A tiny mutation in the coronavirus strain common in the U.S. and Italy has made it far more contagious than other variants of the virus, according to a new study.
The potent version of SARS-CoV-2 has four to five times more "spikes" that allow it to bind to human cells on its surface.
This feature not only makes it more contagious, but also more stable and resistant.
Since the corona virus became a pandemic, scientists have wondered why it appeared to be decimating some states and countries while both its spread and lethality were limited.
Previous research had suggested an apparently stronger burden that struck Italy and Europe and spread to New York City, which quickly became the epicenter of the pandemic.
Now scientists at Scripps Research believe that they have confirmed this theory and identified the mutation that overloaded the particularly infectious variant of the coronavirus.
The corona virus "spike" protein (pictured) consists of two components (shown in purple and green). The two-part composition makes it "unstable" and fragile, but a new mutation makes it more stable by making the entire spike "more flexible" and contagious, according to a study by Scripps Research
Plagued by the mutant coronavirus strain, the number of cases in New York increased, which quickly became the global epicenter of the pandemic
There, the researchers isolated various strains of coronavirus that were identified worldwide based on their genetic signatures.
Then they put together a microscopic cage match and tested how aggressively the respective strains attacked human cells in petri dishes.
One strain was the clear winner – the iteration of the virus with the mutated gene, which gave it more "spike" proteins.
"Viruses with this mutation were much more contagious than those without the mutation in the cell culture system we use," said virologist Dr. Hyeryun Choe, PhD, lead author of the study.
The "spike" is a protein on the surface of the coronavirus – known as SARS-CoV-2 – that makes it possible to bind to receptors on the surface of human cells.
In particular, it binds to ACE2 receptors, which are found both on the surface of lung cells and in blood vessels, which makes these systems the main targets for the coronavirus.
The more tips it has, the more opportunities the virus has to stick to a human cell and hijack its machinery to do more of itself.
And the mutant strain that is common in the United States and Italy has them in the spades.
The strong strain of the corona virus also hit Europe and conquered Italy particularly strongly before it spread to the USA (light blue).
"The number – or density – of the virus' functional tips is four or five times higher due to this mutation," said Dr. Choe.
Not only did it have more spikes, but it also had a particularly good fit.
Its protein tip was flexible rather than rigid. This gives him the same advantage that modern suspension bridges have. Wobble and jostle could bend it – but it won't break.
And the longer and more stable it can hang from receptors, the better the possibility for virus particles to penetrate and take over the human cell without the virus falling to pieces.
"Our data is very clear, the virus becomes much more stable with the mutation," said Dr. Choe.
This mutation belongs to a coronavirus strain known as D614G.
Researchers at the Los Alamos National Laboratory in New Mexico said in March that the mutant strain spread to Europe in early February.
Since then, it has found its way to the United States, where it became the most common – and most aggressive – tribe on the east coast by March, and scientists there said it was now the world's dominant tribe.
The researchers mapped the mutation in the spike protein (shown in green), which enables it to be more flexible and infectious
When scientists first reported Spike D614G in March, it only occurred seven times in the sequences uploaded to an international database.
In the meantime, a lesser burden spread from China to Washington and California, so that the United States was bombarded by two different attacks of different strengths.
"However, a sample of GISAID data in early April showed that the frequency of G614 increased at an alarming rate in March and that geographic distribution continued to expand," the researchers wrote in their report, published online on April 30.
It seems that at some point the G614 mutation and another, the D614 mutation, merged into the D614G mutation.
Together they have become dominant and become more contagious through different modes.
This previous work, coupled with the new study, debunked the "founder effect" theory that the corona virus is not very genetically diverse and comes from just a few seeds, says the Scripps team.
"There were at least a dozen scientific papers that talked about the prevalence of this mutation," said co-author Dr. Michael Farzan.
"Do we only see a" founder effect "?
& # 39; Our data nail it. It is not the founding effect. & # 39;
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