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The coronavirus mutated in a way that helped it spread rapidly around the world, researchers admit. There is also the other – optimistic – side of the coin. The mutation made a change that made SARS-CoV-2 more susceptible to vaccines.
- The coronavirus D614G mutation was identified in February 2020. It has been determined to replicate faster and to be more contagious than the “original” version of the virus
- The D614G mutation has a “flap” on the tip of the spike, which allows it to penetrate the host cells more efficiently
- Scientists suspect that the “flap” will make the D614G variant susceptible to vaccines – thanks to it, antibodies will be easier to inactivate the pathogen
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Coronavirus – like any virus – mutates. Scientists have found that this process is much slower in his case than in the case of influenza or HIV. So far, over 12 thousand. SARS-CoV-2 mutation. In common opinion, however, this phenomenon is associated as something dangerous.
In October, dr hab. Piotr Rzymski from the Medical University of Poznań explained in a statement for PAP: “whenever we talk about mutations, we should remember that while this word is generally treated rather pejoratively, a virus mutation does not necessarily mean something dangerous from our point of view. Many mutations do not play any role in this respect (…) »(after PAP)
- The new mutation of the coronavirus. More contagious and less pathogenic
The research of American scientists presented in the prestigious journal “Science” can be related to the words of the scientist. Scientists at the University of North Carolina at Chapel Hill and the University of Wisconsin-Madison detailed it in detail for a variant of the coronavirus – called D614G (or simply G), explaining why it has spread so much around the world and why it may be susceptible to vaccines.
American scientists have known about the D614G mutation for months (it was identified in February 2020). Previous research has shown that it likely appeared in Europe, then became the most common variant of SARS-CoV-2 in the world. A study by a team from the University of North Carolina at Chapel Hill and the University of Wisconsin-Madison supports this theory, suggesting that the D614G variant replicates faster and is more contagious than a virus that originated in China.
A hamster experiment was conducted to better understand the G variant mutation of the coronavirus. Some animals were infected with the newly identified variant of the coronavirus, others with the older SARS-CoV-2 strain. The infected rodents were then placed in cages next to the cages with healthy hamsters. Air could flow between the cages, but the animals had no physical contact with each other. What did this experiment show? Option G appeared to replicate about 10 times faster than the “original” version of SARS-CoV-2 and was found to be much more contagious.
‘We have seen that the mutant coronavirus is better airborne than its’ original ‘version, which may explain why it dominated humans,’ emphasized research author Yoshihiro Kawaoka. “The D614G virus replicates extensively in nasal epithelial cells, which are a potentially important site of person-to-person transmission,” added epidemiologist and microbiologist Ralph Baric of the UNC Gillings School of Global Public Health.
Why is the Coronavirus G variant so effective? Its strength appears to be due to the changes that took place in the spike-forming protein SARS-CoV-2 (it attaches to the host’s ACE2 protein, which allows it to enter its cell). The D614G mutation was found to have a “flap” at the tip of the spine, allowing it to bind to cells even more effectively.
The stick, however, has two ends. And what allows the G-variant of the coronavirus to attack our cells more effectively could contribute to its ‘collapse’. According to scientists, the said “flap” may help the antibodies to neutralize the pathogen. This suggests that D614G will be susceptible to vaccines.
- What does the coronavirus SARS-CoV-2 look like?
The scientists’ discovery also seems to explain why the mutant virus is more infectious, but not necessarily causing severe complications and death. Already in August, prof. Paul Tambyah, an infectious disease specialist, consultant at the National University of Singapore and head of the International Society of Infectious Diseases, said the world should be relieved to hear about the emergence of the D614G strain. He believed that this was to be expected, as most viruses become less virulent as they mutate.
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Prof. Tambyah emphasized the fact that how easy it is for a virus to infect cells did not necessarily translate into harmfulness. “The virus works in its best interest,” he said. “To survive, it must infect but not kill.” It is completely dependent on people, its hosts and hosts.
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