These coronavirus variants are keeping scientists awake at night
At least four new variants of the coronavirus are keeping scientists awake at night.
One, first identified in southeast England, has now shown up in at least 50 countries and appears to be spreading more efficiently than older variations of the virus. Its appearance has frightened political leaders, who have closed borders and imposed travel restrictions in attempts to curb its spread.
Others, identified in South Africa and Brazil, haven’t traveled as far and wide but show a constellation of mutations that have grabbed the attention of geneticists.
And then there is a new variation that’s shown up in California that may or may not be driving renewed spread there.
“We don’t get much sleep, to be honest, lately,” said Dr. Christian Gaebler, a molecular immunologist at the Rockefeller University who is studying the body’s immune response to coronavirus infection.
So far, none has done what scientists most fear and mutated to the point that it causes more severe disease, or evades the protection provided by vaccination. While some of the new variants appear to have changes that look like they could affect immune response, it’s only by a matter of degree.
At the top of the list for researchers in the US is the B.1.1.7 variant first seen in Britain. The US Centers for Disease Control and Prevention warned last week it could worsen the spread of the pandemic.
While there’s nothing like the phrase “mutant new virus” to grab the attention, scientists say so far they are reassured by what they have found: The human immune system can handle the variants that have sprung up so far.
“It is not any more or less severe. It doesn’t cause different rates of hospitalization or mortality,” Gregory Armstrong, who directs the Office of Advanced Molecular Detection at CDC, told CNN.
“As far as we know it is transmitted in exactly the same way.”
That means the same measures already known to reduce spread will also stop the new variants: mask use, social distancing, avoiding large groups or crowds and frequent handwashing.
The mutations in the variant help it enter cells more easily — which means if someone, says, breathes in a lungful of air that has virus particles in it, those particles are going to be more likely to infect some cells in the sinuses or lungs rather than bouncing off harmlessly. The changes enhance the spike protein that the viruses uses to attach to cells.
Armstrong says the evidence that B.1.1.7 is more easily transmitted is compelling to him.
For one thing, it took over in southeast England during a time when people were supposed to be in lockdown in November and December, infecting 50% more people than the older, so-called wild type virus variants.
“They also looked at what happens with the contacts of these people,” he added. About 11 out of every 100 people in contact with someone infected with wild-type virus would themselves get infected. “But the contacts of people with B.1.1.7. 16 out of 100 would get sick,” Armstrong said. “Contacts of people with B.1.1.7 would get sicker at higher rates.”
Plus there’s evidence people infected with the B.1.1.7 variant have what’s known as a higher viral load — they have more virus reproducing in their bodies. That makes sense if the variant infects cells more easily, because viruses hijack the cells they infect, turning them into virus factories. More infected cells equal more virus.
But Armstrong discounts initial worries that the new variant infects children more easily. Britain left schools open during the lockdown that saw B.1.1.7 spread, he said, and that would easily explain why more children became infected.
All this simply means people need to try harder to prevent spread until vaccination can be sped up.
“In order to interrupt transmission, we are going to need higher rates of what we do to slow transmission,” Armstrong said. “We are going to need to pay more attention to wearing masks. And we will need to increase vaccine coverage.”
Mike Osterholm, who directs the Center for Infectious Disease Research and Policy at the University of Minnesota, doesn’t have a lot of faith that people will do that.
“I do think that the B.1.1.7 is going to have a deadly impact of the number of new cases in 6-8 weeks,” he said. “Hope I’m wrong.”
So far, CDC has reports of 120 cases of people infected with B.1.1.7 in 20 states, although the agency says it’s likely far more common than that. The US doesn’t have many labs doing the testing needed to identify mutated versions of coronavirus.
Biologist Michael Worobey of the University of Arizona said he’s found evidence B.1.1.7 was imported at least five separate times to the US, and likely many more. “It is striking that this lineage may already have been established in the US for some 5-6 weeks before B.1.1.7 was first identified as a variant of concern in the UK in mid-December,” he wrote in a post on a website dedicated to sharing genetic information about the virus. “And it may have been circulating in the US for close to two months before it was first detected, on 29 December 2020.”
