What we know so far about new COVID-19 variants
There are now at least three variants of COVID-19 circulating in the U.S. Each raised international alarms as they spread in the countries they were first detected, each for different reasons.
The emergence and rapid spread of these new viral variants has intensified the push to understand how the coronavirus mutates and how these new versions of the virus might behave. They have the potential to be game-changers, and not in a good way.
The new variants raise a lot of questions. Do we need to change our behavior? Are schools still safe? Will vaccines still work? Are there new variants here in the Northwest? Will things get worse? We’ve tried to slow the deluge of news to answer your most crucial questions.
When writing about COVID-19, it’s normal for news to change even as it’s being reported. The information in this story is up to date, but it represents emerging research, so nothing is written in stone. Still, it’s surprising for a story to change so much while it’s being written: the first U.S. case of the South African variant of COVID-19 was reported Thursday morning. On Friday, Oregon researchers announced they had identified a separate variant from Denmark was found in Oregon. And that’s just the tip of the iceberg.
It’s hard to keep track of it all, but there’s good news: The basic science isn’t going to change, and an understanding of the basics can help you keep track of changing news. So we’ll start there.
The instructions to build a human are written in our genes. The instructions to build a virus are also written in theirs. Instead of an alphabet, that code is written in molecules called “nucleobases.” There are five of them, adenine, cytosine, guanine, thymine and uracil. But usually we refer to nucleobases using the first letter: A, C, G, T, and U.
When our cells make copies of themselves, sometimes those letters are misprinted. The same thing happens when a virus — like the one responsible for spreading COVID-19 — enters our cells and hijacks cellular machinery to copy itself. That misprint is a mutation. Some mutations do nothing at all, but some can make big changes.
Just having a mutation isn’t enough to make a new variant, though.
Both types of genetic material have “coding” portions. The letters in a coding portion of a genome tell a body to build certain amino acids in certain orders. Amino acids are like the Legos of our body: the blocks we build proteins out of. Each amino acid can be coded using a few different three-letter sequences. Sort of like how there are a lot of different words for “cow.”
That means that not all mutations in coding areas actually change anything. If a piece of RNA that used to read “CUU” and now reads “CUA,” that’s OK: It still codes for the same amino acid, Leucine. It’s the equivalent of writing “bovine” instead of “cow.”
But sometimes, mutations can start to change which amino acids, or blocks, the virus builds. If “CUU” gets misprinted as “CCU,” it codes for a new amino acid. It’s like changing “cow” to “caw.” The word has an entirely different meaning.
If these different building blocks change how the virus behaves, it is considered a variant. The most widespread new variant of COVID-19, called B.1.1.7, was first detected in the United Kingdom so it’s sometimes referred to as the U.K. variant. It has at least 22 mutations in coding parts of its RNA.
If a virus changes so much our bodies can’t recognize it, it can be considered a new strain. SARS-CoV-2, is a strain of virus. All the new variants are types of that original strain.
B.1.1.7 first appeared undetected in Kent, in southeast Great Britain, and is the most common variant in the U.K.
Scientists are still learning more about this new variant. Early on, though, it became clear that the virus has a lot of mutations on its “spike” protein. The spike protein helps the virus enter cells, and gives the coronavirus such a, well, spiky surface.
The mutations in B.1.1.7′s spike proteins make it easier for the virus to enter cells. That seems to make it more contagious than previous versions of the COVID-19 virus. There’s also early evidence to suggest it could be more deadly.
In December, British Prime Minister Boris Johnson instituted new social distancing measures across the nation, in an attempt to keep cases low and reopen for Christmas. It looked like it worked everywhere, except in Kent.
Cases there kept rising, so researchers combed through a collection of viral genomes that had been uploaded to a national database to see if there was a reason. The U.K. had been collecting and sequencing the RNA of thousands of viruses from thousands of people with COVID-19.
Scientists identified the B.1.1.7 variant in early December, and the earliest known samples of this lineage had initially been collected in late September.
By mid-December, this new variant had spread widely, and had become the variant causing the most infections in the U.K. and Ireland.
As cases began to skyrocket and hospitals rapidly filled up, the U.K. was forced to tighten social distancing measures. There was no COVID-safe Christmas, though Johnson did lift some restrictions for the holiday, despite the potentially dire consequences. The U.K. is currently in the third week of a third nationwide lockdown, which is expected to last until March.
When it arrives, it spreads quickly. In January, B.1.1.7 has accounted for 20% of the cases in Belgium, where it is now the most common variant found. Denmark is currently in a strict lockdown -- but the variant is still spreading. Scientists believe that despite the lockdown, the variant is increasing by 70% each week. Denmark sequences every COVID-19 sample, so its research is very robust.
