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What you should know about the U.K. mutation and what it means for the end of the pandemic

Andy Larsen answers the big questions about the new COVID-19 variant, including why we don’t know if it is here yet.

(AP Photo/Frank Augstein) Police stand next to an electronic notice notifying about coronavirus testing to help clear a backlog of freight, truck and passengers outside the Port of Dover in Dover, England, Wednesday, Dec. 23, 2020. Freight from Britain and passengers with a negative virus test have begun arriving on French shores, after France relaxed a two-day blockade over a new virus variant. The blockade had isolated Britain, stranded thousands of drivers and raised fears of shortages.

Does 2020 have one last surprise in store for us?

Ever since the pandemic started, there’s been some fear of a mutant, game-changing strain of the virus. So when British scientists discovered a new variant called B.1.1.7 in December, naturally we wanted to find out if our fears have come true.

After a couple of weeks of studying, we’ve gained some real knowledge of what’s going on here — where our fears have been realized and where they’ve not come to pass. Both the science of the variant and its potential consequences are very interesting, so let’s break down the current state of the research. But first, let me answer the question I know is at the front of your mind. Is it here? Is it in the United States or even Utah? The quick answer is we don’t know, keep reading and I’ll explain why.

How did we discover the new variant?

In southeastern England’s county of Kent, scientists were trying to figure out what was behind an unexpected surge in infections. They genetically sequenced samples from some sick people and found something they didn’t expect — a variant of the coronavirus that was significantly different than the one that usually spreads in the area.

In particular, there were 17 mutations in this variant. That’s a really big number, because generally the virus picks up a mutation or two per month.

And it turns out the viral changes could be significant. A lot of times, mutations don’t really do anything — like a sentence with a typo, the meaning of the genetic language stays the same even with a different letter or two. The body reads the sentence in the normal way anyway.

But in this variant, the typos seemed likely to really matter. One of the mutations has been conjectured to make it easier for the virus to bind to human cells. Another mutation may help the virus sometimes sneak past the human immune response.

Gosh. If the virus usually gets one or two mutations per month, how did this variant get 17 changes without us noticing?

The leading hypothesis is that it came from one individual’s long battle with the coronavirus. In some unusual cases that last months, the virus has the chance to replicate so many times that mutations can happen at an accelerated rate. That’s especially true when the virus has to dodge all sorts of medically induced obstacles, from the drug remdesivir to plasma therapy.

Take this example of a 45-year-old man who battled the coronavirus for five months before succumbing to the illness. Scientists sequenced his virus over the course of his illness and found numerous mutations.

One 45-year-old man saw repeated mutations in his coronavirus over the course of a 5-month-long battle with the disease.

Most of the time, these viral changes die with the individual involved. After all, the long-term COVID-19 patient is usually in a hospital, minimizing the chance of giving it to someone else. In this case, though, it seems like the variant escaped into the world.

What’s the difference between a variant and a strain?

It should be noted that we are not dealing with a new “strain” of the coronavirus, but a new “variant.” Essentially, think of it like this: SARS-CoV-2 that caused this pandemic is a different strain than the SARS-CoV-1 virus that caused the 2003 pandemic. The level of mutation that we’re seeing in this virus in the United Kingdom isn’t anywhere near significant enough to rise to the level of the term “strain.”

Does this variant make the coronavirus more contagious?

We’re still figuring that out. To do so, we compare how fast the new variant spreads compared to the other variants in the U.K.

In particular, a preprinted study released Wednesday estimates that this version might be 56% more transmissible. Another estimate said the variant might be 70% more transmissible. Let’s say the former were true. In that case, you could multiply the current contagious number R0 — the measure of how many people are infected by the average person with coronavirus — by 1.56.

Regardless of the number, remember that these estimates are all based on circumstantial evidence. What’s happening in the U.K. could be due to other factors: What if the variant was first spread in a particularly social or careless group of people? That might be enough to explain the differences.

But wait! We’ve also found that people with the variant also have, on average, higher viral loads in their throats. This might explain, in part, why we see the higher spread: Those sick with the variant are able to spread more virus particles around than usual.

