Adriana santagati
03/16/2021 6:00 AM
Clarín.com
Society
Updated 03/16/2021 6:00 AM
The scientists were able to identify where it was that the Covid-19, in its process of “copying itself”, would have made the “mistake” that led to
a much more contagious variant
that spread throughout much of the world.
The UK variant, which was first detected in September, is believed to have arisen in the Duchy of Kent, in a patient who had a disease that compromised his immune system.
For this reason, he had an extremely prolonged clinical picture, in that time
a series of changes
were generated
in the SARS-CoV-2 genome
and, from that zero case, the chain of infections was triggered.
Although it is difficult to confirm 100%, there would have arisen this variant that spread to a hundred countries including Argentina --where it has community circulation--, forced a
lock down
in Great Britain and suspension of flights.
What science does have more certainty now is
why this variant is between 50% and 70% more transmissible
than the original from Wuhan.
And to the surprise of the researchers, the key to the increase in transmissibility seems to be not only the greater eagerness to bind to the receptor of the human cell, but
the dynamics with which it replicates inside it once it enters
.
The research by specialists at the prestigious Mount Sinai School of Medicine in New York is so recent that it has not yet been published in a scientific journal.
But it is shared by the technical scientific director of ANLIS-Malbrán, an Argentine scientific body that has been following the course of the pandemic tirelessly and that has a
strategic collaboration
with the US entity.
The UK variant has 23 mutations of which 8 are in the spicule.
Of these, there is one in particular that would give the virus more affinity to bind to the AC2 receptor of the human cell.
It was believed that this was the reason why this variant is much more contagious, but now it is known that
it is not the only one
.
“These mutations give the virus a much more important replication kinetics.
Today it is known that three hours after the entry of the virus into the human cell, the number of copies equal to that between 24 and 48 in the variant that was circulating at that time.
Its replication dynamics is extremely faster and
if you have a higher viral load, you will spread more
”, explains geneticist Claudia Perandones.
The ANLIS-Malbrán expert says that these same mechanisms were analyzed in the other three VOCs, the acronym in English for variants of concern, which are followed with special attention:
South Africa, Manaus and Rio de Janeiro
(the last two were detected also here).
And they found that although they have a higher replication dynamics than the
wild type
(the original virus), they do not equal that of the United Kingdom.
“Knowing what are the advantages that these variants give to the virus allows us to generate much more targeted therapeutic strategies.
If you have that the difference in viral load is very close to the beginning of the picture,
you have to exacerbate early diagnosis and isolation
", says Perandones, and asks" not to be afraid of the variants. "
In this sense, it takes up an issue that recently caused concern in the scientific community: the identification of two patients in Brazil who had co-infections of two different variants.
“The question was raised as to whether patients were infected with a variant that, by persisting over time, generated changes that would cause another variant to appear.
But genomic studies were carried out in the population and they found that there were two variants, the one from Rio de Janeiro and one from Rio Grande Do Sul, and it was confirmed that they were indeed
co-infections of two different variants
.
They were even able to sectorize in these patients that the upper respiratory tract had an infection from one variant and the lower one from another, as
a respect for the viral territories
.
They are two independent events that did not make the clinical picture more serious ”, he reassures.
It also demystifies that SARS-CoV-2
mutates more than other viruses
.
It is what it may seem to us, perhaps because we are all pending and nobody notices how the influenza virus mutates.
It is that, in fact, the agent that causes the flu has a mutation rate
between 15 and 20 times higher than the Covid
.
Because the virus that keeps the whole world in suspense has a mechanism called
proof reading
(which the influenza does not have), which is like a "reading" when it is replicating and that allows it to control the errors it makes in the generation of copies.
Thus, the amount of errors or mutations is less.
However, there are.
And, says Perandones, there will continue to be.
Because all viruses mutate all the time.
In some cases, as in these variants we are talking about, the mutations confer them selective advantages, such as being more transmissible.
An encouraging piece of information provided by the expert is that in the three detected here (Rio de Janeiro, Manaus and the United Kingdom), convalescent plasmas with a high concentration of antibodies were able to
neutralize the viral effect
.
This is not only positive with respect to the treatments but also "gives the certainty of the vaccine effectiveness".
Regarding vaccines, he insists, as infectologists have already done, that pharmaceutical companies are testing the effectiveness against the different variants that have appeared so far and that the formulations can be corrected, as is the case with the flu.
"Perhaps the situation to consider is that
we are not going to have a vaccine development that will last forever,
" he says.
And finally, can all these virus changes lead to us having
an Argentine variant
at some point
?
"It's possible.
There is no country in the world that can say that it is not going to have a variant of Covid.
That is why it is important to monitor those that are circulating and the potential introductions that travelers may make.
We can have an Argentine variant, but perhaps not all the variants that emerge may be negative, "he concludes.
ACE
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