This video helps understand why does the coronavirus spread so easily between people. My Coronavirus Recommendations Mask …
As the number of coronavirus infections approaches
100,000 people worldwide, researchers are
racing to understand what makes coronavirus
spread so easily.
This video helps understand why does the coronavirus
spread so easily between people.
A handful of genetic and structural analyses
have identified a key feature of the virus
— a protein on its surface — that might
explain why it infects human cells so readily.
Other groups are investigating the doorway
through which the new coronavirus enters human
tissues — a receptor on cell membranes.
Both the cell receptor and the virus protein
offer potential targets for drugs to block
the pathogen, but researchers say it is too
early to be sure.
“Understanding transmission of the virus
is key to its containment and future prevention,”
says David Veesler, a structural virologist
at the University of Washington in Seattle,
who posted his team’s findings about the
virus protein on the biomedical preprint server
bioRxiv.
The new virus spreads much more readily than
the one that caused severe acute respiratory
syndrome, or SARS (also a coronavirus), and
has infected more than ten times the number
of people who contracted SARS.
Spiky invader.
To infect a cell, coronaviruses use a ‘spike’
protein that binds to the cell membrane, a
process that's activated by specific cell
enzymes.
Genomic analyses of the new coronavirus have
revealed that its spike protein differs from
those of close relatives, and suggests that
the protein has a site on it which is activated
by a host-cell enzyme called furin.
This is significant because furin is found
in lots of human tissues, including the lungs,
liver and small intestines, which means that
the virus has the potential to attack multiple
organs, says Li Hua, a structural biologist
at Huazhong University of Science and Technology
in Wuhan, China, where the outbreak began.
The finding could explain some of the symptoms
observed in people with the coronavirus, such
as liver failure, says Li, who co-authored
a genetic analysis of the virus that was posted
on the ChinaXiv preprint server.
SARS and other coronaviruses in the same genus
as the new virus don't have furin activation
sites, he says.
The furin activation site “sets the virus
up very differently to SARS in terms of its
entry into cells, and possibly affects virus
stability and hence transmission”, says
Gary Whittaker, a virologist at Cornell University
in Ithaca, New York.
Several other groups have also identified
the activation site as possibly enabling the
virus to spread efficiently between humans4.
They note that these sites are also found
in other viruses that spread easily between
people, including severe strains of the influenza
virus.
On these viruses, the activation site is found
on a protein called haemagglutinin, not on
the spike protein.
Urging caution.
But some researchers are cautious about overstating
the role of the activation site in helping
the coronavirus to spread more easily.
“We don’t know if this is going to be
a big deal or not,” says Jason McLellan,
a structural biologist at the University of
Texas at Austin, who co-authored another structural
analysis of the coronavirus, which was published
in Science.
Other scientists are wary of comparing furin
activation sites on flu viruses to those on
the new coronavirus.
The haemagglutinin protein on the surface
of flu viruses isn’t similar or related
to the spike protein in coronaviruses, says
Peter White, a virologist at the University
of New South Wales in Sydney, Australia.
And the flu virus that caused the deadliest
recorded pandemic, the 1918 Spanish flu pandemic,
doesn’t even have a furin activation site,
says Lijun Rong, a virologist at the University
of Illinois in Chicago.
Whittaker says studies in cell or animal models
are needed to test the activation site’s
function.
“Coronaviruses are unpredictable, and good
hypotheses often turn out to be wrong,”
he says.
His team is currently testing how removing
or modifying the site affects the spike protein’s
function.
Drug targets.
Li's team are also looking at molecules that
could block furin, which could be investigated
as possible therapies.
But their progress is slow because of the
outbreak.
Li lives on campus and is currently the only
member able to access his team's laboratory.
McLellan’s group in Texas has identified
another feature that could explain why the
new coronavirus infects human cells so successfully.
Their experiments have shown that the spike
protein binds to a receptor on human cells
— known as angiotensin-converting enzyme
2 (ACE2) — at least ten times more tightly
than does the spike protein in the SARS virus.
Veesler’s team also found that the spike
protein binds with high affinity to the ACE2
receptor, which suggests that the receptor
is another potential target for vaccines or
therapies.
For example, a drug that blocks the receptor
might make it harder for coronavirus to enter
cells.
In Conclusion, the virus that causes COVID-19
seems to be spreading easily and sustainably
in the community (“community spread”)
in some affected geographic areas.
Community spread means people have been infected
with the virus in an area, including some
who are not sure how or where they became
infected.
To learn more about what is known about the
spread of newly emerged coronaviruses, then
visit the link in the description below.
https://www.cdc.gov/coronavirus/2019-ncov/about/transmission.html

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