A mutated version of the coronavirus that has
gripped Europe and the West is more infectious because it doesn't break as
often while inside the body, a study has found.
Researchers at The Scripps Research Institute
in Florida say the 'spike protein' that the virus uses to attach to cells in
the airways has adapted since January.
It used to break off regularly while trying
to bind to receptors in people's airways, which it would use to gain entry to
the body, but is now more resilient, they say.
A genetic mutation which scientists around
the world have been picking up on for months appears to have caused this spike
to be less likely to snap, and also to force the coronaviruses to produce more
of them to make itself more infectious.
As a result the virus appears to be
approximately 10 times more infectious than it was when it first jumped to
humans in China at the end of the year, scientists say.
The mutated version of the virus, dubbed G614
- a change from D614 - is a tiny change in its genetic make-up that scientists
weren't sure what to make of when they found it.
But by May research had found it had become
the dominant strain being found in Covid-19 patients across the UK, US, Canada
and Italy.
Lead researcher on the Scripps institute's
study, Dr Hyeryun Choe, told the Washington Post the mutation seemed to have
happened to 'compensate' for the weakness of the spike protein in the past.
The Post reported it appeared to have become
approximately 10 times more infectious as a result of this change.
The way the virus enters the body is by using
its spike to latch onto a receptor - called an ACE-2 receptor - inside
someone's airways.
ACE-2 receptors are essentially tiny gateways
that the virus uses to get into the blood and then multiply rapidly, destroying
cells around them in the process and triggering illness.
Dr Choe and her colleagues examined the
differences between the spike protein s,
dubbed S, on the outside of both versions of the coronavirus.
They found: 'These results show SG614 is more
stable than SD614, consistent with epidemiological data suggesting that viruses
with SG614 transmit more efficiently.'
The spike was stronger, they said, and as a
result the virus was better able to bash through the gateway of the ACE-2
receptors.
Dr Choe told the Washington Post: 'The
epidemiological study and our data together really explain why the [G
variant's] spread in Europe and the US was really fast... This is not just
accidental.'
However, this improved spike strength did not
seem to be making people any sicker - or any less sick.
This, they suggested, could be because the
spike had nothing to do with the virus's ability to reproduce - to replicate -
once it was inside the body.
HOW AND WHY CAN VIRUSES CHANGE OVER TIME?
Viruses are known to change over time because
they are subject to random genetic mutations in the same way that all living
things are.
These mutations can have various effects and
many will only happen briefly and not become a permanent change as newer
generations of viruses replace the mutated ones.
However, some of the mutations might turn out
to be advantageous to the virus, and get carried forward into future generations.
A virus may change its structure by accident
but turn out to be mor e infectious
that way, meaning it can infect more hosts, reproduce more, and become more
dominant than its less fertile predecessor.
Or if a virus becomes less dangerous to its host
- that is, it causes fewer symptoms or less death - it may find that it is able
to live longer and reproduce more.
As a result, more of these less dangerous
viruses are produced and they may go on to spread more effectively than the
more dangerous versions, which could be stamped out by medication because more
people realise they are ill, for example.
The mutation may then be taken forward in the
stronger generations and become the dominant version of the virus.
In an explanation of an scientific study
about HIV, the NHS said in 2014: 'The optimal evolutionary strategy for a virus
is to be infectious (so it creates more copies of itself) but non-lethal (so
its host population doesn’t die out).
'The "poster boy" for successful
long-living viruses is, arguably, the family of viruses that cause the, which
has existed for thousands of years.'
The process of reproduction, and using the
body's resources to achieve this, is how the coronavirus causes illness.
Dr Choe's study added: 'An interesting
question is why viruses carrying the more stable SG614 appear to be more
transmissible without resulting in a major observable difference in disease
severity.
'It is possible that higher levels of functional
S protein observed with SG614 increase the chance of host-to-host transmission,
but that other factors limit the rate and efficiency of intra-host
replication.'
The paper was published online on bioRxiv
without being reviewed by independent scientists.
Researchers in the UK and US had in May noted
that the G614 version of the virus had become 'the dominant pandemic form in
many countries'.
They said it was first found in Germany in
February and had since become the most common form of the virus in patients
worldwide - it appears to force out the older version whenever they clash.
Viruses mutate naturally all the time and it
is not usually cause for alarm but should be studied in case they change so
much they become unrecognisable to the body and immunity from a first infection
cannot protect against them, as is the case with flu.
A study done by scientists at the University
of Sheffield and Los Alamos National Laboratory, New Mexico, found that D614
appeared to have been the virus's original state in humans, and the one found
in Wuhan.
It made up the vast majority of all Covid-19
infections in China, and Asia as a whole, and also seemed to be the first
version of the virus to appear in the countries they studied.
However, the mutated version - G614 - started
to appear soon after in Europe and North America in particular, before going on
to take over as the dominant virus.
'A clear and consistent pattern was observed
in almost every place where adequate sampling was available,' the researchers
said.
'In most countries and states where the
COVID-19 epidemic was initiated and where sequences were sampled prior to March
1, the D614 form was the dominant local form early in the epidemic.
'Wherever G614 entered a population, a rapid
rise in its frequency followed, and in many cases G614 became the dominant
local form in a matter of only a few weeks.'
They said the G614 mutation may give the
virus a 'selective advantage' which makes it better able to bind to cells in
the airways, or to shed viruses which it uses to reproduce and spread.
It could do this because the D614G mutation
appeared to affect the shape of the 'spike' protein that the virus uses to
attach to a person's cells and infect them.
A sample of 447 hospital patients in
Sheffield showed that people had a higher viral load when infected with G614,
meaning they had a higher quantity of viruses circulating in their body.
This could make them more likely to spread
COVID-19 because they could be more likely to show symptoms and have more
viruses on their breath, for example.
The researchers wrote: 'An early April
sampling... showed that G614's frequency was increasing at an alarming pace
throughout March, and it was clearly showing an ever-broadening geographic
spread.'
And they added: 'Through March, G614 became
increasingly common throughout Europe, and by April it dominated contemporary
sampling.
'In North America, infections were initiated
and established across the continent by the original D614 form, but in early
March, the G614 was introduced into both Canada and the USA, and by the end of
March it had become the dominant form in both nations.'
WHAT IS AN ACE-2 RECEPTOR AND WHAT DOES IT
HAVE TO DO WITH COVID-19?
ACE-2 receptors are structures found on the
surface of cells in the lungs and airways which work with an enyzme called ACE
(angiotensin-converting enzyme) to regulate blood pressure.
Its exact function in the lungs is not well
understood but studies suggest it is protective against lung damage and low
levels of it can worsen the impact of viral infections.
Scientists say that the coronavirus which
causes COVID-19 enters the body through the ACE-2 receptor, which the shape of
it allows it to latch on to.
This means that someone with more ACE-2
receptors may be more susceptible to a large viral load - first infectious dose
of a virus - entering their bloodstream.
People who have higher than usual numbers of
ACE-2 receptors may include those with diabetes or high blood pressure because
they have genetic defects which make them produce more.
High levels of ACE-2 receptors may also be
protective, however.
They are thought to be able to protect the
lungs during infection and a study on mice in 2008 found that mice which had
ACE-2 blocked in their bodies suffered more damage when they were infected with
SARS, which is almost identical to COVID-19.
Smoking has in the past been repeatedly
linked to lower than normal levels of ACE-2 receptors, potentially increasing
the risk of lung damage from COVID-19.
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