British public health officials were mystified. National restrictions reduced the spread of coronavirus in much of the country in late November. But in one part of the south-east of England, the infections were inexplicably growing.
Epidemiologists have launched an investigation, initially assuming that some sort of wider event has occurred or that people are ignoring the rules of social distancing at work, in illegal home parties, or elsewhere. They found nothing. Surprised, they turned to a team of scientists who monitor mutations in the genome of the virus.
On December 8, a group known as the Covid-19 Genomics UK Consortium found a new variant of the virus, with 23 mutations, in a sample taken from a patient in Kent, near the center of the outbreak in late September. They found the same variant in someone tested in London a day later.
Some of the new mutations may have increased virus transmission.
“The merging of genome data and details of the Kent epidemic has led to a key link,” said Sharon Peacock, a microbiologist at the University of Cambridge who leads the genomics team. In an email, she said it was a “light bulb moment” by scientists.
The UK has raised restrictions after announcing a new variant of the coronavirus that appears to be more transmissible.
New information continued to arrive and the British government first publicly expressed concern about the variant on December 14, when Health Minister Matt Hancock told British lawmakers that it was responsible for 1,000 cases in London and south-east England and was expanding.
“Initial analysis suggests that this variant is growing faster than the existing ones,” Hancock said.
Meanwhile, scientists have dug deeper into the nature of mutations in new variants.
Viruses mutate all the time – although coronaviruses are slower than some other common viruses like the flu. What was pointed out in the new variant was that a larger number of mutations than usual affected the code of amino acids that produce proteins that make up the virus.
One mutation alters the spike virus of a virus in a way that is known to make it easier for the virus to stick to cell walls and enter the body. Together with the other two mutations, the change may give the variant a possible advantage over previous versions in human infection.
It was a variant not seen before – and the number and nature of its mutations were, scientists say, unprecedented.
“It’s kind of on the branch, it’s actually really impressive that it’s so different from everything else in the UK,” said Dr. Peacock.
At the time of the discovery of the new variant, it accounted for 62% of all cases recorded in London. And the infections continued to grow rapidly.
The latest data show that the seven-day average of cases in the UK in the week to 23 December rose by 61% compared to the previous week, even though the number of cases is falling in most of the rest of Europe. Hospitalizations and death – indicators of the spread of the virus – increased by 16% and 20%, respectively.
“The ‘basic mechanism that drives rapid spread’ is not entirely clear – it can happen because the virus replicates faster, which means you get a higher viral load, which means you’re more infected,” Peter Horby, president of New Emerging Respiratory Virus Threats An advisory group informing the British government told lawmakers on December 23.
The second hypothesis is that a shorter time could elapse between exposure and infection, leading to faster transmission. “Or it could mean that the duration of contagion is longer,” said Dr. Horby.
Researchers are now working to answer two key questions: Will the new variant cause a more serious disease and will it be able to avoid vaccines?
British scientists say they currently do not have enough evidence to give a definitive answer, but are working hard to find out.
The vaccine tests blood samples of people who had the vaccine against the new variant to determine if they show a different response from the one caused by the previous version.
The widespread opinion among Pfizer / BioNTech vaccine scientists and developers is that the vaccine produces antibodies that attack different sites on the virus, so changes in a small area are unlikely to destroy the strength of the vaccine.
About the severity of the disease caused by the new variant, they are waiting for data on hospitalization and death, which are lagging behind in the number of cases, in order to tell them more.
As they embarked on a new variant, British researchers have spent the last few weeks in a silent hunt for zero patient. They reviewed the contacts of two people who first identified with the variant, neither of whom was ill, and others who became infected early.
One of the hypotheses is that the variant originated in a person with a damaged immune system. People with a lack of immune system are often the hosts when viruses go through a large number of mutations, because the virus can survive in their system for so long.
“Ideally, you would know who the case with the index is,” said Dr. Peacock. “We don’t even know if this happened to a patient in the UK or if it has already been introduced, we can’t say categorically at the moment.”
In the week after the new variant was released to the public, new data and epidemiological modeling have made British scientists increasingly convinced that the new variant reproduced faster than its predecessors. Some models have suggested that it is 50% to 70% more portable than other versions.
By December 18, as new infections in the region continued to accelerate, a meeting of government officials and scientists had upset the government, causing a significant shift in policy.
The next day, Prime Minister Boris Johnson announced new blockades for regions where the virus was spreading rapidly and reduced the planned five-day Christmas easing of restrictions to just one day in the rest of the country.
This article was published in The Wall Street Journal.