At once the coronary virus seems to have changed.
For months, Dr. Stephen Kemp, an infectious disease specialist, scanned a global library of the coronavirus virus genome. .
Then, in late November, Camp made an astonishing match: some of the same mutations found in the patient, along with other changes, appeared again and again in people who were recently infected, particularly in the UK.
Worse, the changes focused on the prickly protein that the virus uses to attach to human cells, suggesting that a virus that has already wreaked havoc around the world has evolved in a way that could make it even more contagious.
“There is a load of mutations that occur together with the same frequency,” he wrote on December 2 to Dr. Rabinandra Gupta, a Cambridge virologist. Listing the most disturbing changes, he added, “All of these sequences have the following mutations.”
The two researchers still did not know it, but they found a new version of a highly contagious coronary virus, which has since stamped across the UK, shaken scientists’ understanding of the virus and threatened to bring back the global recovery from the pandemic.
The rumor skyrocketed through a consortium of British pathologists, veteran torch-bearers in genomics who helped track Ebola and Zika epidemics. They came together in lax conversations and video calls, comparing comments while chasing clues – including a tip from scientists in South Africa on another new version there. Others have since emerged in Brazil.
For almost a year, scientists have only observed cumulative changes in the coronary virus and expected more of the same. The new versions forced them to change their thinking, and introduced a new stage in the epidemic in which the virus could develop long enough to undermine the effectiveness of vaccines.
British lawmakers announced the news on December 14, warning that the version was spreading faster than its predecessors.
The road to its discovery, however, was set for little praise in March, when Britain decided to start a series of Coron virus virus samples en masse. The country produces half the world inventory of the coronary virus genome, and provides an unparalleled view of how the virus changes and how people brought it to the UK last year and are now carrying out the version.
For the UK, the discovery came too late to prevent a punitive new wave of COVID-19 that put hospitals on the brink of denying life-saving treatment. The version had already spread rapidly, and was done by the government’s loose restrictions in the fall and early winter.
But Britain sounded the alarm to the world, allowing countries to close their borders and start frantically searching for a version they might not otherwise have noticed for months. British scientists quickly published studies that convinced skeptics of its power.
“In the UK, a lot of things have gone wrong with this epidemic – mostly, without learning lessons about the importance of early response,” said Neil Ferguson, a public health researcher and government adviser. “But the UK has a rather unprecedented surveillance system for COVID. We can track very small changes in the virus.”
Laboratories across the UK, after testing swabs to detect the virus, send the remnants of the material in refrigerated vans to the Wolcom Sanger Institute, a genomics lab, where they are stored in vigilant freezers.
There, robots separate the positive samples and deposit them in wells of tiny muffin-shaped plates. Machines then map their genome, said Jeffrey Barrett, who runs the sequence project and produces 30,000 letter-length genetic codes uploaded to an Internet library. The task of logic in mutations rests with biologists like Andrew Rambo, a professor in Edinburgh, who determine where they fit into the evolutionary tree.
The effort has created more than 165,000 sequences in the UK. The United States, with five times as many people, floor about 74,000 genomes. Germany has a floor of about 3,400, less than half of what Britain put into the global pool alone on Thursday.
“It’s made a complete revolution in dealing with the virus,” said Judith Breuer, a virologist at University College London.
The campaign was formed on March 4, before 100 coronary heart disease infections were found in the UK, when a Cambridge microbiologist, Sharon Peacock, sent email letters to British genomics asking each of them: “Can you call me, please?
Within two weeks the newly formed consortium had promised government funding £ 20 million, about $ 27 million.
“This is a close-knit community here, and in March it actually put aside any rivalry, any ego, and simply said ‘we can play a critical role in managing the plague,'” said Thomas Connor, a Wales scientist who built the platform. For genome collection and analysis.
Among the samples sequenced last summer were those of a man in his 70s with lymphoma, who were hospitalized in May at a Cambridge hospital for treatment with COVID-19. Gupta, a part-time clinician, began treating a patient whose anti-cancer drugs had corrupted his immune response. The patient was stressed in an isolation room, and struggled to breathe. Even after several rounds of treatment, including plasma with recovered antibodies from patients, the virus did not disappear.
Instead, it’s a mutation. Britain’s sequential efforts have opened a window to those changes: for 101 days in the hospital, the sequence of viral particles passing through a man’s lungs 23 times, a treasure trove of clues.
The patient died in August, ostensibly without infecting anyone else. But in the end the mutations in his virus provided scientists with a leading theory as to the origin of the British version: by evading the immune defenses of someone like a Cambridge patient who had a weakened immune system and long-term infection.
“We call this the standard gold patient for evaluating different viral populations in a host,” Kemp said.
One mutation that a patient had, labeled 69-70del, changes the shape of the barbed protein. Another, N501Y, can help a protein bind more strongly to human cells.
Kemp sought these changes every few days in the global database, and found little cause for concern. Then, in late November, he suddenly noticed many genomes, mostly from the UK, that had the same mutations and a host of others that could change the way the virus entered human cells. He summoned Gupta to his computer to take a look.
Eventually, British scientists discovered 23 mutations that distinguished this genome from the earliest known version in Wuhan, China – enough to be considered a new version, since it was labeled B117. On an evolutionary tree made by Kemp, it stood separately like a solitary, upper branch.
“I did not expect anything like that,” Gupta said. “At the end of November everything was related to the vaccine and there was no variation of new versions.”
The number of mutations in the spike protein particularly affected him, he said, calling it a “wow ‘moment.”
At the same time, public health experts in the UK have been puzzled by an unexplained outbreak of coronary heart disease cases. Lock has calmed the virus across England, but not in Kent, a traveling county in London and a fruit orchard in the south-east. Cases have appeared in schools. One in 328 residents is infected.
It was only on December 8, in their regular meeting with genomics, that public health officials concluded that the cause was most likely a new version. Looking back through their databases, scientists discovered that it was first collected in September and spread when people returned to offices and towered over restaurants and pubs at government demand.
In the end, the researchers were convinced that the version, in fact, is more transmitted – about 30-50% more – but only after putting together patches of less cutting clues.
“There is no absolutely unequivocal line of evidence; science produces this kind of certainty over longer periods of time,” said Oliver Phibus, an evolutionary biologist at Oxford. “It was more a case of different and independent lines of evidence uniting.”
After the scientists presented their Dec. 11 conclusion to a government advisory body, Ferguson, a public health researcher, was concerned that it “would almost certainly require us to get into another lock.” He sent a message to Prime Minister Boris Johnson’s chief scientific adviser, warning of the version.
By Dec. 22, government scientists said strict measures, including closing schools, were needed to suppress the version. But Johnson allowed people in parts of England to gather for Christmas and did not impose a lock all over England until January 4th.
It is estimated that the version accounts for more than 80% of positive cases in London and at least a quarter of infections elsewhere in England and has occurred in more than 50 countries. U.S. health officials warned Friday that the British version may be the dominant source of infection in the United States by March.
In recent days, Gupta and Kemp have begun using blood serum from vaccinated people to determine if the version may weaken the strength of the vaccines.
“The world has long been told that the mutations are not really important from the coronary virus,” Gupta said. “But we found that the mutations did come, and they affected the ability of the virus.”