Our bodies are pretty good at killing viruses; we have a lot of defenses. While a virus is in our lungs or in our blood stream it’s at the mercy of an inhospitable environment, made even less hospitable by our immune systems. But once it enters a cell, it’s usually safe from our immune systems, and it can start to replicate. Eventually, we get sick.
Some viral mutations can make it easier for a virus to spread through the air, or survive outside of a human. So that can mean we’re more likely to get exposed.
It’s easier for B.1.1.7 to get into our cells. That means it’s more likely for an exposure to actually infect you. Scientists estimate the U.K. variant of the COVID-19 virus could be 70% more transmissible than the original variant, and may be 30% more lethal, according Patrick Valance, U.K. Prime Minister Boris Johnson’s chief scientific adviser.
So things that were relatively safe before might not be as safe any longer. But since we know that our risk of getting infected if we are exposed has increased, it’s a good idea to reduce our risk of getting exposed.
While a thin cotton mask may have stopped enough of the virus to keep you from getting sick before these more contagious variants were so widespread, now a thicker, medically-rated mask may be better.
Some experts recommend doubling up masks. European countries responded to the new variant by requiring medical grade masks in public. Those masks are still harder to come by in the U.S., but President Joe Biden’s coronavirus plan involves importing more personal protective equipment and producing more within the country.
You should also limit the places you visit. If you went to the grocery store once a week before, consider going every other week. Or if you already go every two weeks, why not try every three? Be even more careful about indoor gatherings.
We also may need to prepare to see our reopening strategies shift. If the U.K. variant spreads, state, local, and federal government agencies may need to consider more strict lockdown measures.
For example, the U.K. was able to keep schools open for most of the fall, as cases declined. When cases rose, businesses closed, but schools stayed open. That’s no longer the case. Schools across Europe are closing, including in the U.K. The Netherlands closed schools after B.1.1.7 was found to be responsible for an outbreak that infected 15% of students and teachers in a primary school.
A more contagious virus means that fast outbreaks are more likely, and if more people are sick there will be more people who are hospitalized and more who die. That affects how the virus spreads, and the measures we take to slow the spread.
If this variant does prove to be more deadly than others, plans designed to keep hospital intensive care units from being overrun will need to be adjusted. We currently assume that a certain percentage of diagnosed people will need to be hospitalized. A subset of that may require treatment in an ICU, or require oxygen and be placed on a ventilator. A more deadly virus changes all of that math.
Unlike some countries, the U.S. does not have any sort of nationwide COVID-19 genomics surveillance program. But when the virus first arrived in the U.S., a number of universities realized that they had the capacity to survey the virus’ genes, and already had a network set up to do so: the same network we use to track the flu.
In April, a small team of Oregon Health & Science University researchers opened a lab to sequence and survey COVID-19 as it spread.
“We had that expertise and saw an opportunity to become involved in trying to add genome surveillance on top of the existing testing that was happening,” said Ben Bimber, a virologist on the COVID-19 genomic surveillance team.
But it’s a secondary job for the people who work on the team — Bimber’s day job involves studying HIV and tuberculosis — so team members can only run a few hundred samples a week. And because OHSU is based in Portland, most of the samples they sequence come from Portland, too.
That is hard to say. So far, there’s only been a handful of B.1.1.7 cases identified in Oregon. Only one was identified by OHSU’s lab.
”But there’s obviously far more cases in Oregon and in general,” Bimber said. “Our data also generally lags at least a week, possibly more, behind. As we get more and more batches of data, we expect to see more cases.”
So far, OHSU has sequenced over 1,600 COVID-19 viral genomes. But OHSU’s head pathologist Dr. Donna Hansel said on “Think Out Loud” that OHSU has thousands of banked samples waiting to be processed, if they can find the lab capacity.
Think of it like the early days of the COVID-19 outbreak. Tests were so limited, they weren’t able to provide a good measure of how fast COVID-19 was spreading. The tests told us where people were getting tested, not where the virus was.
One crucial detail: All of the cases of the U.K. coronavirus variant found in Oregon so far shared no common connections.
“Typically, when you see something like this happening, we are assuming that there is broader spread in the community than we are actually detecting,” Hansel said.
We are still in the early stages of research on this variant, but scientists using fairly simple models have been able to run through a few scenarios. Given how fast the variant spread in the U.K., one paper published in the Center for Disease Control and Prevention’s Morbidity and Mortality Weekly Report estimated that B.1.1.7 could be the dominant variant in the U.S. by the end of March.
There are dozens of variants of COVID-19, but three have the caused most international concern: a strain from Brazil (called P.1), one in South Africa (B.1.351), and one associated with large outbreaks in California that originally came from Denmark (L452R.)
