As of May 2020, over 5.2 million people have
been infected with COVID-19, of which 338
thousand have died. Scientists around the
world are working tirelessly to fight this
disease. In this episode of [Simple Science
with Jumbo Eggs], we will learn about some
of the ways scientists have been looking into,
for us to enjoy once again spending time with
one another outside of our homes.
COVID-19 is the name of the disease that is
a pandemic right now, and SARS-CoV-2 is the
name of the virus that causes this disease.
But it’s kind of difficult to pronounce
the virus’s name, so we’ll just call it
COVID-19 virus in this video.
When you think about fighting COVID-19, the
vaccine is probably the first thing that comes
to your mind. You’re right! Currently, the
vaccine is probably the most promising way
to fight this disease. Vaccines have already
worked wondrously well against the other viral
diseases like polio and smallpox, so it’s
not a completely new method that nobody has
ever heard of. The fact that we are familiar
with vaccines in general is a good thing,
because when the vaccine for COVID-19 finally
comes out, we are almost certain it will work.
Many scientists believe it will take about
12 to 18 months for the vaccine to be developed,
although some think this can be done by as
early as Fall 2020.
So why does this take so long? Didn’t Edward
Jenner in 1796 just take some cowpox stuff
and put it into a random boy and call it a
day? Well, actually, it almost took three
more years for the vaccination to be given
to the public, but let’s not go too deep
into the history of vaccination, lest we digress.
The real problem is that, even though making
vaccines with today’s technology is trivially
easy, making them safe and effective is an
entirely different matter.
Like all drugs, vaccines can have side effects.
To minimize the risk of serious side effects,
every vaccine and drug in development need
to be initially tested in human volunteers,
in a process called a clinical trial. This
is because what scientists find using cell
culture or lab animals often give very different
results than what they find in people. The
clinical trial has three phases: Phase I,
Phase II, and Phase III. Each phase can take
several months, which is why it takes at least
a year to develop any vaccine. If the vaccine
does pass all of these trials in the end,
then it can be made available to the public.
One interesting type of COVID-19 vaccine currently
in clinical trials is an mRNA vaccine. Historically,
vaccines are made from either proteins isolated
from germs, or live, but weakened germs. But
preparing these materials takes a lot of time
and money, so it’s difficult to scale up
the production fast enough to meet the huge
demand in a pandemic. The mRNA vaccine works
by just giving people the mRNAs that code
for the proteins found in the germs. When
these mRNAs enter our body, our cells make
the germ proteins using these codes. These
proteins are then presented on the outside
of the cells, which the immune cells recognize
and develop immunity toward them.
Another potential treatment for COVID-19 you
may have heard about are chloroquine and hydroxychloroquine.
These drugs are usually used to treat malaria,
but why do people think these will work for
COVID-19?
One reason is that the chloroquines can help
tone down the immune system. People with COVID-19
can sometimes have overreactive immune system
called cytokine storm. When this happens,
the immune system tries to do everything it
can to kill the virus, even if it means killing
the person. It’s kind of like if you have
bed bugs and they’re annoying the hell out
of you, you set your house on fire to kill
them. Yeah, you don’t have bed bugs anymore…but
your house is gone now. But the chloroquines
are known to have immunosuppressive effects,
which may help calm the immune cells down
so they don’t end up destroying their own
hosts. Another reason scientists think the
chloroquines can help fight COVID-19 is because
they can prevent the virus from entering our
cells. The virus binds to a protein on our
cells called ACE2, and this triggers the cells
to engulf the virus particles. The chloroquines
can interfere with this process so the virus
particles stay outside.
Unfortunately, chloroquine and hydroxychloroquine
don’t appear to be an effective treatment
in this case, according to a recent study
. In this study, 96,032 COVID-19 patients
from 671 hospitals who were treated with chloroquine
or hydroxychloroquine, among others, were
followed. The authors concluded that the patients
on chloroquine or hydroxychloroquine had increased
number of deaths and also even a higher possibility
of getting disturbed heart rhythm , which
doesn’t really sound that bad, but it’s
actually pretty serious because it can kill
people. So you probably want to think twice
about taking these medications for COVID-19.
