. Another mutation deletes two amino acids from the spike protein; this has been associated with a reduced immune response, but is typically only found in combination with other mutations (as it is here).
Finally, another mutations is next to a site where the spike protein is cut into two smaller fragments, something that’s essential for its function. While the mutation hasn’t been characterized, its location is suggestive.
Another mutation found in B.1.1.7 eliminates a viral protein (called ORF8) entirely. A different mutation that damages this gene was found in Singapore earlier in the year, and seems to cause less severe symptoms among those infected. But, due to Singapore’s successful control of the pandemic, there are no longer any active infections with that strain, so we’ve got no further data there.
There’s also some suggestive information that can be gathered from the collection of mutations found in B.1.1.7 as a whole. Of the 17 mutations that characterize it, 14 alter the proteins encoded by the virus; only three produce no changes. That’s a very high percentage and is often an indication of evolutionary selection for some of the changes.
The high rate of mutation that’s necessary to produce B.1.1.7 in a relatively short time has also been seen before, in immunocompromised individuals who have infections. In these individuals, the infection can take over a month to resolve, and they’re often given treatments that directly target the virus, like convalescent plasma and remdesivir. Thus, it’s possible that at least some of the changes seen here were due to the selective evolutionary pressure exerted by these treatments. (The researchers behind this analysis note that this is a hypothesis, rather than anything we’ve reached conclusions about.)
While all of these differences are suggestive, it’s important to emphasize that we have no definitive evidence that any of them alter the behavior of the virus. So, while the data on its spread is dramatic, we’re still not even certain that’s a product of these mutations, and their impact on the course of viral infections is largely a matter of speculation. While we wait for biologists to come to grips with the changes found in B.1.1.7, the WHO’s advice remains simple: be extra certain to take the measures that public health experts have been advising for months.