A variant first seen in South Africa called B.1.351 or 501Y.V2, has a different pattern of mutations that causes more physical alterations in the structure of the spike protein than B.1.1.7 does. One important mutation, called E484K, appears to affect the receptor binding domain — the part of the spike protein most important for attaching to cells.
It could help the virus partly escape the effects of vaccines. “There is more concern about immune escape,” Armstrong said. Vaccine makers and academic researchers are testing samples of this variant, along with others, to see if it can evade the immune response caused by vaccination.
Dr. Michel Nussenzweig of Rockefeller University doesn’t think so, however.
He and colleagues have been studying the immune response to coronavirus infection and say the body produces hundreds of different types of antibodies to attack the virus.
People are born with some of them, and once there is an infection, the immune response matures and becomes even better at targeting the virus, Nussenzweig’s team reported in the journal Nature Monday.
“We have a reservoir of antibodies that are preformed,” said Gaebler, who worked in the study.
“The immune system goes to that pool and sees what fits well. Once it finds those antibodies, it can refine them and make them even better.”
That should reassure people, Nussenzweig said. The human immune system adapts very well to viral mutations, he said, and produces hundreds of different antibodies that can attack coronavirus.
“For sure there is a breadth of different kinds of antibodies that can neutralize the virus. These kinds of things in plasma are likely to be resistant to the emerging mutations,” Nussenzweig said.
Vaccines produce a similar immune response to natural infection. So even if a new variant emerges with mutations that allow it to dodge some of the immune response, the body is producing antibodies that can see undisguised parts of the virus.
Nonetheless, officials in South Africa say this variant is now the most common version of the coronavirus found in several areas. It’s also common in neighboring Zambia and has been detected in 20 countries. It has not been found in the US yet.
P.1 and P.2
Two variants of concern have shown up first in Brazil. One, called P.1., has been found in 42% of specimens in one survey done in the Brazilian city of Manaus, and Japanese officials found the variant in four travelers from Brazil. “The emergence of this variant raises concerns of a potential increase in transmissibility or propensity for SARS-CoV-2 re-infection of individuals,” CDC said. P.1 also carries the E484K mutation.
P.2, also first seen in Brazil, caused a flurry of alarm when it turned up in Britain last week in 11 people.
Finally, there’s a new variant seen in California. “We don’t know yet what the significance of that one is,” said Armstrong. It also has a mutation in the receptor binding domain of the spike protein. The new California variant is called L425R and while it’s being found commonly, it’s not yet clear if it’s more transmissible.
Any viral strain can become more common because of what’s known as the founder effect. “The founder effect is a matter of a virus being in the right place at the right time,” Armstrong said. If a particular strain happens to be circulating when transmission increases because of human behavior, that strain will ride along and become more common not because it spreads more easily, but simply because it was there.
In a pre-print — a study that’s posted online but not reviewed by a medical or scientific journal — a team at Cedars-Sinai in Los Angeles said they found this variant in 36% of samples taken from 192 patients at the hospital in late November and December, and in 24% of samples from southern California
The California Department of Public Health said the variant was “increasingly” turning up around the state.
Right now the US is doing a poor job of what’s known as genomic surveillance, Armstrong said. “We don’t have gold standard sequencing-based surveillance like the UK has,” Armstrong said. That may explain why the UK spotted B.1.1.7 before the US did.
Staffers who might be doing this kind of testing instead are running tests to diagnose coronavirus infections in people. “State labs have just been overwhelmed. A lot of staff that were doing sequencing are doing PCR testing instead,” he said.
So the appearance of L425R may just be a function of labs in California starting to look for the variants and finding them.
CDC is working to increase the capacity to do this kind of testing, stepping up efforts with state and local health departments, funding academic labs to do more testing and working on deals with commercial testing labs, Armstrong said. “Within two to three weeks, we’ll be getting 5,000 sequences a week from those companies,” Armstrong said.
It will take more study to show whether these variants can increase the already astronomical spread of the virus. The US has more than 24 million diagnosed cases and close to 400,000 deaths.