You may have seen headlines about a now-dominant strain of the coronavirus spreading that is more contagious than the original. According to researchers, a mutation occurred in the virus as it began spreading in Europe in early February and it rapidly became the dominant form. This news comes from a research paper from scientists at Los Alamos National Laboratory and has not been peer reviewed. There is some skepticism that any mutations have changed the general contagiousness or lethality of COVID-19. Sarah Kaplan, reporter at the Washington Post, joins us for what to know.
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Speaker 1 (00:00):
It's Friday, May eight. I'm Oscar Ramiras from the Daily
Dive podcast in Los Angeles, and this is your daily
coronavirus update. You might have seen headlines about a now
dominant strain of the coronavirus spreading that is more contagious
than the original. According to researchers, a mutation occurred in
the virus as it began spreading in Europe in early February,
(00:20):
and it rapidly became the dominant form. This news comes
from a research paper from scientists at Los Alamos National
Laboratory and has not been peer reviewed. There is some
skepticism that any mutations have changed the general contagiousness or
lethality of COVID nineteen. Sarah Kaplan, reporter at the Washington Post,
joins us for what we know. Thanks for joining us, Sarah,
(00:41):
good to be here. It was a pretty scary headline
earlier this week. Scientists say a now dominant strain of
the coronavirus could be more contagious than the original. Right away,
people started getting very scared about this. Talks of the
coronavirus mutating being a much more contagious strain. Nobody knew
really what was going on right away. There was a
(01:03):
lot of experts that were skeptical of what was going on.
But this all came from a research paper from scientists
at Los Alamos National Laboratory. So tell us a little
bit what we know about this. This paper is actually
what's called a preprint, so it's research that has not
yet been published by a scientific journal. And usually when
(01:24):
scientific papers are published in a journally undergo a review
process where other scientists read through the paper, make sure
the conclusions are valid and provide feedback. And so the
idea is that that is a way to make sure
that the results are robust. But in this era of
science really happening at warp speed and researchers wanting to
get information out there as quickly as possible, scientists have
(01:46):
been posting their research to these preprint servers where they're
available online even before they've been published in a journal.
And best what this paper was and basically what it
found is that the strain of the virus that is
now the most common, that is the most abundant around
the world has a mutation in the gene that influences
(02:06):
one of the proteins on the surface and their idea
is that somehow that have made that strain more transmissible
and more contagious. And they're saying that this particular strain
was something that came out of Europe, not in Wohan, China,
where they say that the stars Cove two the thing
that causes COVID nineteen, where it really originated. So this
(02:26):
strain is coming out of Europe. This thing to remember
is that all viruses mutaps. We hear mutation and we
think X men or some kind of like crazy lab experiment,
but mutations are very common viruses. The way they work
is they break into ourselves and they use our cellular
machinery to make copies of themselves and their sloppy out it,
and so a lot of mistakes get introduced. This virus
(02:48):
has about thirty thousand based pairs and its genomes, So
you can think of that as a book that's thirty
thousand words long. You change one word in the book
and it probably won't change the book very much. And
so all of these strains that we talk about that
have been circulating, they carry kind of different genetic fingerprints, markers.
They've picked up mutations, and now you can recognize that
as distinct lineages. That doesn't necessarily mean that they're functionally different,
(03:11):
and in fact, the consensus from scientists so far is
that all of these strains are actually functionally the same.
We're all getting the same version of the coronavirus. They
just have some slight changes to them. So this strain,
the one that has been described with the mutation on
the gene that colodes for its spike proteins, that is
one that emerged in Europe and it has become very
(03:32):
abundant around the world, the dominant stream that's circulating in
the US as well. And this hypothesis that the reason
that it is so abundant is because it's more contagious.
That's one interpretation, but a lot of the critics of
this paper have said there are other explanations beyond mutation
that increases contagiousness. You think about this virus being introduced
(03:53):
to northern Italy way back in January. It was a
very vulnerable population and a society that was largely unprepared
to contain the threat, and so they say, you know,
it's the founder effect. The reason this virus is so
abundant is because it got to a soft target and
then spread a lot, and so now we're seeing that everywhere.