Perhaps one of the most intuitive way to fight
COVID-19 aside from the vaccine is to get
help from the survivors. When a person recovers
from an infection, they develop antibodies
against the pathogen. In the case of COVID-19,
these antibodies can either inactivate the
virus so it can’t enter our cells, or tag
it so it’s easier for the immune cells to
find and get rid of it. One approach is to
ask these survivors to donate their blood
to help sick patients recover. This is called
convalescent plasma. Convalescent means a
person who is recovering after an illness,
and plasma means the watery part of blood
where you can find the antibodies. Preliminary
studies do show that this does seem to help
the patients recover faster. But the problem
with this therapy is limited availability.
To treat a disease with antibodies, you need
a lot of the antibodies. This is because one
antibody molecule can bind and inactivate
only one protein. And since a virus particle
can have many copies of the protein the antibody
can target, you would need the antibody molecules
to be many times the number of the virus particle.
Coupled with the fact that you can only get
them from healthy volunteers without other
infectious diseases, it’s difficult to treat
COVID-19 patients with convalescent plasma
therapy. What if we make these antibodies
in a lab? Even though it’s technically possible,
the production process is time consuming and
expensive because antibodies are very large
molecules. We also need to make sure these
antibodies are safe, which isn’t always
the case, because the immune system may react
to them and cause an allergic reaction or
even deadly cytokine storm.
There are a few other ways scientists have
learned to fight COVID-19 by exploiting the
weakness in the virus itself. Viruses can
sometimes mutate enough that the preexisting
vaccines no longer work against them. We would
be in trouble if we finally get the vaccine
after the long wait, but the virus has mutated
so the vaccine doesn’t work. Also, vaccines
do not work well in the elderly and very young
babies because their immune systems do not
work well. So these next approaches can provide
a second line of defense we can use in cases
like these.
The first method works by stopping the viral
genome from replicating. The COVID-19 virus
has an RNA genome, and this replicates by
a viral protein called RNA-dependent RNA polymerase.
It’s a mouthful, but it just means this
protein uses a piece of RNA as a template
to make another piece of RNA, which in this
case, is the viral genome. This protein works
a bit differently than human RNA polymerases,
so it can also use RNA pieces it’s not supposed
to use. This is where the drug called remdesivir
comes in. Remdesivir looks similar to a normal
RNA building block, but when the viral RNA
polymerase picks this up, it can stop the
RNA production altogether. This decreases
the number of viral genomes, slowing down
the virus replication to buy the immune system
time to clean them up.
The second part of the COVID-19 virus scientists
target is the S protein. S stands for spike,
because, well, it looks like a spike. Once
the virus enters our body, the tips of the
S proteins are processed and cut off by our
own enzymes in our bodies called furin and
TMPRSS2. This is how the virus can only infect
certain species. For example, if we take a
bat coronavirus and put it in us, the virus
would not be able to enter our cells. But
if we cleave off the S protein and then put
it in us, then it would be able to go into
our cells. This means if we block furin from
cleaving the S proteins, then then the COVID-19
virus will become much less efficient at infecting
us. Currently, drugs called Camostat Mesylate
and Emodin aim to target the S protein’s
function.
The third method aims to block the virus’s
own protein cleaving function. When the COVID-19
virus makes its own proteins, these are first
made into long strips of a larger protein.
Then, a viral protein called main protease
cuts this large protein into different pieces.
This is kind of like getting a large candy
roll and cutting it into smaller pieces to
make the final candy product. Since this main
protease is only found in viruses, scientists
are studying if we can stop this protein from
working to stop the virus from replicating.
Lopinavir and ritonavir are currently being
used to stop HIV from replicating by exploiting
this exact method, so scientists are studying
if these drugs can also be used in the case
of COVID-19.
Last but not least, assembly of the viral
particle itself can be blocked so the virus
can’t be formed. The outside structure of
the COVID-19 virus is organized by proteins
called M and E. If we can disturb these proteins
so they don’t find each other, it would
be possible to slow their replication. According
to computer simulations, Belachinal and Macaflavanone
E are some of the chemicals found to potentially
work this way.
These were seven of many ways to fight COVID-19.
We hope that one day, all of this effort will
help bring a swift end to this pandemic so
it becomes just a thing of the past, just
like how it did with the 1918 flu pandemic.
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