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A new variant of Covid-19 in England

Dosen Pengampu
Peter Manuputty, S.Pd., M.Pd

Disusun Oleh
Nama : Chitra Ayu Triyani Wijaya
NIM : 2020RB1104
Matkul : Writing

ENGLISH DEPARTMENT
FACULTY OF TEACHER TRAINING AND EDUCATION SCIENCE
VICTORY UNIVERSITY OF SORONG
A scary new strain of Corona Virus, innocuously named B.1.1.7, has recently
exploded across southeast England, prompting the government to tighten lockdowns
on the region. Though we don't know all the details, experts are increasingly
confident it is more easily transmitted than other strains. Here's everything we know
so far about this novel strain.

1. What is it?
The B.1.1.7 strain of SARS-CoV-2 is a version of the virus with 23 mutations, eight of
which are in the spike protein the virus uses to bind to and enter human
cells, Science Magazine reported. 

2. Where did it come from?

It was first detected Sept. 21 in Kent County in England, then took off and spread in
November, according to the World Health Organization.
Since then, it has become the most common variant in England, representing more
than 50% of new cases diagnosed between October and Dec. 13 in the U.K.,
according to the WHO.

However, some scientists now believe that the virus may have mutated in a person
who was immunocompromised, according to Science Magazine.

That's because, unlike the flu, the novel coronavirus can correct mistakes when it
replicates, and so tends to have a fairly stable genome, Live Science previously
reported. However, studies have shown that people who have weakened immune
systems — because they are taking immunosuppressant drugs or are being treated
with chemotherapy, for instance — may harbor infectious virus for months. That, in
turn, would give the virus many chances to acquire mutations that help it replicate or
evade the immune system.

3. What do these mutations do?

We don't know for sure. Viruses mutate all the time, and most of these changes don't
affect how deadly or infectious the virus is. In this case, some of these mutations
may have arisen purely by chance and may not affect the function of the virus. 
But three mutations in particular have worried experts.

One, a two amino-acid deletion known as 69-70Del, was first detected separately in
a patient being treated with immunosuppressants who developed COVID-19. The
patient received remdesevir, convalescent plasma and neutralizing antibodies, but
died months later. Though the virus did not initially have this deletion, it acquired it
over months, researchers reported in a preprint article published Dec. 19 to
the medRiv database (It has not been peer-reviewed.) The authors suspect it
evolved to evade the immune system. Another wrinkle associated with this deletion
is that it can make one of the targets of SARS-CoV-2 PCR tests — known as the S
gene — falsely test negative. Some tests only look for positives in this S gene and
would therefore miss the new variant. Most PCR assays, however, look for three
separate regions of the spike protein, so those assays won't be affected, the WHO
said.

Another mutation, known as N501Y, alters the key amino acids that make up the so-
called receptor-binding domain of SARS-CoV-2, where amino acid asparagine (N)
has been replaced with tyrosine (Y) in the part of the virus that latches onto the
ACE2 receptor on human cells, according to the Centers for Disease Control and
Prevention. A September study in the journal Cell found this variant binds more
tightly to the ACE2 receptor than other versions of the coronavirus — at least in a lab
dish.
Dozens of samples of SARS-CoV-2 from South Africa and Australia have tested
positive for this mutation, but lab tests suggest the South African and U.K. variants
separately evolved the same mutation. That suggests it may provide an evolutionary
advantage to the virus.

The third suspicious mutation is P681H, which is also in the receptor-binding domain
of the virus. According to preliminary information posted by the COVID-19 Genomics
Consortium UK, this mutation sits next to the "furin cleavage site," which is where the
spike protein must be cleaved in order for the virus to enter cells, according to Science
Magazine.

4. Does it spread more easily?

Yes. Experts now think the new variant is between 50% and 74% more transmissible
than other dominant strains, according to a study by the Center for Mathematical
Modeling and Infectious Diseases (CMMID)  that has not yet been peer-reviewed.
The WHO estimates this would tack on 0.4 to the basic reproductive number R,
which dictates how many people each infected person would spread the virus to.

Based on models of that growth, the new variant could be responsible for 90% of all
new COVID-19 cases in London and East and South England by mid-January, that
study found. 

Another study from the U.K., published Dec. 27 to medrXiv and also not peer
reviewed, found higher viral loads in PCR tests that are negative for the S gene.
Testing negative for the S gene means the virus has the 69-70Del mutation and so
such S-gene dropouts are thus a proxy for, but not a certain indication of, the
samples coming from the B.1.1.7 variant. And a higher viral load makes it easier for
the virus to spread.
 5. Is it more deadly?
We don't know, but experts suspect it is not. However, if it spreads much more
easily, that means more people will be hospitalized. Once hospitals become
overwhelmed, the quality of care of the sickest patients drops, which can lead to
higher death rates than would otherwise be expected.

The CMMID study found that the new variant could explain an uptick in
hospitalizations in southeast England, largely due to increased spread, not
necessarily because the virus is more dangerous.

Another study, also not peer-reviewed, by CMMID, used a mathematical model to

see whether the virus' rapid growth in London was due to increased infectiousness,
or due to it being more severe. The latter didn't fit the data well, whereas the former
fit nicely. 

6. Will vaccines work against the new virus?

Most experts think the newly developed vaccines will still work against the novel U.K.
variant. When vaccines stimulate the immune system, the body builds an arsenal of
cells to bind to many different parts of the virus. Mutations in a handful of spots will
likely not be enough to make the vaccine less effective, according to the CDC.

Given that 99% of the proteins on the new variant are identical to the strain the
Pfizer-BioNtech mRNA vaccine targets (the Moderna vaccine is very similar), it is
highly likely that the vaccine will work, BioNTech CEO Uğur Şahin said at a news
briefing. 

It's possible that over time a variant could emerge that will evade some of our
vaccines, similar to how the flu vaccine needs to be updated every year. However,
the new mRNA vaccines could be updated to reflect new mutations in about six
weeks, Şahin told the Financial Times.

7. What can we do to stop this?

The new variant still spreads the same way as the ordinary form of the coronavirus.
That means the same things everyone has been doing to prevent the spread of the
virus since March will also work for the new U.K. variant: washing hands, physical
distancing, masks and good ventilation. Adhering strictly to those rules and avoiding
unnecessary outings will help prevent its spread.