So while we don’t know for sure, we have a proposed biological mechanism for increased contagion, an epidemiological mechanism for increased contagion, and when we count cases, we see increased contagion. I think the conclusion that the variant is more contagious is relatively safe, though we’ll want to do more research to nail down exactly how much more contagious.

Does the variant cause more severe disease?

We don’t have evidence of that at the moment. According to the European version of our Centers for Disease Control and Prevention, neither higher mortality nor poorer clinical outcomes have been reported.

However, officials offer a limitation: Most of those who have had their coronavirus infections sequenced are under 60 years old. It’s good we’re not seeing this variant kill huge swaths of young people, but we don’t really know what happens with older people.

It’s worth remembering, though, that viruses usually evolve to become more contagious and less severe. As Science’s Derek Lowe puts it, “Remember, it’s not the job of a virus to make people deathly ill: It’s the job of a virus to make more virus. Overall, that is generally better served by strains that are easier to catch and that don’t rip into their hosts too viciously.”

Is the new variant in the U.S.?

We haven’t found it, but that’s due to a curious difference in how many coronavirus samples we sequence in our country vs. the United Kingdom. As of Wednesday, the United States had sequenced 37 coronavirus samples in all of December. In the U.K., researchers have sequenced 3,774 samples in that same time frame.

Epidemiologist Trevor Bedford looks at the quantity of specimens sequenced over time in the U.K. vs. the U.S. (Source: https://twitter.com/trvrb/status/1341806686965665792)

Given that about 60% of London cases are the new variant right now, it seems like it probably would have slipped into the U.S. at some point, but we just don’t know if it has or where it is. The U.S. really needs to up the speed and quantity of its coronavirus sequencing.

Will the vaccines work on the new variant?

We think the vaccines will almost certainly still work, but we’re checking to make sure.

It’s reasonable to be a little bit scared — after all, many of the mutations are in the section of genetic code that creates the virus’s spike protein, which also happens to be the part that our vaccines target. If that spike changed too radically, the vaccines could be rendered ineffective.

But if that were the case, the variant would likely also evade the antibodies that are created when people get the coronavirus. That would mean people who have already been sick could get sick again. But in England, they’re not seeing reinfections. In short, the natural antibodies still work, and so there’s good reason to think the vaccine antibodies will work, too.

There is a chance the vaccine won’t be as effective on this variant as others, but we’re talking percentage points, not game-changing failure. Both Moderna and Pfizer say their scientists will run experiments to find out more.

What impact will the variant have on the late stages of the pandemic?

Well, it could cause havoc.

In America, most states have put in place limited coronavirus restrictions because they’ve proved to be enough to keep the virus from spiraling out of control, while still allowing people to live their everyday lives. As a result, most of America sees an effective contagion number around 1 — which means every infected person is infecting one other, so cases are growing or shrinking pretty slowly. Utah’s R is currently estimated to be 1.01, for example.

Rt.live's breakdown of the effective contagion rate — Rt — in America's 50 states as of December 24.

But if the new variant were to start spreading in the U.S., and did so faster than we can vaccinate people, our current containment measures wouldn’t be enough. Our R of 1 would turn into an R of 1.56 or so, and we’d see cases begin to double in a couple of weeks. Without changes, they’d keep exponentially growing, and our hospitals would get overrun.

That’s why the U.K. is locking people down again, requiring them to stay at home except in cases of urgent travel, medical appointments and outdoor exercise. Most flights have been canceled, restaurants shut down, and so forth.

Our hope is that Britain’s containment efforts have been somewhat successful, and that we can ramp up vaccinations in time to beat the new variant. Giving at least 60% of people a vaccine that’s 90% effective is a really effective way to reduce the coronavirus in a community.

But the variant does have the potential to increase the pressure of the vaccination race, there’s no doubt about it. Getting doses in as many people as possible as quickly as possible has always been important, but especially so in the case of a changing coronavirus that’s especially contagious.

Andy Larsen is a data columnist. He is also one of The Salt Lake Tribune’s Utah Jazz beat writers. You can reach him at alarsen@sltrib.com.

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