The new SARS-CoV-2 strain circulating in the UK (technically called SARS-CoV-2 VUI 202012/01, or B.1.1.7 – see “what’s in a name” below) has raised a lot of concern internationally. The fact that we have a mutant strain of the virus isn’t surprising. There are countless mutant strains out there already. Viruses like this naturally change over time. Usually the changes are fairly irrelevant in terms of how the virus behaves, though they can still be useful for tracking purposes. However, depending on the type of mutation and location on the virus genome, it can impact what the virus does in either a good way, or a bad way. Mutations are random, but if a certain mutation helps the virus survive and spread, those mutant strains tend to become more common.
What’s the deal with B.1.1.7 (or whatever you want to call it)?
This strain has multiple mutations (compared to other commonly circulating strains), and many of those mutations affect the spike protein. The spike protein is what the virus uses to attach to ACE2 receptors, which are found on the surface of human and animal cells. The better the match between the spike protein and the ACE2 receptor, the greater ability of the virus to attach to and infect cells. Differences in the ACE2 receptors impact species susceptibility (e.g. a person’s ACE2 receptor is a good match for the virus, so people can be infected. A bird’s ACE2 receptor is a very poor match so birds are resistant). The mutations in B.1.1.7 seem to make the spike protein a better match for human ACE2 receptors.
That’s likely why this strain seems to be much more transmissible to people than other strains, and it’s rapidly become a common strain the UK. It’s also been found in various other countries (typically with an epidemiological link to the UK).
How did B.1.1.7 emerge?
The ECDC’s Threat Assessment Brief mentions three main potential mechanisms for the emergence of this particular strain. They considered gradual accumulation of the collection of mutations in the UK to be unlikely, since this strain is a big jump from other strains in that country (i.e. intermediate generations of the virus with smaller numbers of these mutations weren’t found in the population before B.1.1.7 suddenly appeared). That left the following main considerations:
- Prolonged infection of a single patient with SARS-CoV-2, which allows more mutations to occur quickly, with subsequent spread back into the general population.
- Infection of an animal, with mutation in the animal and then transmission back to people.
- Gradual emergence of the strain in another country that has little sequencing data, and then introduction of the strain to the UK.
I assume this strain originated in a person. However, movement of viruses between species can foster selection of mutants, and that’s why we’re paying close attention to how SARS-CoV-2 behaves in animals, especially large groups of animals like mink farms where there can be a lot of transmission. It’s also one reason we’re worried about infection of wildlife, as sustained spread in wildlife could potentially create lots of new strains.
What is the impact of B.1.1.7 on animals?
Increased affinity for human cells doesn’t necessarily mean increased affinity for other species’ cells. It might, or it might result in decreased affinity. Hopefully someone’s looking into that.
- If this virus is equally transmissible to animals as its predecessor, we still have more human cases and that means more animal cases, just from more human-to-animal exposures.
- If this strain can more easily infect certain animal species, we could see even more human-to-animal transmission, i.e. a higher occurrence of the spillover infections we’re already seeing.
- Another concern is whether any new strain could infect species that are resistant to the current SARS-CoV-2 virus, including livestock and wildlife species. I doubt this set of mutations is enough to change the host range, but it needs to be considered.
How can we find out how B.1.1.7 affects animals?
Experimental studies are one way, but they’re not ideal in this case for a number of reasons. Field studies can be useful, looking at transmission of the new strain to animals in contact with infected people, as well as ongoing surveillance of animals in settings like mink farms. The issue is there are very few researchers doing things that way. Logistical challenges, as well as lack of coordination with the human health measures and testing, hamper timely testing of in-contact animals. We need to test animals when infection in their human contacts is first detected if we want to recover virus from them. Cooperation of local and provincial health authorities has been a challenge here, an understandable one though given the stress the system is under trying to manage the pandemic. It’s another example of why planning for this type of thing needs to be done in advance (as I said repeatedly post-SARS-CoV-1, and as I tried to address with the province in January 2020, with no response). The odds are good that animals won’t play a role in dissemination of this virus, but it would be nice to base that on data, not hope.
Will this new strain impact the most impressive vaccination development drive in human history?
Hopefully not. There is confidence that this mutation will not impact the efficacy of the current vaccines. However, it’s a reminder that we still have to control transmission as much as possible while vaccines roll out. Less transmission means fewer illnesses, fewer deaths and fewer mutations. We need to buy time until vaccines are available to everyone, everywhere, to reduce disease and the risk of significant mutations.
What does it mean for Canada (or the US, or any other country)?
It means we need to:
- Control the spread of SARS-CoV-2, whatever the strain
- Sequence more viruses to understand the presence and spread of different strains
- Investigate potential animal sources
- Vaccinate, vaccinate, vaccinate
What’s in a name? When it comes to a virus…
Just like we quickly tried to move away from calling SARS-CoV-2 the “Wuhan coronavirus,” we are trying to avoid calling this new strain a “UK variant.” It’s best referred to as a strain first found in the UK, or by its technical name (which unfortunately isn’t particularly short or catchy). We shouldn’t be “shaming” countries that find pathogens or their variants and report them. Just because this new strain was first found in the UK doesn’t mean it originated there. We don’t want fear of blame, travel bans or things like that to be a disincentive for countries to test and report. Even if the virus emerged there, it’s not the UK’s fault (beyond the fact that more virus spread overall means more risk of a mutation like this occurring). A mutation like this could have happened anywhere in the world and been imported to the UK, and then spread rapidly there after it arrived.