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 might mean for the pandemic.
Fast forward to April, and the matter has grown a lot more complicated. We now have three major coronavirus variants on our plate, with a couple of other minor ones at risk of making waves, too. There’s a dizzying amount of research about them all, and, most importantly, we’ve been able to actually see some of the real-world consequences of the variants compared with what we’ll call Coronavirus Classic, both here in America and abroad.
Suffice it to say, it can be overwhelming to digest all of the news about those variants — especially when some warn they are a “category 5 hurricane” while other stories say not to panic. What’s actually going on, and how worried should you be?
Here’s the breakdown:
Overview of variants
Right now, there are three major coronavirus variants you need to worry about: B.1.1.7, B.1.351 and P.1.
That’s a lot of letters and numbers together to remember. It reminds me of how Mercedes-Benz or Lexus just throw together some letters for car model names. It sure would be a lot easier to talk about the cars if we could just call them by regular words! Sometimes, you’ll see these coronavirus variants referred to as the U.K. variant, the South African variant, and the Brazilian variant, respectively, from where they were first discovered and where they are currently the dominant strain.
But there’s a problem with that, because it tends to stigmatize those locations. That has real-world consequences for people from those areas — something we’ve seen with a rise in anti-Asian racist incidents since some insisted on calling the coronavirus the “China Virus or the “Wuhan flu.” So while it’s more difficult, there are good reasons to stick with the alphanumeric soup.
In an effort to make it easier, here’s a table for you to help keep the variants straight:
There have been other variants that have popped up as the virus continues to mutate, included in these are B.1.427 (the “California variant”) and A.VOI.V2 (the “Tanzania variant”). So far, these have spread less than the three major variants listed above, but this 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 be most aware of for the next few months.
What’s sort of remarkable is that these variants, evolving in different places around the world, have mutated in some of the same ways.
For example, all three have the “N501Y” mutation. This naming convention means that, in the billions and billions of times that the virus has replicated itself in humans, at spot No. 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 that chemical replacement essentially makes the virus more sticky to human cells. So wherever this accident happens, it tends to replicate. Repeatedly, we see areas where similar or identical mutations lead to enhanced virus performance.
What, exactly, does “enhanced virus performance” mean?
The variants are more contagious
These variants all appear to be more contagious than Coronavirus Classic by varying degrees, thanks to those mutations. Essentially, this means when the average person gets a coronavirus variant, that person spreads it to more people.
Researchers found that the B.1.1.7 variant, for example, increased transmission by about 70% compared with the normal coronavirus, when looking at viral growth in the U.K., Denmark, Switzerland and the U.S. This result has been approximated in a handful of studies, now, so we have a pretty good idea that it’s true.
Now that the B.1.1.7 variant is so common in America, you can even see this in various states — B.1.1.7 steadily increases its share of coronavirus cases because it’s so much more contagious. In fact, 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.
The good news is that we’re still in the early stages of this in Utah. While B.1.1.7 cases have increased since January like they have everywhere else, overall they’ve only represented 2.1% of all sequenced coronavirus cases in the state — 226 cases of B.1.1.7 have been positively identified so far. That’s been continually increasing over the course of the past few months, so it’s higher than 2.1% now, but we’re not at 50% to 75% like some of the worst states.
What about the other major variants? We just have less data. One computer model from South Africa guessed that B.1.351 could be 50% more transmissible. Two studies looked at Brazil: One found that P.1 is somewhere between 40% and 120% more transmissible, the other found it to be 160% more transmissible.
Because these two variants have spread in fewer places than B.1.1.7, it’s harder to pin down how much of the increases in transmissibility are due to the virus itself and how much are due to other factors, like relaxed precautions. With P.1 now spreading in a big way in Canada, we’re about to get more data quickly. In Utah, so far, we have three confirmed cases of P.1.
The variants appear to be more severe
Thanks to studies in the U.K., we have a pretty good idea that these variants are more severe, too.
A study in the British Medical Journal looked at the outcomes of 109,000 cases in Britain — half of which had the B.1.1.7 coronavirus, and half of which had Coronavirus Classic. Results show 227 of the people in the first group died, compared with 141 in the second group, a result that indicates that B.1.1.7 is more deadly, by about 64%.
