The
complex mutation of covid-19
Coronaviruses — like all viruses — change small parts of their
genetic code all the time.
"Viruses mutate
naturally as part of their life cycle," says Ewan Harrison, scientific
project manager for the COVID-19
Genomics UK Consortium,
a new project that tracks the virus in the United Kingdom.
Like flu and measles,
the coronavirus is an RNA
virus. It's a
microscopic package of genetic instructions bundled in a protein shell. When a
virus infects a person, the string of genetic instructions enables the virus to
spread by telling it how to replicate once it enters a cell. The virus makes
copies of itself and pushes them out to other cells in the body. Infectious
doses of the virus can be coughed out in droplets and inhaled by others.
Inevitably, viruses
"make mistakes in their genomes"(genetic coding mistakes) as they
copy themselves, says Harrison. Those changes can accumulate and carry over to
future copies of the virus. Researchers are using these small, cumulative
changes to trace the pathway of the virus through groups of people.
TWO
strains of the killer coronavirus are spreading around the world – and 70% of
infected patients have caught the more aggressive and contagious type, study
claims
coronaviruses are also
one of the largest RNA viruses. They're about 30,000
nucleotides long —
double the size of flu viruses. But at 125 nanometers wide, they're still microscopic;
800 of them could fit in the width of a human hair.
Nonetheless, their relatively larger size means "they have
a lot more tools in their tool belt" compared with other RNA viruses, says
Menachery — in other words, more capability of fighting off a host's immune
system and making copies of themselves.
The coronavirus has mutated into at least two
separate strains since the outbreak began in December, according to Chinese
scientists.
Researchers say there are now two types of
the same coronavirus infecting people – and most people seem to have caught the
most aggressive form of it.
At least 94,000 people have been infected
around the world and almost 3,200 have died, while 50,000 have recovered from
the disease.
The team of experts from Beijing and Shanghai
said 70 per cent of people have caught the most aggressive strain of the virus
but that this causes such bad illness that it has struggled to spread since
early January.
But now scientist says that L the most aggressive
one has become less common as the outbreak has gone on, with it apparently
struggling to spread since early January, while S the older and milder has
become more common.
S is less aggressive but is thought to be the
first strain of the virus which made the jump into humans and is continuing to
infect new patients.
This could be because the disease it causes
is less severe, meaning people carry it for longer before ending up in hospital,
increasing the risk of them passing it on.
In the paper the researchers, led by
Professor Jian Lu and DrJie Cui, said: 'Whereas the L type was more prevalent
in the early stages of the outbreak in Wuhan, the frequency of the L type
decreased after early January 2020.
The scientists' explanation suggests that,
because the L strain surged at the beginning of the outbreak and made people so
ill, those who caught it were quickly diagnosed and isolated, meaning it had
less opportunity to spread widely.
This 'human intervention' is thought to be
the hospitalisation of people with the virus, disinfecting the areas and the
lockdown of areas where it was spreading fast.
Knowing that the virus can mutate may make it
harder to keep track of or to treat, and raises the prospect that recovered
patients could become reinfected.
The experts cautioned that the study that
discovered the mutation only used a tiny amount of data – 103 samples – so more
research is needed, and another scientist added that it is normal for viruses
to change when they jump from animals to humans.
Scientists in Beijing and
Shanghai said 'human intervention measures' may have forced the most aggressive
strain of the coronavirus into submission
The good news is that the small genetic changes that researchers
have observed so far don't appear to be changing the function of the virus.
"I don't think we're going to see major new traits, but I do think that
we're going to see different variants emerge in the population," says
Bahl.
As so far virus function is not changing so it helps scientist
to observe virus genetic function and make a suitable vaccine or drug.
And that slower rate of
change is potentially good news for treatments and vaccines. Researchers think
that once a person gains immunity against SARS-CoV-2, either by recovering from
an infection or by getting a future vaccine, they will
likely be protected against the strains in circulation for "years rather
than months," predicts Trevor
Bedford, an
evolutionary biologist at the Fred Hutchinson Cancer Research Center, in an
assessment shared
on Twitter.
But Researchers are also on alert and worried for changes that
might affect how the coronavirus behaves in humans. For instance, if the
coronavirus developed ways to block parts of our immune system, it could hide
out in our bodies and establish itself better. If it evolved to bind more
strongly to human cells, it could enter them more efficiently and replicate
more quickly.
Selective pressures could come from introducing treatments and
vaccines that are effective against a narrow group of coronavirus strains. If
that happens, strains that aren't targeted by these measures would likely
proliferate.
If people with a certain strain of the virus
are taken into hospital faster than those with another strain, this limits the
number of other people that strain can infect.
If the virus is prevented from infecting a
lot of people, that strain may die off and evolution – via survival of the
fittest – will allow another strain which can infect more people to become the
dominant one.
The S strain may be winning because it causes
milder symptoms so patients take longer to realise they're sick, increasing the
risk of them passing it on.
Professor Jian and DrJie added: 'These
findings strongly support an urgent need for further immediate, comprehensive
studies that combine genomic data, epidemiological data, and chart records of
the clinical symptoms of patients with coronavirus disease 2019 (COVID-19).'
A British scientist who was not involved with
the research said it was too early to say how accurate the claim of the virus
splitting into two was.
The University of Leeds's Dr Stephen Griffin
said: 'It is usually the case that when RNA viruses first cross species
barriers into humans they aren’t particularly well adapted to their new host
(us!).
'Thus, they usually undergo some changes
allowing them to adapt and become better able to replicate within, and spread
from human to human.
'However, as this study hasn’t tested the
relative "fitness" of these viruses when they replicate in human
cells or an animal model, it isn’t really possible to say whether this is
what’s happened to SARS-CoV2.
'It is also difficult to say how/why human
interference may have impacted upon one strain relative to the other for
similar reasons.'
He added that the difference between the two
strains did not offer any insight into how likely someone was to die if they
caught it.
The study was published in the
scientific journal National Science Review, which is managed by the Chinese
Academy of Sciences.
However Projects such as
the COVID-19
Genomics UK Consortium will
use these genetic drifts to track the path of the virus and figure out if there
are hospitals or community hubs that are hot spots for contagion, according to
Harrison. This will give public health officials a sense
of where and how the virus is being transmitted now.
Will the coronavirus surge when schools reopen? Will new strains
emerge that develop resistance to drugs or vaccines that are introduced? To
answer such questions, Harrison says, the long-term plan is to track the virus
in real time — and see how it changes as it spreads.
Conclusion:
So
far it is seen that s type strain of corona virus is more dominant in effecting
population and the s type has milder symptoms or asymptomatic unlike ltype
which is quickly diagnosed and hospitalized to undergo treatment. The patient
who is s type covid-19 affected show milder symptoms or no symptoms and the
time they reach hospital the contagious virus already affected many people that
were around that patient. protecting oneself from effecting S type only way is isolation so the strain
die off and less evaluate, which has
noticed by scientist so far that stype is not evaluating so its easy to unlock
its coding and develop a vaccine or drug as soon as possible but it take year
to pass a treatment after much trials.
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