What you need to know about the British mutation and what it means for the end of the pandemic

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Andy Larsen answers the big questions about the new COVID-19 variant, including why we don’t know if it’s already out there.

(AP Photo / Frank Augstein) Police stand next to an electronic message reporting coronavirus testing to clear a backlog of cargo, trucks and passengers outside the port of Dover in Dover, England, on Wednesday, December 23, 2020. Freight from Great Britain and passengers with a negative virus test have started arriving on French shores after France relaxed a two-day blockade for a new virus variant. The blockade had isolated Britain, stranded thousands of drivers and raised fears of shortages.

| 27 December 2020, 1:00 PM

Does 2020 have one last surprise in store for us?

Since the start of the pandemic, there has been some fear of a mutant, pioneering strain of the virus. So when British scientists discovered a new variant called B.1.1.7 in December, we naturally wanted to know if our fears have come true.

After a few weeks of studying, we’ve gained some real knowledge of what’s going on here – where our fears were realized and where they didn’t come true. Both the science of the variant and its possible consequences are very interesting, so let’s break down the current state of the research. But first let me answer the question that I know comes to 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 the county of Kent in south-east England, scientists were trying to figure out what was behind an unexpected wave of infections. They genetically sequenced samples from a number of sick people and found something they didn’t expect – a variant of the coronavirus that was significantly different from the one that usually spreads in the area.

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

And it turns out that the viral changes can be significant. Often times, mutations don’t really do anything – like a sentence with a typo, the genetic language meaning remains the same even with a different letter or two. In any case, the body reads the sentence in the normal way.

But in this variation, the typos probably seemed to really matter. One of the mutations is believed to make it easier for the virus to bind to human cells. Another mutation can sometimes help the virus sneak past the human immune response.

Oh dear. 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 arose from one person’s long battle with the coronavirus. In some unusual cases in recent months, the virus has the chance to replicate so often that mutations can occur at an accelerated rate. This is especially true when the virus has to avoid a variety of medically induced obstacles, from the medication remdesivir to plasma therapy.
Take this example of a 45-year-old man who fought the coronavirus for five months before succumbing to the disease. Scientists have sequenced his virus over the course of his illness and have found numerous mutations.

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

Usually these viral changes die along with the affected person. After all, the long-term COVID-19 patient is usually in a hospital, which minimizes the chance that he will give it to someone else. In this case, it appears that the variant has escaped into the world.

What is the difference between a variant and a species?

It should be noted that we are not dealing with a new “strain” of the coronavirus, but a new “variant”. Think of it essentially like this: SARS-CoV-2 that caused this pandemic is a different strain from the SARS-CoV-1 virus that caused the pandemic in 2003. The mutation level seen in this virus in the UK is not nearly significant enough to rise to the level of the term ‘strain’.

Does this variant make the corona virus more contagious?

We are still figuring that out. To do this, we compare how quickly the new variant spreads compared to the other variants in the UK

In particular, a preprinted study published Wednesday estimates that this version could be 56% more transferable. Another estimate said the variant could be 70% more transferable. Let’s just say the first was true. In that case, you could multiply the current infectious 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 is happening in the UK could be due to other factors: What if the variant was first spread to a particularly social or careless group of people? That may be enough to explain the differences.

But wait! We have also found that people with the variant also have a higher viral load in their throat on average. This could partially explain why we’re seeing the wider spread: People who are sick with the variant may spread more virus particles than normal.

So although we are not sure, we have a proposed biological mechanism for increased contamination, an epidemiological mechanism for increased contamination, and when we count cases we see increased contamination. I think the conclusion that the variant is more contagious is relatively safe, although we want to do more research to determine how much more contagious it is.

Does the variant cause a more serious illness?

We currently have no proof of that. According to the European version of our Centers for Disease Control and Prevention, neither higher mortality nor worse clinical outcomes have been reported.

However, officials offer a limitation: Most of those who have been sequenced for their coronavirus infections are under the age of 60. It’s good that we don’t see this variant killing huge groups of young people, but we don’t really know what happens to older people.

However, it’s worth remembering that viruses usually evolve to become more contagious and less serious. As Science’s Derek Lowe puts it, “Remember, the job of a virus isn’t to make people deadly ill: it’s the job of a virus to make more viruses. In general, that’s generally better served with species that are easier to catch and that don’t rip too viciously into their hosts. “

Is the new variant in the US?

We didn’t find it, but that’s because of a curious difference in the number of coronavirus samples we sequence in our country versus the UK. As of Wednesday, the United States had sequenced 37 samples of the coronavirus by December. In the UK, researchers sequenced 3,774 samples over the same time frame.

Epidemiologist Trevor Bedford looks at the number of samples sequenced over time in the UK versus the US (Source: https://twitter.com/trvrb/status/1341806686965665792)

Considering that around 60% of cases in London are currently the new variant, it looks like it probably would have sneaked into the US at some point, but we just don’t know if this is the case or where it is. The US really needs to increase the speed and amount of their coronavirus sequencing.

Do the vaccines work on the new variant?

We think the vaccines will almost certainly still work, but we are definitely checking.

It’s fair to be a little scared – after all, a lot of the mutations are in the part of the 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 become ineffective.

But if it did, the variant would likely also avoid the antibodies that are produced when people get the coronavirus. That would mean that people who have already been sick could get sick again. But in England they don’t see reinfections. In short, the natural antibodies still work, so there is good reason to think that the antibodies in the vaccine will work.

There’s 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 conduct experiments to find out more.

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

Well, it can wreak havoc.

In America, most states have put in place limited coronavirus restrictions as these have proven to be enough to keep the virus from getting out of control while still allowing people to go about their daily lives. As a result, most of America sees an effective infection rate around 1 – meaning every infected person infects each other, so cases grow or shrink quite slowly. For example, the R of Utah is currently estimated at 1.01.

Rt.live’s breakdown of the effective infection rate – Rt – in the 50 US states as of Dec. 24.

But if the new strain started to spread in the US, and do so faster than we can vaccinate humans, our current containment measures would not be enough. Our R of 1 would turn into an R of 1.56 or so, and we’d see the cases start to double in a few weeks. Without change, they would continue to grow exponentially and our hospitals would be inundated.

That is why the UK is again locking people up and requiring them to stay at home, except for urgent travel, medical appointments and outside physical activity. Most flights have been canceled, restaurants closed, and so on.

We hope that the UK 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 is 90% effective is one really effective way to reduce the coronavirus in a community.

But the variant has the potential to increase the pressure of the vaccination race, there is no doubt about that. Getting doses to as many people as possible as soon as possible has always been important, but especially in the case of an evolving coronavirus that is 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 [email protected].

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