February 23, 2021 • 40 mins
This is our final interview for Season 1 and it's our biggest one to date: we got a chance to interview Dr. Keith Gagnon, an associate professor of chemistry and biochemistry at SIU whose lab has uncovered a U.S.-specific coronavirus variant that accounts for about half of the cases in the nation! He has been featured on many major news outlets as more information about this mutation is uncovered. We were so honored he took time out of his busy schedule to talk to us and frankly he filled us with a lot of hope for the future - while the topic of conversation is scary, we were grateful he was able to explain things in layman's terms. We learned a lot and think you will too!
Stay tuned for our end of Season 1 wrap-up episode and our kick-off of Season 2 as we commemorate the one-year anniversary of the pandemic. There are many great things in store and we can hardly wait to share them with you!
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Caroline Raymond (00:00):
Hi, I'm Caroline Amos. And I'm Raymond
(00:02):
McAnally. And we are FATIGUED(laughter).
Caroline Amos (00:13):
All right, Dr.
Keith gagnant. Tell us a littlebit about yourself.
Dr Keith Gagnon (00:19):
Well, I'm an associate professor here at
Southern Illinois, IllinoisUniversity in Carbondale. So
SEIU been here for six and ahalf years, I grew up in New
England, went to college and didmy PhD in North Carolina, did
some postdoctoral work inDallas, Texas area, I have three
(00:39):
kids and beautiful wife. I playbasketball when the gym is open,
and there's not a pandemic goingon. I like to work on cars, with
my hands around the house.
And I love my job becausescience is a nice a merger or
marriage of working with yourhands, but also getting to think
critically.
Caroline Amos (00:59):
Oh, I love that.
That's awesome. Yeah, man, manyfacets then I guess. So.
Congratulation.
Raymond McAnally (01:07):
And for our audience, what is what is your
area of expertise?
Dr Keith Gagnon (01:11):
So I traditionally trained as an RNA
biochemist. So RNA is the cousinmolecule to DNA doesn't quite
get as much fanfare, but itperforms many important roles in
the cell and in biology. Sothat's what I learned when I was
an undergraduate graduatestudent was how to work with RNA
and the many roles it plays inbiology. So that's my background
(01:36):
sort of RNA biology or on RNAbiochemistry. And the two major
areas we've worked on the most.
Before we started working onSARS, COBie two was a disease
called Lou Gehrig's disease.
This is also known as a myatrophic lateral sclerosis, or
ALS, was the devastatingneurological disorder. And so we
(01:56):
try to understand more aboutwhat's going on at the molecular
cellular level, and are thereways we could come up with
strategies to treat it. And theother area is, like gene therapy
development, there is a type ofenzyme called CRISPR. And CRISPR
is being it's a bacterial enzymethat's being co opted or
developed as a gene therapytool. very promising, but it's
(02:20):
got some it's got some problems,it's not quite perfect, it
didn't evolve to work. Andpeople evolved to work in
bacteria to fight against, youknow, bacteria phages. So it
needs a little bit ofengineering. And so that's kind
of what my lab does is we dosome of the engineering of this
enzyme, so it can be hopefullysuitable for human gene therapy
or human use. That's very cool.
And of course, we startedsequencing, SARS, COVID, two
(02:42):
viruses this year, so yeah,well, so that's the whole reason
we wanted to talk to you today.
As you can read in the news, Dr.
Keith, or Dr. G, as I like tocall him now has part of his lab
was important in discovering thenew mutation of COVID-19.
Caroline Amos (03:07):
Tell us a little bit more about what the process
of discovering a mutation of avirus looks like?
Dr Keith Gagnon (03:15):
Well, it starts with a lot of painstaking
sequencing, a lot of calledmolecular biology, you have to
get access to some of thesesamples, that took a long time
to come up with an agreementwith the state where we could
access clinical samples. There'ssome important equipment and
expertise. So we had to set allthat up. And then we were able
(03:38):
to eventually start sequencingthe genome of the virus. And for
those who are not reallyhardcore scientists, what we're
talking about is, the genome isall those sort of letters that
make up the the book of what thevirus is, you know, think of it
as a book with 30,000 letters init that make up words and
(03:59):
sentences and chapters and allthat. And so that's sort of like
what a genome is, it has all theinformation to reproduce another
organism or, in this case,another virus. And so what we do
is we look at every single oneof those letters to see if any
of them have changed. Now, wedon't do this manually. We have
computers, which we've trainedto screen through and scan
(04:20):
through this very, very quickly.
And we look for changes in thatsequence. And we compare this
these sequences of differentviruses all against each other,
essentially See, how much doesit change from maybe the first
Coronavirus in China? versus howmuch does it change from one
that we sequenced last month,you know, in Illinois, so we can
(04:41):
track all this. And by doingthis, we can determine if we're
getting any significant changesor important changes, maybe a
recurring change that we seeover and over again and multiple
viruses, and then that sort ofconstitutes a new family or a
new variant of the virus. That'skind of the process that we go
through. And a lot of people areworking in this area around the
(05:04):
world looking for these variantsand trying to keep our finger on
the pulse, if you will, to makesure we don't get caught with
our by surprise.