The idea is that maybe what is distinguished distinctive about
(04:16):
the strain of the virus is not the viruses DNA,
but it's US. It's the fact that it got to
Europe and then North America and we proved to be
very easy targets. The same could be said for US
here in the United States. Obviously, there was reports a
little bit ago that the strain that was going around
in New York City, who was obviously been so hard
(04:36):
hit for US in the United States, that that strain
was a mutated strain that came from Europe also, but obviously,
again you know, a population unprepared for it, it's going
to spread like wildfire, and that's kind of exactly what happened.
So they're saying that this new strain possibly more contagious,
but probably not any more lethal. In fact, once these
(04:56):
things kind of keep mutating and passing on to more
and more people a lot of times with viruses, it
loses its effectiveness. The idea is that it's not in
a virus's best interest to kill its host. A virus
that is extremely lethal isn't able to spread very far
because from the viruses perspective, you want your hosts to
be up and moving around and affecting other people, and
(05:19):
so some of the most successful viruses from a kind
of biological perspective are ones that don't actually cause that
much destruction to a person. And example is the herpes virus,
which has been with the human lineage for six million years.
So when we were closer to our great ape cousins
than we are to modern humans today, we had herpes
(05:39):
virus and you know, it's not deadly, and so it
stayed with us a really long time. The evolutionary pressure
on viruses is to become more contagious and less virulent,
and that is a hope, you know, it's a long
term hope that one day this virus may become less virulent.
But the other thing to keep in mind is that
this virus actually mutates more slowly than other viruses do.
(06:02):
Most viruses are not able to fix mistakes in their
genetic material when they make copies of themselves, and this
virus is able to fix some mistakes, so that means
it picks up mutation about one tenth as frequently as
something like the influenza virus. So researchers don't expect this
virus to mutate in a way that produces functional changes,
(06:25):
changes in the way it affects us or the way
it infects us. They're not expecting that to happen rapidly.
If anything, it will be a matter of many more
months or years. Yeah, this virus has remained relatively stable,
so I wanted to bring you on to talk a
little bit about it. Obviously, we still don't know that
much about the novel coronavirus. We're learning as we go.
(06:46):
We're still waiting for more effective treatments. We're still waiting
for a vaccine to hopefully eventually come through. And you
hear a headline like that, you know, it gets pretty
scarier right away. You think it's changing, and as it is,
people already talking about second waves and things like that.
So I wanted to talk a little bit about you,
just so everybody can know that this might be a
second strain that you taated in Europe. But it's not
(07:07):
anything necessarily that we need to worry about right now.
It's not that we don't need to be worried, but
it's just that our response is the same the recommendations
that we've been getting from public health officials and epidemiologists
and scientists are still true. We should be physically distancing,
we should be wearing masks, we should be washing our hands.
(07:27):
I mean, I understand kind of the thirst for information
about this virus. There's so many uncertainties, and that's very
hard to live with because we want to know what
is the right thing to do, what is the best
way to stay safe. But I think that this is
really forcing us all sort of undergo a little bit
of a scientific literacy crash course. And it's just a
reminder to be cautious when you read studies. Science is
(07:52):
not single breakthrough. It's the accumulation of research that all
points to the same thing. And so this one study
is not going to change the way we fight coronavirus.
But as researchers look into these questions of you know,
what are these mutations and how do they affect the
virus and how is it spreading, that's what's going to
enable them to understand it and develop effective tools against it.
(08:14):
You know, approach everything with interest, but maybe with caution
and with context. Think about what is the broader picture
of what the research is telling us, and make sure
it fits in with everything else. There's a Carl Sagan
quote that extraordinary claims require extraordinary evidence, and so anything
that seems a little too extraordinary is maybe something to
take with a great assault. Sarah Kaplan, reporter at the
(08:37):
Washington Post, thank you very much for joining us. Thank you.
