The highly infectious coronavirus variant “Kent” was already in the US six weeks before the UK sounded the alarm, according to a study.
Researchers at the University of Arizona say that progeny B.1.1.7 – as it is scientifically known – was behind a group of cases in California that were followed until November 6.
Another outbreak of the variant occurred in Florida on November 23, according to scientists.
Top scientific advisers in the UK – who have called for a blockade to stop the rapid spread of the variant – told the government about the new variant only in mid-December.
The team studied the genomes of 50 infected patients whose samples tested positive for the variant, tracking their offspring to estimate when the mutant virus first appeared in the country.
This retrospective study has the advantage of genomic analysis and retrospective, and the first real case of the Kent strain was not diagnosed in an American until December 29.
“It is striking that this parentage could have already been established in the US for about 5-6 weeks before B.1.1.7 was first identified as a variant of concern in the UK in mid-December,” the researchers write. .
“And it may have been in the United States for almost two months before it was first detected on December 29, 2020.”
The Kent variant was designated as a variant investigated by the United Kingdom on 8 December and reclassified as a “variant of concern” on 18 December.
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New variants of coronavirus have mutations in the spike protein, which are essential for the immune system’s antibodies to block and destroy it. Changing their shape makes it harder for the body to catch the virus
The study has not yet been evaluated by colleagues, but is available online as a pre-print.
The exact origin of the Kent variant is unknown, but it is believed to have appeared in mid-September.
Dr. Susan Hopkins, a senior public health official in England (PHE), said in December that there was initially “nothing to point out in particular that this is a major concern, as the options come and go.” leaves”.
Virus mutations occur all the time, the vast majority of which are harmless or harmful to the pathogen.
However, by chance, sometimes changes to the viral code give it a survival advantage and increase its success, often becoming more infectious and easier to spread.
This is thought to have occurred in variant B.1.1.7, which previous studies have found to be more abundant in the upper respiratory tract.
A mutation in the spike protein – which comes out of the coronavirus and hijacks human cells – has made it better for infecting humans.
This so-called N501Y mutation is also found in the South African and Brazilian variants that have been identified since then.
Researchers in Arizona found that all cases in California have another minor mutation, which is seen in only 1.2% of European cases B.1.1.7.
This, they say, indicates a single introductory event, probably from international travel, that sowed the variant in California, where it then spread from person to person.
A similar trend was observed for the group of Floridian cases, which were very similar to the most common type of B.1.1.7 observed in the United Kingdom.
This is a “strong indication that they are also descending from a single introductory event,” say scientists.
At least three major variants of coronavirus have been observed in the UK in recent months – from Kent, South Africa and Brazil – and appear to be evolving to spread faster and to evade parts of the immune system, although people of Science still does not believe that there is yet to go so far as to completely get rid of vaccines
When the British government revealed that the variant was probably the reason for an increase in local cases in the UK in mid-December, it plunged south-east London and eastern England into Level 3 restrictions.
The British government’s scientific advisers have proclaimed that it is up to 70 percent more infectious than the previous dominant variant and encourage people to stay home to prevent transmission.
It is now believed to account for more than 60% of all cases in the UK, but in California, between 27 December and 2 January, only 0.4% of cases were Kent. At a comparable time in the UK, this figure was 1.2%.
“This suggests that the dynamics of B.1.1.7 may be somewhat less explosive in California than its original epicenter in England,” say the researchers.
“Florida’s Class 2 (21 million inhabitants), on the other hand, showed a faster movement of non-B.1.1.7,” the researchers write.
Here, it accounted for 0.7 per cent of cases 34 days after first appearing in the state and “at a comparable time in the B.1.1.7 outbreak in England B.1.1.7 accounted for about 0.1 percent of all cases ”.
Therefore, although obviously younger than the offspring of California Clade 1, the offspring of Florida Clade 2 is already a larger proportion of the Florida SARS-CoV-2 epidemic than class 1 of the California SARS-CoV-2 outbreak.
Line B.1.1.7 currently accounts for only 0.3% of coronavirus infections in the United States, the researchers say.
The reason for the different rate at which B.1.1.7 overcomes pre-existing spots remains unknown, but researchers offer some possibilities in their study.
“One possibility is that the advantage of B.1.1.7 transmission may vary depending on the intensity of the attenuation,” they say.
“Perhaps this parentage of SARS-CoV-2, with demonstrably higher viral loads in the upper respiratory tract than other variants, is able to sow over-spreading events with relative ease when attenuation efforts are relatively lax, but its advantage transmission is less acute when playing the field is leveled by, for example, the widespread use of masks and avoiding the crowd inside.
“Another possibility is that non-B.1.1.7 offspring circulating in the US, especially in California, may be more transmissible than non-B.1.1.7 offspring in England with which B.1.1.7 has competed, offering B.1.1.7 a lower transmission advantage and thus a slower travel rate of non-B.1.1.7 lines. ‘