These coronavirus variants are keeping scientists awake at night

One, first identified in southeastern England, has appeared in at least 50 countries and appears to be spreading more efficiently than older variants of the virus. Its emergence frightened political leaders, who closed borders and imposed travel restrictions in an attempt to curb its spread.

Others, identified in South Africa and Brazil, did not travel as much, but show a constellation of mutations that caught the attention of geneticists.

And then there is a new variation that has appeared in California that may or may not be generating a new spread there.

“We haven’t slept much, to be honest, lately,” said Dr. Christian Gaebler, a molecular immunologist at Rockefeller University who is studying the body’s immune response to coronavirus infection.

So far, none have done what scientists fear most and have mutated to the point of causing more serious illnesses or evading the protection provided by vaccination. Although some of the new variants appear to have changes that appear to affect the immune response, it is only a matter of degree.

B.1.1.7

At the top of the list of researchers in the USA is variant B.1.1.7 seen for the first time in Britain. The US Centers for Disease Control and Prevention warned last week that this could worsen the spread of the pandemic.

While there is nothing like the phrase “new mutant virus” to draw attention, scientists say they are so far at ease with what they have discovered: the human immune system can handle the variants that have emerged so far.

“It is neither more nor less serious. It does not cause different rates of hospitalization or mortality,” Gregory Armstrong, who directs the CDC’s Office of Advanced Molecular Detection, told CNN.

“As far as we know, it is broadcast in exactly the same way.”

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This means that the same measures already known to reduce the spread will also prevent the new variants: wearing a mask, social distance, avoiding large groups or crowds and frequent hand washing.

Mutations in the variant help you get into cells more easily – meaning that if someone, say, breathes air with virus particles, those particles are more likely to infect some cells in the sinuses or lungs instead of bouncing harmlessly. The changes increase the peak protein the virus uses to bind cells.

Armstrong says the evidence that B.1.1.7 is more easily transmitted is convincing to him.

On the one hand, he took over southeastern England during a time when people were supposed to be stranded in November and December, infecting 50% more people than the older variants, called wild-type viruses.

“They also looked at what happens to these people’s contacts,” he added. About 11 out of 100 people in contact with someone infected with the wild-type virus would be infected. “But the contacts of people with B.1.1.7. 16 out of 100 would be sick,” said Armstrong. “Contacts from people with B.1.1.7 would be sicker at higher rates.”

In addition, there is evidence that people infected with variant B.1.1.7 have what is known as the highest viral load – they have more viruses reproducing in their bodies. This makes sense if the variant infects cells more easily, because viruses hijack the cells they infect, turning them into virus factories. More infected cells equate to more viruses.

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But Armstrong dismisses initial concerns that the new variant will more easily infect children. Britain left schools open during the blockade that saw B.1.1.7 spread, he said, and that would easily explain why more children were infected.

All of this simply means that people need to do more to prevent spread until vaccination can be accelerated.

“To stop the transmission, we will need higher rates than we do to slow the transmission,” said Armstrong. “We need to pay more attention to wearing masks. And we need to increase vaccination coverage ”.

Mike Osterholm, who heads the University of Minnesota’s Center for Infectious Disease Research and Policy, does not believe that people will do that.

“I really think B.1.1.7 will have a deadly impact on the number of new cases in 6-8 weeks,” he said. “I hope I’m wrong.”

So far, the CDC has reported 120 cases of people infected with B.1.1.7 in 20 states, although the agency says it is probably much more common than that. The United States does not have many laboratories doing the necessary tests to identify mutant versions of the coronavirus.

University of Arizona biologist Michael Worobey said he found evidence that B.1.1.7 was imported at least five different times into the United States, and probably many more. “It is striking that this strain was already established in the United States for about 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 United States for almost two months before it was first detected, on December 29, 2020.”

B.1.351

A variant seen for the first time in South Africa called B.1.351 or 501Y.V2, has a different pattern of mutations that causes more physical changes in the structure of the peak protein than B.1.1.7. One major mutation, called E484K, appears to affect the receptor-binding domain – the part of the spike protein most important for binding to cells.

It can help the virus to partially escape the effects of vaccines. “There is more concern about immune escape,” said Armstrong. Vaccine manufacturers and academic researchers are testing samples of this variant, along with others, to see if it can escape the immune response caused by the vaccination.

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Dr. Michel Nussenzweig, from Rockefeller University, does not think so.

He and his colleagues have studied 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 as soon as an infection occurs, the immune response matures and becomes even better at fighting the virus, reported Nussenzweig’s team in the journal Nature Monday.

“We have a reservoir of antibodies that are preformed,” said Gaebler, who worked on the study.

“The immune system goes to that pool and sees what fits well. Once you find these antibodies, you can refine them and make them even better. ”

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This should reassure people, said Nussenzweig. The human immune system adapts very well to viral mutations, he said, and produces hundreds of different antibodies that can attack the coronavirus.

“There are certainly a range of different types of antibodies that can neutralize the virus. These types of things in the plasma are probably resistant to emerging mutations,” said Nussenzweig.

Vaccines produce an immune response similar to natural infection. So even if a new variant appears with mutations that allow it to evade part of the immune response, the body is producing antibodies that can see undisguised parts of the virus.

However, officials in South Africa say that this variant is now the most common version of the coronavirus found in several areas. It is also common in neighboring Zambia and has been detected in 20 countries. It has not yet been found in the USA.

P.1 and P.2

Two variants of concern emerged first in Brazil. One, called P.1., Was found in 42% of specimens in a survey conducted in the Brazilian city of Manaus, and Japanese authorities found the variant in four travelers from Brazil. “The emergence of this variant raises concerns about a potential increase in transmissibility or propensity for reinfection in individuals with SARS-CoV-2,” said the CDC. P.1 also carries the E484K mutation.

P.2, also seen for the first time in Brazil, caused a wave of alarm when it appeared in Britain last week in 11 people.

L425R

Finally, there is a new variant seen in California. “We still don’t know what that means,” said Armstrong. It also has a mutation in the receptor-binding domain of the spike protein. The new California variant is called the L425R and, although it is commonly found, it is not yet clear whether it is more transmissible.

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Any viral strain can become more common because of what is known as the founding effect. “The founding effect is that the virus is in the right place at the right time,” said Armstrong. If a particular strain is circulating when transmission increases because of human behavior, that strain will continue and become more common not because it spreads more easily, but simply because it was there.

In a prepress – a study posted online but not reviewed by a medical or scientific journal – a Cedars-Sinai team in Los Angeles said it found this variant in 36% of the samples collected from 192 patients at the hospital in late November and December, and in 24% of Southern California samples

The California Department of Public Health said the variant was “increasingly” appearing in the state.

At the moment, the United States is doing a terrible job with what is known as genomic surveillance, said Armstrong. “We don’t have surveillance based on gold standard sequencing like the UK,” said Armstrong. This may explain why the UK detected B.1.1.7 before the USA.

Employees who may be doing this type of testing are running tests to diagnose coronavirus infections in people. “State laboratories have become overwhelmed. Many employees who were doing the sequencing are doing PCR tests,” he said.

Therefore, the appearance of the L425R may be just a function of California laboratories starting to look for variants and find them.

The CDC is working to increase the capacity to do this type of testing, stepping up efforts with state and local health departments, funding academic laboratories to do more testing and working on agreements with commercial test laboratories, said Armstrong. “In two to three weeks, we will be receiving 5,000 sequences a week from these companies,” said Armstrong.

Further studies are needed to show whether these variants can increase the already astronomical spread of the virus. The USA has more than 24 million diagnosed cases and about 400,000 deaths.

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