Heck, due to the number of cases and deaths in the U.K. from B.1.1.7, we can even give estimates based on age ranges and gender. In studying about 5,000 deaths from the U.K., scientists in Nature reported that the average 55- to 69-year-old male has about a 0.9% chance of death from the new variant, compared with a 0.6% chance of death from the old one.
Again, with the B.1.351 and P.1 variants, we don’t have enough data yet to establish whether they also lead to more severe sickness or death. We did see increased deaths in both cases, but that could also be a symptom of overrun hospitals. I would say that it’s likely they lead to more severe disease, but it’s hard to know for sure.
One interesting aspect of all three variants has been worse outcomes for young people. For example, deaths in Brazil are 2.7 times higher among those 20 to 39 years old in the P.1-fueled second wave compared with the first wave; those older saw deaths rise 1.15 times higher. On the other hand, it might just be spreading more among young people in the second wave, because those people went back to work at higher rates than the elderly population did. So while we see this increase in bad outcomes among young people, it’s hard to know for sure that it’s due to the virus.
Still, the increase in severity and fatality has surprised some scientists. That’s because viruses typically mutate to become less deadly rather than more deadly — a dead body isn’t very good at replicating the virus, and viruses care only about making more virus. But these variants, because they’re better at infecting human cells, seem to have found an unfortunate happy medium that results in rougher sicknesses for those who are infected with it.
Are antibodies from vaccines and previous infections still effective?
This is where we’ve seen the greatest amount of research into these three variants, because of the consequences involved: If these variants weren’t responsive to the antibodies created by vaccines or infection for the standard coronavirus, it’d basically be like starting the pandemic all over.
So here’s the good news: Clearly, all three variants are at least usually neutralized by those antibodies.
The best news is for B.1.1.7 — the most prevalent of the variants in Utah and the U.S. Both Pfizer and Moderna did studies on how well their vaccine worked against B.1.1.7, and both found that they worked essentially just as well as they did against Coronavirus Classic. Johnson & Johnson, AstraZeneca and Novavax’s vaccines saw only single-digit percentage-point reductions. Reinfections have occurred at only 0.7%, which scientists believe is about the same rate as reinfections for the standard coronavirus.
For B.1.351, the news is worse. There was a lot of attention on AstraZeneca’s vaccine being found only 10% effective against B.1.351 in South Africa. Suffice it to say, 10% effective is not what you want from your vaccines.
Other vaccines have proved to give better protection, albeit still less than normal. A study of Pfizer’s vaccine was found to be 77% effective against B.1.351, compared with 94% against the previous type. Johnson & Johnson’s was found to be about 64% effective, while Novavax was 60% effective in South Africa.
Why was AstraZeneca’s vaccine basically useless, while the others weren’t? It seems that AstraZeneca’s vaccine creates a slightly different version of the coronavirus spike protein than the others do, and it doesn’t 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 with the others.
As for P.1, the news is in between the other two variants. The Pfizer and Moderna vaccines appear to be just as effective, while Johnson & Johnson’s efficacy falls only to 68%, compared with 72%. However, it appears 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 its original vaccine but with an updated code. The National Institutes of Health started testing that last week. They’re also testing different dosing strategies. The idea is that we want to see if it’s best for people to get a third dose of variant vaccine or to substitute the second dose with the variant vaccine — or if there’s no difference.
B.1.351 has been reported in 31 U.S. states, but not in Utah, to this point. Clearly, though, it hasn’t spread as quickly as B.1.1.7, so this vaccine trial is mostly about preparedness here. There’s a good probability we won’t have to use it.
Overall, you can see why the variants have caused as much trouble as they have in Michigan, Canada, Brazil, Europe and Africa. They’re more contagious, and once people have been infected, they’re more likely to become hospitalized or die. That’s a pretty bad combo!
On the other hand, the situation is better than it could be, thanks to our still-effective vaccines against all three variants. It all highlights the importance of vaccinating everyone as quickly as possible to reach herd immunity. We’re in a race against time here — one that some other locales have lost, but we could 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 firstname.lastname@example.org.