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The theory was simple and compelling: Children are less vulnerable to the new coronavirus because they carry antibodies against other common coronaviruses that cause colds. The idea could also explain why some people infected with the new virus show mild symptoms while others – likely without antibodies to the cold coronaviruses – are much more severely affected.
The notion gained popularity, especially among those who argued that this existing protection would quickly bring human populations to herd immunity, the point at which the spread of a pathogen slows down as it lacks hosts to. infect. A study in the journal Science, published in December, strongly revived the hypothesis.
But for all its appeal, the theory doesn’t hold up, according to a new study published Tuesday in the journal Cell. Based on carefully conducted experiments with live viruses and with hundreds of blood samples taken before and after the pandemic, the new research refutes the idea that antibodies to seasonal coronaviruses have an impact on the novel coronavirus. , called SARS-CoV-2.
“By entering this study, we thought we would learn that people who had pre-existing and pre-pandemic antibodies to SARS-CoV-2 would be less susceptible to infection and would suffer from less severe Covid-19 disease,” said Scott Hensley, an immunologist at the University of Pennsylvania. “This is not what we found.”
He and his colleagues concluded that most people are exposed to seasonal coronaviruses by the age of 5. As a result, about one in five people carry antibodies that recognize the novel coronavirus.
But these antibodies aren’t neutralizing – they can’t disarm the virus, or lessen the severity of symptoms after infection, the team found.
The researchers also compared antibodies to the common cold coronaviruses in children and adults and found no difference in the amounts. In contrast, the Science study reported that about 5% of adults carried these antibodies, compared to 43% of children.
This study “reported very high levels of pre-pandemic cross-reactive neutralizing antibodies in children, which we did not find,” said Dr Hensley. (The term “cross-reactive” refers to antibodies capable of attacking similar sites on more than one type of virus.)
“I don’t have an explanation for the difference from the scientific study, honestly,” he added.
Perhaps the difference in location – Pennsylvania, in his study, compared to Britain in previous research – could account for part of the gap, he said.
Other experts said they find Dr Hensley’s study more compelling of the two and more consistent with the circumstances under which large groups of people are infected with the new coronavirus.
For example, a single person infected with the novel coronavirus at a summer camp in Wisconsin sparked an outbreak that affected 76% of the other participants, noted John Moore, a virologist at Weill Cornell Medicine in New York.
Likewise, on a fishing trawler that set sail from Seattle, only three sailors who had antibodies to the novel coronavirus before the trip remained virus-free. These aren’t the infection rates you would see if the protective antibodies were widely distributed in the population, Dr. Moore said.
“The idea that having snuff some time ago somehow protected you from infection with SARS-CoV-2 always left me cold, but it ‘is a lingering urban legend throughout the pandemic,’ he said. “Hopefully this new paper will finally chill everyone and put such thoughts in the freezer.”
Experts also praised the new study’s cautious and rigorous approach.
“It’s really nice to have such a well done study,” said Shane Crotty, virologist at La Jolla Institute of Immunology in San Diego.
The theory that existing antibodies can protect people against the new virus “certainly has great appeal because at first glance it can explain much of the pandemic,” said Dr Crotty. “But a great idea doesn’t make it true.”
Dr Hensley and his colleagues examined samples from 251 people who had donated blood at the University of Pennsylvania before the pandemic and then developed Covid-19.
These people carried levels of antibodies able to recognize the new coronavirus that were no different from those seen in blood samples taken from 251 people who were not infected. And the levels showed no relation to the clinical outcome in any of the patients.
“It’s hard to find those kinds of samples – I was just impressed,” said Marion Pepper, an immunologist at the University of Washington in Seattle. “It’s like three different studies put together into one.”
The most important part of the coronavirus is the spike protein on its surface, which attaches to human cells. The spike is also the most distinctive part of the virus, so it makes sense that antibodies to seasonal viruses are unlikely to recognize and disarm it, Dr Pepper said.
“There are very specific parts of these viruses that are critical for infection, and most of that cross-reactivity is not directed at those parts,” she says.
But George Kassiotis, an immunologist at the Francis Crick Institute in London who led the study published in Science, disagreed with the findings of the new research. It “broadly confirms rather than contradicts our main findings,” he said, adding that the new study was too small to rule out any role for existing antibodies.
But even though people did carry antibodies to the coronavirus from childhood infections, the protection they confer isn’t powerful enough to matter, said Jesse Bloom, evolutionary biologist at the Fred Hutchinson Cancer Research Center in Seattle.
“If there is no measurable effect in a study with hundreds of people in both the infected and uninfected groups, then the effect is certainly minimal,” said Dr Bloom.
Most of the vaccines developed for the novel coronavirus focus on the spike protein. Some scientists have argued that antibodies to other parts of the virus may also be essential for protection. But the new study suggests that other antibodies are of minimal importance in protecting people against SARS-CoV-2.
Experts all said the new study did not rule out the role of immune cells, called memory B cells and T cells, produced in response to seasonal coronaviruses. These cells could recognize parts of the new virus and attack it, reducing the severity of symptoms.
Yet the cells would not prevent infection, Dr Crotty said. When exposed to the new virus, immune cells can be awakened “quickly enough that you have an asymptomatic infection that you never noticed,” he said. “But no, they wouldn’t stop the infection.”
Testing for T cells is laborious and expensive, so analyzes of their contribution to immunity have not yet been completed. In the meantime, the new study rules out at least one important role for existing antibodies, Dr Hensley said: “We’ve kind of written a chapter here, but there’s still so much to learn.
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