I'm oscar A Mirrors and this has been your daily
coronavirus update. Don't forget today's big news stories. You can
check me out on the Daily Dive podcast every Monday
through Friday. So follow us on my Heart radio or
wherever you get your podcast
It's Friday, May eight. I'm Oscar Ramiras from the Daily
Dive podcast in Los Angeles, and this is your daily
coronavirus update. You might have seen headlines about a now
dominant strain of the coronavirus spreading that is more contagious
than the original. According to researchers, a mutation occurred in
the virus as it began spreading in Europe in early February,
(00:20):
and it rapidly became the dominant form. This news comes
from a research paper from scientists at Los Alamos National
Laboratory and has not been peer reviewed. There is some
skepticism that any mutations have changed the general contagiousness or
lethality of COVID nineteen. Sarah Kaplan, reporter at the Washington Post,
joins us for what we know. Thanks for joining us, Sarah,
(00:41):
good to be here. It was a pretty scary headline
earlier this week. Scientists say a now dominant strain of
the coronavirus could be more contagious than the original. Right away,
people started getting very scared about this. Talks of the
coronavirus mutating being a much more contagious strain. Nobody knew
really what was going on right away. There was a
(01:03):
lot of experts that were skeptical of what was going on.
But this all came from a research paper from scientists
at Los Alamos National Laboratory. So tell us a little
bit what we know about this. This paper is actually
what's called a preprint, so it's research that has not
yet been published by a scientific journal. And usually when
(01:24):
scientific papers are published in a journally undergo a review
process where other scientists read through the paper, make sure
the conclusions are valid and provide feedback. And so the
idea is that that is a way to make sure
that the results are robust. But in this era of
science really happening at warp speed and researchers wanting to
get information out there as quickly as possible, scientists have
(01:46):
been posting their research to these preprint servers where they're
available online even before they've been published in a journal.
And best what this paper was and basically what it
found is that the strain of the virus that is
now the most common, that is the most abundant around
the world has a mutation in the gene that influences
(02:06):
one of the proteins on the surface and their idea
is that somehow that have made that strain more transmissible
and more contagious. And they're saying that this particular strain
was something that came out of Europe, not in Wohan, China,
where they say that the stars Cove two the thing
that causes COVID nineteen, where it really originated. So this
(02:26):
strain is coming out of Europe. This thing to remember
is that all viruses mutaps. We hear mutation and we
think X men or some kind of like crazy lab experiment,
but mutations are very common viruses. The way they work
is they break into ourselves and they use our cellular
machinery to make copies of themselves and their sloppy out it,
and so a lot of mistakes get introduced. This virus
(02:48):
has about thirty thousand based pairs and its genomes, So
you can think of that as a book that's thirty
thousand words long. You change one word in the book
and it probably won't change the book very much. And
so all of these strains that we talk about that
have been circulating, they carry kind of different genetic fingerprints, markers.
They've picked up mutations, and now you can recognize that
as distinct lineages. That doesn't necessarily mean that they're functionally different,
(03:11):
and in fact, the consensus from scientists so far is
that all of these strains are actually functionally the same.
We're all getting the same version of the coronavirus. They
just have some slight changes to them. So this strain,
the one that has been described with the mutation on
the gene that colodes for its spike proteins, that is
one that emerged in Europe and it has become very
(03:32):
abundant around the world, the dominant stream that's circulating in
the US as well. And this hypothesis that the reason
that it is so abundant is because it's more contagious.
That's one interpretation, but a lot of the critics of
this paper have said there are other explanations beyond mutation
that increases contagiousness. You think about this virus being introduced
(03:53):
to northern Italy way back in January. It was a
very vulnerable population and a society that was largely unprepared
to contain the threat, and so they say, you know,
it's the founder effect. The reason this virus is so
abundant is because it got to a soft target and
then spread a lot, and so now we're seeing that everywhere.
