Confused about all the coronavirus variants? Here is the explanation.

Back in December, I wrote about a new aspect of the coronavirus landscape – a variant that had just been discovered in the English county of Kent – and what it could mean for the pandemic.

Fast forward to April, and the matr has become much more complicated. We now have three major coronavirus variants on our board, with a few other minors at risk of making waves as well. There is a dizzying amount of research on all of them, and most importantly, we were able to actually see the effects of the variants compared to what we would call Coronavirus Classic, here in America and abroad.

Suffice it to say: it can be overwhelming to digest all the news about these variants – especially if some warn that they are a “category 5 hurricane”, while other stories do not panic. What’s really going on, and how worried should you be?

Here is the explanation:

Overview of variants

Currently, there are three major coronavirus variants to be concerned about: B.1.1.7, B.1.351 and P.1.

These are many letters and numbers you need to remember. It reminds me of how Mercedes-Benz or Lexus just throw together a few letters for car model names. It would be much easier to talk about the cars if we could just call it in plain words! Sometimes you see these coronavirus variants, the UK variant, the South African variant and the Brazilian variant, respectively, from where it was first discovered and where it is currently the dominant strain.

But there is a problem with that, because it tends to stigmatize those locations. It has real consequences for people from those areas – something we have seen with an increase in anti-Asian racist incidents, as some have insisted on calling the coronavirus the ‘China virus’ or the ‘Wuhan flu’. Although it is more difficult, there are good reasons to stick to the alphanumeric soup.

In an effort to make it easier, here is a table for you to keep the variants right:

There have been other variants that have emerged as the virus continues to mutate, and these are B.1.427 (the “California variant”) and A.VOI.V2 (the “Tanzania variant”). So far it has spread less than the three main variants above, but it is an evolving picture (no pun intended). However, given their ubiquity, B.1.1.7, B.1.351 and P.1 are the three variants to pay the most attention to over the next few months.

What is remarkable is that these variants, which develop in different places around the world, have mutated in the same ways.

All three, for example, have the “N501Y” mutation. This naming convention means that the amino acid asparagine (given the symbol N), at number 501 of the virus’ genetic code, the amino acid asparagine (given the symbol N) was randomly replaced by the amino. acid tyrosine (given the symbol Y).

It turns out that making the chemical replacement essentially makes the virus more sticky to human cells. Wherever this accident happens, it tends to recur. We repeatedly see areas where similar or identical mutations lead to improved virus performance.

What exactly does ‘improved virus performance’ mean?

The variants are more contagious

These variants appear in different degrees thanks to the mutations more contagious than Coronavirus Classic. In essence, this means that when the average person gets a coronavirus variant, the person spreads it to more people.

Researchers found that the B.1.1.7 variant, for example, increased transmission by about 70% compared to the normal coronavirus when looking at viral growth in the United Kingdom, Denmark, Switzerland and the USA. This result has been approximated in a handful of studies, now, so we have a good idea that it is true.

Now that the B.1.1.7 variant is so common in America, you can even see it in different states – B.1.1.7 is gradually increasing its share of coronavirus cases because it is so much more contagious. The Centers for Disease Control and Prevention said Wednesday that B.1.1.7 is now the most common form of coronavirus in the United States.

New York Times presents data from Helix, a virus-sequencing company. Helix unfortunately does not estimate the distribution of B.1.1.7 in Utah due to the limited sample size compared to states with larger populations. (Https://www.nytimes.com/interactive/2021/04/06/us/variants-cases-spread.html)

The good news is, we’re still in the early stages of this in Utah. While B.1.1.7 cases have increased since January as elsewhere, they have generally represented only 2.1% of all coronavirus cases in the state – 226 cases of B.1.1.7 have been positively identified so far. It has been steadily increasing over the last few months, so it is now higher than 2.1%, but we are not 50% to 75% like some of the worst states.

Data from the Utah Public Health Lab on confirmed cases of coronavirus cases in Utah. Note that the cases collected over the past two weeks are unlikely to be followed up yet. Only a small percentage of Utah coronavirus-positive cases are followed up.

What about the other great variants? We just have less data. One computer model from South Africa guessed that B.1.351 could be 50% more transferable. Two studies looked at Brazil: one found that P.1 is somewhere between 40% and 120% more transmissible, and the other one 160% more transmissible.

Because these two variants have spread in fewer places than B.1.1.7, it is more difficult to determine how many of the increases in transmissibility are due to the virus itself and how much of it is due to other factors, such as relaxed precautions. With P.1 now widely distributed in Canada, we are going to get more data quickly. In Utah, we have so far had three confirmed cases of P.1.