A number of others have been found in states and countries around the world. But they’re either not spreading fast enough to raise alarm bells yet, or — if they’re behaving differently than other variants — they’re spreading in places with less scientific surveillance.
As of Thursday, the U.K., Brazil, and South Africa variants have been found in the U.S. The first case of B.1.351, which is the South Africa variant, was found in South Carolina on Thursday, and the first case of P.1, the Brazil variant, was found in Minnesota on Monday.
On Friday, OHSU’s surveillance lab announced that it has identified cases of the Danish L452R variant in Oregon.
While we know a bit more about B.1.1.7, in part because of the U.K.’s robust viral surveillance program, there’s a lot of basic research that still needs to be conducted on these new lineages of COVID-19 as they emerge.
”We need to do more work characterizing these variants,” Bimber said. “Simply saying that a variant is spreading or dominant doesn’t tell you much about the properties of that virus. You have to measure the infectivity, look at its pathology, and look at whether it can evade antibodies.”
From the research done on B.1.1.7, it appears that antibodies from people vaccinated against COVID-19 work against the U.K. variant. That’s a strong piece of evidence that the vaccines can work, and so far it’s supported by data from outbreaks. Vaccine makers have felt safe enough to confidently say that vaccines are effective against this variant.
That may not be the case for other viruses, however. Early research shows that the South African variant, B.1.351, may be better at evading vaccine antibodies than B.1.1.7 and the original COVID-19 lineage. And preliminary data from Moderna shows that its vaccine produces six times fewer neutralizing antibodies for B.351 than the initial variant. Fortunately, the Moderna vaccine was incredibly effective to begin, so according to Moderna, the antibody response their vaccine creates is still enough to create immunity.
The Brazillian variant, P.1, appears to be very infectious. It is estimated that 75% of the people living in the Amazonian city of Manaus contracted the variant before it peaked there in May of 2020. Antibodies derived from COVID-19 patients are often used to treat severe forms of the disease. Those antibodies do not appear to be as effective against the virus circulating in Brazil. Though it’s not a study of antibodies produced by a vaccine, it suggests that vaccines may not be as effective against this variant, as well.
In a press conference Friday, Dr. Anthony Fauci, the U.S.’s top infectious disease expert, said the arrival of these new variants, particularly B.1.351 from South Africa, is a “wake up call.” The U.K., France and Germany have implemented new travel bans to prevent its spread.
Yes. Some mutations are beneficial to humans, some aren’t. Some mutations that benefit the virus also benefit us: Some viruses become less lethal over time and become better at spreading as a result.
But it’s a numbers game. So far, most mutations have been small and slow, and there has been some overlap between mutations of different variants. They all arose individually. As these new variants circulate and infect more people, they could change too.
There’s evidence that the Pfizer and Moderna vaccines currently being distributed are less effective against the new COVID-19 variants from South Africa and Brazil.
Preliminary research from Novavax, which is in the final stages of a COVID-19 vaccine trial, show it appears to be slightly less effective against the UK variant than the original strain, and even less effective against the South Africa strain.
Johnson & Johnson announced the results of a large scale trial of their new single-dose vaccine Friday. The vaccine was 72% effective at preventing severe illness in the U.S. portion of the trial. But its efficacy rating dropped to 57% in South Africa, where the B.1.351 variant dominates.
That could change even more: each time a copy is made, the virus has a chance to accumulate more mutations that help them evade vaccines or spread more effectively. But there’s another way a COVID-19 virus could change really rapidly, in a sort of nightmare scenario.
More virus circulating means more mutations. But viruses also have ways to share bits of genetic material. It’s called viral recombination.
Viral recombination happens when viruses from two or more viruses of the same strain, but different lineages infect the same cell. Sometimes, the cell will produce new viruses that contain bits and pieces of genetic material from all the parent viruses. Just like with more simple mutations, the change can help the virus or hurt it.
Some scientists suspect a recombination event helped the COVID-19 virus make it into humans, but so far there’s no hard evidence.
The more variants there are spreading, the better chance is of someone getting infected with more than one variant at a time. And if there are many new variants infecting lots of people, the chances of an event like that happening get even higher.
You’re probably used to hearing this by now but here’s the thing: COVID-19 is still a brand-new disease. It’s been very slow to build up mutations, which means new lineages were slow to emerge. New variants are, well, new, and so is research into recombination events.
What little research there is seems to be mixed. Research into similar coronaviruses found recombination. Some studies have found evidence that SARS-CoV-2, the virus that causes COVID-19, has undergone many recombination events this year. Other studies using different methods have failed to find that evidence.
So it’s still uncertain. But we do know that viral recombination happens. It’s been responsible for most of the influenza pandemics over the last century, including outbreaks of avian influenza, also known as bird flu.
Copyright 2021 Oregon Public Broadcasting