The idea is that maybe what is distinguished distinctive about
(04:16):
the strain of the virus is not the viruses DNA,
but it's US. It's the fact that it got to
Europe and then North America and we proved to be
very easy targets. The same could be said for US
here in the United States. Obviously, there was reports a
little bit ago that the strain that was going around
in New York City, who was obviously been so hard
(04:36):
hit for US in the United States, that that strain
was a mutated strain that came from Europe also, but obviously,
again you know, a population unprepared for it, it's going
to spread like wildfire, and that's kind of exactly what happened.
So they're saying that this new strain possibly more contagious,
but probably not any more lethal. In fact, once these
(04:56):
things kind of keep mutating and passing on to more
and more people a lot of times with viruses, it
loses its effectiveness. The idea is that it's not in
a virus's best interest to kill its host. A virus
that is extremely lethal isn't able to spread very far
because from the viruses perspective, you want your hosts to
be up and moving around and affecting other people, and
(05:19):
so some of the most successful viruses from a kind
of biological perspective are ones that don't actually cause that
much destruction to a person. And example is the herpes virus,
which has been with the human lineage for six million years.
So when we were closer to our great ape cousins
than we are to modern humans today, we had herpes
(05:39):
virus and you know, it's not deadly, and so it
stayed with us a really long time. The evolutionary pressure
on viruses is to become more contagious and less virulent,
and that is a hope, you know, it's a long
term hope that one day this virus may become less virulent.
But the other thing to keep in mind is that
this virus actually mutates more slowly than other viruses do.
(06:02):
Most viruses are not able to fix mistakes in their
genetic material when they make copies of themselves, and this
virus is able to fix some mistakes, so that means
it picks up mutation about one tenth as frequently as
something like the influenza virus. So researchers don't expect this
virus to mutate in a way that produces functional changes,
(06:25):
changes in the way it affects us or the way
it infects us. They're not expecting that to happen rapidly.
If anything, it will be a matter of many more
months or years. Yeah, this virus has remained relatively stable,
so I wanted to bring you on to talk a
little bit about it. Obviously, we still don't know that
much about the novel coronavirus. We're learning as we go.
(06:46):
We're still waiting for more effective treatments. We're still waiting
for a vaccine to hopefully eventually come through. And you
hear a headline like that, you know, it gets pretty
scarier right away. You think it's changing, and as it is,
people already talking about second waves and things like that.
So I wanted to talk a little bit about you,
just so everybody can know that this might be a
second strain that you taated in Europe. But it's not
(07:07):
anything necessarily that we need to worry about right now.
It's not that we don't need to be worried, but
it's just that our response is the same the recommendations
that we've been getting from public health officials and epidemiologists
and scientists are still true. We should be physically distancing,
we should be wearing masks, we should be washing our hands.
(07:27):
I mean, I understand kind of the thirst for information
about this virus. There's so many uncertainties, and that's very
hard to live with because we want to know what
is the right thing to do, what is the best
way to stay safe. But I think that this is
really forcing us all sort of undergo a little bit
of a scientific literacy crash course. And it's just a
reminder to be cautious when you read studies. Science is
(07:52):
not single breakthrough. It's the accumulation of research that all
points to the same thing. And so this one study
is not going to change the way we fight coronavirus.
But as researchers look into these questions of you know,
what are these mutations and how do they affect the
virus and how is it spreading, that's what's going to
enable them to understand it and develop effective tools against it.
(08:14):
You know, approach everything with interest, but maybe with caution
and with context. Think about what is the broader picture
of what the research is telling us, and make sure
it fits in with everything else. There's a Carl Sagan
quote that extraordinary claims require extraordinary evidence, and so anything
that seems a little too extraordinary is maybe something to
take with a great assault. Sarah Kaplan, reporter at the
(08:37):
Washington Post, thank you very much for joining us. Thank you.
I'm oscar A Mirrors and this has been your daily
coronavirus update. Don't forget today's big news stories. You can
check me out on the Daily Dive podcast every Monday
through Friday. So follow us on my Heart radio or
wherever you get your podcast
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