Caroline Amos (05:14):
Yeah.
Raymond McAnally (05:17):
What, um, when you say viruses, you're Are you
referring to the theseindividual samples that you're
able to obtain?
Dr Keith Gagnon (05:26):
That's correct.
So these are samples that werebasically mouth swabs are called
nasal pharyngeal swabs, the NPswabs from patients. And so
that's what's collected duringthe time of testing. And then,
if the test comes up positive,those samples typically get
archived in the freezer. Andthen my lab later gets access to
those and we can sequence thosepositive samples to see what
(05:48):
kind of variant that virus was.
What kind of mutations it hadits genome.
Caroline Amos (05:55):
Wow,
Unknown (05:56):
are you?
Raymond McAnally (05:56):
Are you limited to the samples that you
have physical access to? Or arethere labs like you're sharing
the genome information?
Dr Keith Gagnon (06:06):
That's a great question. So, so the types of
some analyses are limited towhat we have on hand that we
generate, but but the vastmajority of the analyses we do
can be done with lots of data byother groups. And so my lab,
we've only sequenced about maybeclose to 600 genomes so far. But
(06:26):
there is about 450,000 that havebeen sequenced globally around
the world. And these are allactually, I think there's more
than that. But they're alldeposited in these databases,
where then researchers like me,we can go, we can pull those
out. And so this is how we sortof identified this one variant
that my lab recently sort ofreported, is, we were looking at
(06:49):
our Illinois data, our localdata, and we saw some trends.
And then we just simply want toask, Is this trend true in the
United States? How does thistrend look around the world? And
so we were able to pull thatdata and analyze that at larger
scale? And so your answer isyes, the answer to your question
is yes, there's a lot of peoplewe're all sharing our data. And
(07:10):
that's, that's sort of key tocatching these new variants.
So...
Raymond McAnally (07:13):
Yeah, I can only imagine is it? Is it a
situation where that has thatsharing has improved? We've
heard, you know, you hear in thenews, or, to be honest, I
imagine, we think we know itfrom movies and TV shows more
than anything that that labs,kind of, for reasons for funding
(07:35):
and, and research and kind oftheir own r&d. Stay a little bit
siloed. Is that is that true ofthe real science world? Or is
this something that new that'shappening, that that all this
information is being sharedglobally?
Dr Keith Gagnon (07:52):
So, so yes, and no to that question, let me pick
this apart a little bit, becauseI know I asked about three
questions. I mean, they're allvery related, it's a great
question, to see if we canunpack a little bit. So
traditionally, yes, academicscientists were a little bit
protective of our of our data,you know, we put a lot of blood
sweat and tears into collectingthis data, trying to make sense
(08:15):
of it. And then, you know, wehave to publish and disseminate
that. And unfortunately, forbetter or worse, our careers,
whether we get funding or we cancertain things depends on what
we publish and, and whatjournals we publish in. And so
sort of naturally, people are alittle protective. Buta couple
of these databases in particularone called, it's pronounced, he
(08:37):
said, er g said, it's sort ofthe one of the big major
databases out there for puttingthese genomes into. And they
have, then they were aroundbefore the pandemic, and but
they, they've been heavily usedduring the pandemic. And they
have tried to go out of the wayto sort of share openly, but at
the same time, protect therights, if you will, scientists
(09:00):
with their data. So when wepulled all that data from the
gisa, database, we, we have tomake sure we cite the people who
contributed that data. And so wemade sure we had, you know, gave
them credit for all for sharingtheir data with us. And the same
goes for my lab, we, we submitit on there, and it's shared
with others. So there is alittle bit of a protectiveness
(09:23):
naturally, but during thepandemic, people have let our
we've let our guard down alittle bit for the better good
of you know, the world reallywell. That's good. Yeah. And the
data sharing is much is gettingbetter and better. And it
doesn't go as fast as it could.
And there's still some groups orplaces around the world that a
little hesitant to share withshare their data. But I think in
(09:45):
general, it's very open and it'sgetting better. And one of the
few silver linings of thepandemic is just how do we come
together to tackle these bigproblems? data sharing,
important part.
Caroline Amos (09:58):
Yeah, that's really encouraging to hear. Nice
to see everybody work together.
And yeah, for a change. Yeah,that's great. I'm really curious
to know, in this new mutationthat you've discovered, the one
that was, I was doing someresearch before we talk to you
today. And it was discovered,the earliest known case of it
(10:22):
was in Houston, Texas?
Dr Keith Gagnon (10:27):
Yeah, that's correct. Using the global
database, where we coulddownload sequences from
everybody else, we look for theearliest case, the earliest
genome sequence that had the keykey signature, or Hallmark
Hallmark mutations of thisvariant, and we traced it back
to may 20, in the Houston, Texasarea.
