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They discover a "key" that helps the coronavirus to enter and spread rapidly in the human body

2020-10-21T20:12:57.160Z


The finding would explain why the SARS-CoV-2 virus is much more infectious than the previous SARS-CoV.Vanesa Lopez 10/21/2020 17:00 Clarín.com Society Updated 10/21/2020 5:00 PM A group of researchers found a new explanation for why the coronavirus is so infectious and can spread rapidly in human cells. The findings were published Tuesday in the scientific journal  Science. ​It was already known that the SARS-CoV-2 virus - which causes covid-19 disease - uses the ACE2 receptor to infect human c


Vanesa Lopez

10/21/2020 17:00

  • Clarín.com

  • Society

Updated 10/21/2020 5:00 PM

A group of researchers found a new explanation for why the coronavirus

is so infectious and can spread rapidly

in human cells.

The findings were published Tuesday in the scientific journal 

Science.

It was already known that the SARS-CoV-2 virus - which causes covid-19 disease - uses the ACE2 receptor to infect human cells.

Now they discovered that it also uses another "gateway", it is

another receptor, called neuropilin-1

(NRP1).

"Viruses often use multiple factors to

maximize their infectious potential

," Giuseppe Balistreri, head of the research group, from the University of Helsinki, Finland, said in a statement.

Unlike other respiratory viruses, SARS-CoV-2 also infects the upper respiratory system, including the nasal mucosa, and consequently spreads rapidly.

"This virus can leave our body even

when we simply breathe or speak

," Balistreri noted.

Artist's rendering of how the 'spike' of the coronavirus protein (red) could bind to the cellular ACE2 receptor (dark green) and the neuropilin-1 receptor (light blue) on the surface of cells (yellow).

Photo University of Helsinki.

The starting point of the study was the question of why SARS-CoV - the coronavirus that caused an outbreak much smaller than the current one in 2003 - and the current SARS-CoV-2

spread in such a different way

, even when they use the same main receiver, the ACE2.

To try to explain these differences, the researchers looked at proteins on the viral surface.

These are

spikes

 , which are proteins that protrude and give the virus its characteristic corona shape (hence its name, "coronavirus").

These spikes or spikes, as if they were hooks,

anchor the virus to the cells

.

“When the SARS-CoV-2 genome sequence became available in late January, something surprised us.

Compared to its older relative (SARS-CoV), the new coronavirus had acquired

an 'extra piece'

in its surface proteins, a piece that is also found in the spikes or spikes of many devastating human viruses, including Ebola, HIV , and highly pathogenic avian flu strains, among others, Balistreri noted.

This difference could be the key to understanding why SARS-CoV-2 spreads in the human body much more than SARS-CoV.

And research carried out in collaboration by the University of Helsinki, the Federal Polytechnic School of Zurich (Switzerland) and the University of Tartu (Estonia), confirmed that hypothesis.

Scientists discovered that SARS-CoV-2 has an 

extra "key" to enter cells

, which is neuropilin-1 (NRP1), a receptor that is very abundant in human tissues such as the respiratory tract, blood vessels and neurons.

In parallel, a group of researchers from the University of Bristol (United Kingdom) obtained similar results and were able to confirm that the spike or spike of the current coronavirus binds directly to neuropilin-1.

Therefore, the two studies complement each other.

By specifically blocking neuropilin-1 with antibodies, the researchers were able

to significantly reduce infection

in laboratory cell cultures.

“If you think of ACE2 as a lock on the door to enter the cell, then neuropilin-1 could be a factor that

directs the virus to that door

.

ACE2 is expressed at very low levels in most cells.

Therefore, it is not easy for the virus to find doors to enter.

Other factors, such as neuropilin-1, could help the virus to find its door ”, exemplified Balistreri.

Could this contribute to the development of new drugs?

“It is too early to speculate whether direct neuropilin blockade could be a viable therapeutic approach, as this could lead to

side effects

.

This should be evaluated in future studies ”, indicated the researcher.

Currently, the University of Helsinki laboratory is testing the effect of new molecules that have been specifically designed to

interrupt the connection between the virus and neuropilin-1

.

And they assure that the preliminary results are very promising.

LGP

Look also

The Coronavirus as you never saw it

They discover how the coronavirus "camouflages" itself to enter cells without being detected by the immune system

Source: clarin

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