What you need to know about the British 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 do not yet know if it is here.

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

Does 2020 hold one last surprise in the offing?

Since the pandemic began, there has been fear of a mutant, changing strain of the virus. When British scientists discovered a new variant called B.1.1.7 in December, we naturally wanted to find out if our fears had come true.

After a few weeks of studying, we gained a real knowledge of what was going on here – where our fears were realized and where they did not take place. Both the science of the variant and its potential consequences are very interesting, so let’s set out the current state of research. But first let me answer the question I know. Is it here? Is it in the United States or even Utah? The quick answer is that we do not know. Read on and I will explain why.

How did we discover the new variant?

In the south east of England, Kent, scientists have been trying to figure out what is behind an unexpected surge in infections. They genetically traced samples from some patients and found something they did not expect – a variant of the coronavirus that differs significantly from the one usually spread in the environment.

In particular, there were 17 mutations in this variant. This is really a large number, because generally the virus takes on a mutation or two a month.

And it turns out that the virus changes could be significant. Many times mutations do not actually do anything – like a sentence with a typo, the meaning of the genetic language remains the same, even with a different letter or two. The body reads the sentence in the normal way anyway.

But in this variant, the typing errors seem to really matter. One of the mutations is thought to make it easier for the virus to bind to human cells. Another mutation can help the virus sometimes sneak through the human immune response.

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

The main hypothesis is that it stems from the long struggle of one individual with the coronavirus. In some unusual cases in recent months, the virus has the chance to recur so many times that mutations can occur at a rapid rate. This is especially true when the virus has to evade all kinds of medically induced barriers, from the drug inhibitor 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 identified his virus in the course of his illness and found numerous mutations.

One 45-year-old man has seen repeated mutations in his coronavirus during a five-month battle with the disease.

These virus changes usually die in the person concerned. After all, the long-term COVID-19 patient is usually in a hospital, which reduces the chance of giving it to someone else. In this case, however, the variant seems to have 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 with a new “variant”. Think of it this way: SARS-CoV-2 that caused this pandemic is a different species than the SARS-CoV-1 virus that caused the 2003 pandemic. The level of mutation we see in the United Kingdom is not nearly significant enough to rise to the level of the term ‘tribe’.

Does this variant make the coronavirus more contagious?

We’re still figuring it out. To do this, we compare how fast the new variant spreads compared to the other variants in the UK

In a pre-printed study released on Wednesday, it is particularly estimated that this version could be 56% more transferable. According to another estimate, the variant could be 70% more transferable. Suppose the former was true. In that case, you can 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 happens in the UK may be due to other factors: what if the variant is first distributed in a particularly social or indifferent group of people? This may be enough to explain the differences.

But wait! We also found that people with the variant also have on average higher virus load in their throats. This may partly explain why we are seeing the greater spread: those who are sick with the variant may spread more virus particles than usual.

Although we do not know for sure, we have a proposed biological mechanism for increased infection, an epidemiological mechanism for increased infection, and if we count cases, we see increased infection. I think the conclusion that the variant is more contagious is relatively safe, but we would like to do more research to determine exactly how much more contagious.

Does the variant cause worse diseases?

We have no evidence of that at the moment. According to the European version of our Centers for Disease Control and Prevention, no higher deaths or worse clinical outcomes have been reported.

However, officials offer a limitation: most people with their coronavirus infections are younger than 60 years old. It’s good that we do not see this variant killing large sections of young people, but we do not really know what happens to older people.

However, it is worth remembering that viruses usually become more contagious and less serious. As Derek Lowe of Science puts it, “Remember, it is not the job of a virus to make people fatally ill: it is the job of a virus to make more viruses. In general, it is usually better served by strains that are easier to catch and that do not end up too badly in their hosts. ”

Is the new variant in the US?

We did not find it, but it is due to a remarkable difference in how many coronavirus samples we follow in our country versus the UK. As of Wednesday, the United States has sequenced 37 coronavirus samples in December. In the UK, researchers followed 3774 samples in the same time frame.

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

Since about 60% of London business is currently the new variant, it looks like it would probably have slipped to the US at some point, but we just do not know if it is or where it is. The US really needs to increase the speed and amount of the coronavirus sequence.

Will the vaccines work on the new variant?

We think the vaccinations will almost certainly still work, but it’s sure we’m sure.

It’s reasonable to be a little scared. After all, many of the mutations are in the section of genetic code that causes the protein of the virus, which also happens to be the part on which we target vaccines. If the peak changes too drastically, the vaccines can be rendered ineffective.

But if this were the case, the variant would probably also evade the antibodies that arise when humans get the coronavirus. This would mean that people who were already ill could become ill again. But in England they do not see reinfections. In short, the natural antibodies still work, so there is good reason to think that the antibodies against vaccine will work as well.

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

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

Well, it can wreak havoc.

In America, most states have introduced limited coronavirus restrictions because it is enough to prevent the virus from getting out of control while people can still lead their daily lives. As a result, most of America sees an effective number of infections around 1 – meaning that each infected person infects each other, so the cases grow or shrink fairly slowly. Utah’s R is currently estimated at 1.01.

Rt.live’s outline of the effective infection rate – Rt – in America’s 50 states from December 24th.

But if the new variant were to start spreading in the US and do it faster than our people could vaccinate, our current restraint measures would not be enough. Our R of 1 would change to an R of 1.56 or so, and we would see that business would start to double in a few weeks. Without change, they will continue to grow exponentially, and our hospitals will be overrun.

That is why the UK is re-locking people up and requiring them to stay home, except in cases of urgent travel, medical appointments and outdoor exercise. Most flights were canceled, restaurants closed, and so on.

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

But the variant can increase the pressure of the vaccination match, there is no doubt about it. Getting doses from as many people as possible has always been important, but especially in the case of a changing coronavirus that is particularly 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].