The coronavirus is mutating, and scientists are concerned about one mutation in particular: D614G.
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Back when researchers
first analyzed the genome of a brand-new coronavirus in Wuhan, its genetic sequence looked like this. Three weeks later, researchers
sequenced the genome of the same virus in a patient in Seattle. It had changed
here and here and here. These changes are happening
all over the world. The coronavirus is mutating. It’s changed hundreds of times
since January but researchers are concerned
about one mutation in particular. So my question is, is the coronavirus
becoming more dangerous? I’m Cleo Abram,
and this is “Answered, by Vox.” Well there’s two ways
one can think about danger. First is that the virus
causes a more severe disease and that doesn’t appear to be the case. That’s professor of immunology
Michael Farzan. He says the second way that mutations
could make the virus more dangerous is if it becomes more contagious. But before we get there,
here’s the good news. My understanding
is that most mutations, in the coronavirus
but also in every virus, don’t actually change
how it behaves in our bodies at all, is that right? Yes, most mutations
do not change very much. They actually are
just part of the process of sort of selection
and they go away. A virus, at its most basic,
is just a bunch of genetic material packed into a protein shell. In the case of the coronavirus,
that genetic material is RNA, which is made up of four
nucleotide bases. You might remember the bases
A, C, T, G from DNA. With RNA it’s just U, not T. When the virus gets into your body,
its goal is to copy itself which means it needs to produce
more RNA and more proteins. A virus doesn’t always make
an exact copy of its RNA. And when it makes a random mistake
in that copying process, that’s a mutation. But it’s when it’s copying the proteins
that things really get interesting. Within that newly copied RNA, each group of three nucleotides,
called a codon, can instruct your cells to produce
one building block of protein called an amino acid. Amino acids all come
with letter names too: D, G, Y, I–
you get the idea. Different amino acid combinations
mean different proteins. But as it turns out… Several different codons encode
for the same amino acid. So, for example,
say the nucleotides “ACU” mutated into “ACG.” It’s still gonna tell your cell to produce
the exact same amino acid, T. This mutation doesn’t change
the protein at all. We call those silent mutations. But even if it’s a non-silent mutation,
something that does actually change the amino acid
and changes the protein, that doesn’t always necessarily change
how a virus behaves in our bodies, right? That’s absolutely right.
In fact, the genetic code is designed
to be conservative. Meaning that changes
that it’s likely to make, are likely to have a minor effect
on the function of the proteins they encode for. So in general,
mutations are expected in the course of an epidemic
or pandemic. Most of these mutations
do not have a strong impact on the severity of the virus
or even the transmission of the virus. Of course,
that’s not always the case. And for COVID-19, scientists are concerned about
one mutation in particular that might have an impact
on how the virus spreads. The formal name is D614G and that is a code for
the individual amino acids at position 614 of this spike protein
that have changed. I see, so it’s the 614th amino acid – and it changes from D to G?
– Correct. Unfortunately D614G
just so happens to be in the part of the genetic sequence that encodes for
the viral spike proteins, those key proteins that the coronavirus
uses to invade cells. The red protein that everybody sees on the surface of
the pictures of the coronavirus, there’s more of those on viruses
with that change than on viruses without this change. Dr. Farzan and his team
found that with more spiked proteins, the mutated virus is more likely
to infect cells in culture in their lab. But infecting cells in culture
is really very different from it being more infectious
out in the world between people, right? It is certainly more likely
to infect a cell in culture. What the next step is to demonstrate that our results in cell culture translate to human-to-human transmission. So just to be super clear,
we don’t know that this mutation causes the virus to pass more easily
between humans. It does seem to be more transmissible
between cells in a lab and it also seems to become
the dominant form of the virus as it spreads. Where is this mutated version
of the coronavirus now? Actually, everywhere. The first detection of this virus
might have been in Germany in late January and then you would see that virus
sort of grow up in Europe and you would see
a mixture of viruses in the United States but then over time,
you would see more and more virus with this mutation. So what we know right now
is that researchers believe the mutations we’re seeing aren’t making
cases of the coronavirus more severe. They are concerned that
the D614G gene mutation might make the virus
more contagious. But the research so far
is limited to cells in a lab. And scientists just aren’t sure yet how the mutation will affect
contagion rates in the real world. And if you just remember one thing,
it’s this: does what we know about this mutation change anything that people
should be doing in their daily lives to prevent
themselves and their loved ones from getting or transmitting coronavirus? No, it’s just a reminder that
this is a very transmissible virus. It always has been. It might have gotten
a little bit more transmissible and you should be very careful at every point to make sure
that people are protected. Thanks for watching. That was an episode of Vox’s
first ever daily show. It’s called Answered it’s on a new streaming app called “Quibi” and every day we take on a question
about what’s happening in the world right now from the history of curfews to cicada season. So, if you want to check out more, all you need to do is go to the link in the description or download the Quibi app on your phone and search for “Vox” or “Answered”. I’ll be there everyday.
