NEWSCASTER: Researchers have identified a new double mutant variant of the virus.
PARDIS SABETI: We've long known that these viruses mutate.
So SARS-CoV-2 could always pick up a mutation that could just change the game.
NEWSCASTER: As more contagious variants continue to spread younger Americans are feeling the
brunt of this latest surge.
SABETI: One of the things that a lot of people kind of feel complacent about is that it seems
to affect people -- they're mostly elderly or you know mostly not them.
But at any point a virus could change and you know affect them.
It can become more lethal, it can become more lethal to our children, it can evade our vaccines.
And so it's one of those things where you just don't want to give it a minute to change
in a way that's particularly bad.
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NEWSCASTER: The World Health Organization just declared this a global health emergency.
SABETI: Right when the outbreak hit we were in a really good position, because we caught
this virus early, and we had a head start and even though the virus is moving quickly
we kind of have never gotten this kind of data this fast out into the world.
NEWSCASTER: This now makes the first coronavirus death confirmed in the US.
SABETI: Looking back now it's so frustrating to see that we did lose all of that lead
NEWSCASTER: Doctors say they have now detected the first two cases of the variant which originated
in the UK
SABETI: The virus mutated again and again and again as it was expected to do and we
might not have seen the worst of it.
SABETI: I'm a computational geneticist.
My lab develops new technologies in genomics and then uses those to track infectious diseases.
We are actively working in a number of states in the US doing sequencing and identifying
variants.
The way that we identify virus is that you take a sample wherever the virus is shedding.
We see it in our nasal passages and we see it in our saliva.
You can take that and you can basically access the genome of the virus in the sample and
there's a lot of molecular tools like PCR, which is just a way of amplifying that part
of the virus and and seeing that it's present.
We can just take it a step further and not just amplify and say that they're not there
but read out exactly what the genome of the virus that's there is, and that gives us much
more information about what version of the virus are we seeing, how is it related to
other versions.
With microbes in general, we really get to see evolution in real time.
In a year you can just see generations and generations of things happening.
And what we've seen is what we expect to see -- that the virus keeps picking up mutations
that make it better or spread more easily and evade therapies and those are the ones
that are going to keep propagating.
SARS-CoV-2 is a very big virus as as viruses go.
Coronaviruses in general, they're very big genomes -- they're 30 kilobases -- and so
that's a lot of information that they've got a lot that can change that we need to understand
and deconstruct and decode.
They are also RNA genomes so we know that those mutate fast relative to other organisms,
and so we have to be mindful and watching what they're doing all the time.
One of the things I think is interesting about Covid is it has forced an entire collective,
an entire generation of scientists to look at it, and to study it and to generate a lot
of data.
I think that's one of the things that's special about it, is just the number of eyes that
have been on it
A genome is this long kind of code where there's four letters that are strung together in this
in this way and a lot of times if you can decipher that there's a lot of information
there.
So mathematics becomes really really important in deciphering this.
We use a lot of statistical tools to mine the data of the 30,000 bases of the SARS CoV
genome.
In the hundreds of thousands of genomes have been sequenced you can find patterns using
mathematics.
So my lab, one of the big things we do is we build algorithms to mine this data and
to look for patterns.
You can trace the origin, you can date when the virus likely entered the population, you
can get a sense of how it's transmitting and whether or not it's coming in from multiple
infections from the environment or if it's likely that the disease is spreading from
person to person in a close amount of time
In the case of Ebola, for a long time into the outbreak, people believed that ebola was
being transmitted from the environment.
Around the world, all the messaging was don't touch monkeys, don't touch bats, don't touch
fruit that might be touched by those animals.
It was really always thinking -- assuming -- that every case was coming from the environment.
It didn't really make sense with how quickly it was spreading.
Our data was pretty strongly indicating that this was transmitting from human to human,
that they were all -- all of the viruses descended from one likely original infection that probably
entered the human population once and was was from there transmitting from human to
human.
So that was like a kind of thing that was revelatory for Ebola, and since then we have
a better understanding that that's a pretty common phenomenon can happen.
In SARS-CoV-2, it's similar that we can see that all of the cases that we're looking at
originated from one common ancestor, suggestive of like one long transmission chain.
You know there's a question of, could it infect animals and come back out and infect humans,
and that's possible but that we know that the primary mode of transmission is from human
to human.
When you give a virus more opportunities to transmit from human to human than ever before,
you're going to see a lot of changes.
Most of those changes don't really matter -- like most mutations are probably detrimental
or just get cleared out -- but when you give it that many chances, it will stumble upon
things that help it, and when those, you know, things emerge, they're more likely to reproduce
and pass on.
The fewer their viruses are out there, and the fewer those viruses transmit, the less
mutations we're going to see.
It's it's a pretty kind of direct correlation between, you know, the number of infection
cycles you have, the number of opportunities you have for new mutations to arise, and so
the best thing we can do is to get the infection rates to zero, so that the virus has no opportunities
to mutate and change.