The variants appear to be more serious

Thanks to studies in the UK, we have a good idea that these variants are also worse.

A study in the British Medical Journal looked at the outcomes of 109,000 cases in Britain, half of which are the B.1.1.7 coronavirus and half the Coronavirus Classic. Results show that 227 of the people in the first group died, compared to 141 in the second group, a result indicating that B.1.1.7 is more lethal, with about 64%.

Due to the number of cases and deaths in the UK from B.1.1.7, we can even give estimates based on age groups and gender. In studying about 5,000 deaths from the UK, scientists in Nature reported that the average 55- to 69-year-old man has about a 0.9% chance of dying from the new variant, compared to a 0.6% chance of death of the old one. .

Again, with the B.1.351 and P.1 variants, we do not yet have enough data to determine whether this also leads to worse disease or death. We have seen increased deaths in both cases, but it can also be a symptom of excessive hospitalization. I would say that it probably leads to serious illnesses, but it’s hard to know for sure.

One interesting aspect of all three variants was poorer outcomes for young people. The deaths in Brazil, for example, are 2.7 times higher among those aged 20 to 39 years in the second wave fueled by P.1, compared to the first wave; the older people mortality rates rose 1.15 times higher. On the other hand, in the second wave it may just spread more among young people because those at higher prices go back to work than the older population did. Although this increase in bad outcomes is seen among young people, it is difficult to know for sure that it is due to the virus.

Yet the increase in severity and mortality rate has surprised some scientists. This is because viruses usually mutate to become less lethal rather than lethal – a dead body is not very good at replicating the virus, and viruses only give to make more virus. But these variants seem to have an unfortunate happy medium that infects human cells because it is better to infect human cells, leading to a more difficult disease for those infected with it.

Are antibodies from vaccines and previous infections still effective?

This is where we saw the most research into these three variants, because of the consequences associated with them: If these variants do not respond to the antibodies created by the standard coronavirus through vaccines or infections, it would be basically like to start the pandemic everywhere.

So that’s the good news: it’s clear that all three variants are usually neutralized by those antibodies.

The best news is for B.1.1.7 – the most common of the variants in Utah and the US. Both Pfizer and Moderna have done studies on how well their vaccine works against B.1.1.7, and both have found that they work essentially just as well as against Coronavirus Classic. Johnson & Johnson, AstraZeneca and Novavax vaccines have only reduced percentages by one figure. Re-infections occurred only 0.7%, which according to scientists is about the same rate as re-infections for the standard coronavirus.

For B.1.351, the news is worse. There was a lot of attention to the fact that AstraZeneca’s vaccine found only 10% effective against B.1.351 in South Africa. Suffice it to say: 10% effective is not what you want from your vaccinations.

Other vaccines have been shown to provide better protection, although even less than normal. A study of Pfizer’s vaccine is 77% effective against B.1.351, compared to 94% against the previous type. Johnson & Johnson’s are approximately 64% effective, while Novavax was 60% effective in South Africa.

Why was AstraZeneca’s vaccine basically useless, while the others were not? The AstraZeneca vaccine seems to create a slightly different version of the coronavirus peak protein than the others do, and it does not look as much like B.1.351 as the others. As a result, the immune system rarely attacks the B.1.351 virus after doses of AstraZeneca’s vaccine, but usually does so with the others.

As for P.1, the news is between the other two variants. The Pfizer and Moderna vaccines appear to be just as effective, while the efficacy of Johnson & Johnson drops to only 68%, compared to 72%. However, it appears that there are more reinfections of people who had the first coronavirus, with a probability of about 6.4%.

Since B.1.351 is the most dangerous of the three from this perspective, Moderna has created a new vaccine for the variant using the same technology as the original vaccine, but with an updated code. The National Institutes of Health began testing it last week. They also test different dosing strategies. The idea is that we want to see if it is best for people to get a third dose of variant vaccine or to replace the second dose with the variant vaccine – or there is no difference.

B.1.351 has so far been reported in 31 U.S. states, but not in Utah. However, it is clear that it did not spread as fast as B.1.1.7, so this vaccination test is mostly about readiness here. There is a good probability that we will not have to use it.

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In general, you can see why the variants have caused so many problems as in Michigan, Canada, Brazil, Europe and Africa. They are more contagious, and once infected, they are likely to be hospitalized or die. This is a pretty bad combination!

On the other hand, the situation is better than it could be, thanks to our still effective vaccines against all three variants. It all emphasizes the importance of vaccinating everyone as quickly as possible to achieve herd immunity. We’re here in a race against time – one that some locals have lost, but we can still win.

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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