Caroline Amos (10:48):
Now, what makes this mutation different than
what we have been experiencingin the United States as a whole
over this time?
Dr Keith Gagnon (10:57):
So this variant that we found, we call it 20cUS.
Raymond McAnally (11:01):
Is there a media term for it that people
would be more familiar with?
Dr Keith Gagnon (11:07):
No 20cUS - it's not like the quote unquote, UK
variant. Brazil is a variantthat was first observed in South
Africa. So it doesn't have oneof those names. There are some
different naming schemes thatare used, for example, the
variant that was first found inthe UK, they call it some people
just call it colloquially the UKvariant. It's also known as B
(11:31):
117.
Raymond McAnally (11:32):
That sounds like a Star Wars character.
Dr Keith Gagnon (11:36):
Yep. Yep. I think it's, there's another one
it's called 20I or 501YV1. Sothere's there and they're trying
to work out the the namingsystem so that it's more we have
a single one to use. But yeah,so ours is B12, is one naming
system for us also often called20G, because it matches really
(11:57):
closely with a with one that'scalled 20G.
Caroline Amos (12:00):
20G is like a really fun name. I like that.
Dr Keith Gagnon (12:02):
Yeah. So we can call it 20 G, we can go with
that. You got 20 G's.
Raymond McAnally (12:09):
Yeah. 20G's albums gonna drop next fall.
Dr Keith Gagnon (12:12):
Yeah!
Caroline Amos (12:13):
So tell us more about 20 G.
Dr Keith Gagnon (12:15):
Yeah, so. it's actually picked up a couple
mutations really, either reallyrapidly or almost at the same
time. And so that set ofmutations is what defines is not
a single one, but a group. Andso same with the variant that
first was found in the UK, ithas a set of mutations which
distinguish it clearly from allthe other virus variants out
(12:37):
there. And so this set ofmutations for the 20cus or the
20g variant, it looks a littlebit vanilla, or mundane on the
surface, it doesn't have themutations that some of the other
variants in the world have. Andso we've actually been kind of,
I don't want to say brushed off,but a little bit, you know, not
taken very seriously, because itdoesn't have those telltale
(13:00):
mutations that everybody'slooking for, which is number
one, why it got missed in thefirst place, and it grew. In the
US, it's now the the probablythe most dominant one, it's
right around between 40 to 50%of all the variants are derived
from this particular 20 G. Andso it basically took over our
backyard without us even knowingOh, and of course, it doesn't
(13:23):
have those telltale mutations.
So everybody's like, well, itcan't be that big of a deal. Or
is it is the point I'm trying tomake? And I'm saying how did
this thing, gain prevalence andgain dominance in the US with
all the other variants floatingaround, especially during a
massive third pandemic wave? Andthere's so many other variants
that that could have taken over.
(13:44):
But this one did. So I'm arguingit's not entirely by chance.
This is not by accident, I dobelieve and we're working on
experiments to sort ofdemonstrate that, that this
variant has some unique featuresto it. So the good news is,
though, when you look at and youdo some correlations and you
say, okay, our case, our deathsper cases, they call case
(14:07):
fatality rate, has that changeddramatically? In the US? No, it
hasn't. It's actually gone down.
So and there's a lot of factorsthat feed into that. The other
end we looked at is what abouthospitalization rates? Have
those gone up per patients withCOVID-19? And no, they're both
that sort of a little, a littlewavy pattern to them, but that
hasn't really changed. So wedon't think this variants
(14:31):
necessarily more dangerous, butit's it may be it may be more
transmissible it, that means itmay spread a little faster. We
may have some other advantagesthat other viruses other
variants don't have. So we'regoing to watch that carefully.
The last thing I'll say aboutits mutations is that it's now
starting to pick up and acquiresome of the mutations that the
(14:53):
UK variant, the South Africanvariant, the Brazilian variant
have and these are the ones whocall variants of concern that
everybody's worried about,because those particular
mutations have been up notproven, but highly linked to
evading the immune system,reducing the effectiveness of
the vaccine. And the point Iwant to make is that this, this
(15:14):
variant that's in the US thatgained dominance without any of
those mutations, is nowacquiring those mutations. And
so my question is, what doesthat leave us with? What What
happened? about what's in ourwhat's in our own backyard?
Yeah. And the answer is, Yes, weshould. And that's kind of where
I feel like the role my lab isplaying is everybody's looking
for the other variants, as theyshould be. What I'm more
(15:38):
concerned with what's alreadyhere, and what we have to deal
with, if we're not watchingcarefully. So sorry, I talked a
lot. But...
Caroline Amos (15:46):
No, no, this is the reason we wanted to bring
you on this is this stuff thatwe're really interested to learn
a lot more about.
Raymond McAnally (15:53):
I would imagine, because it has taken
over so much - that that itsability to do so is kind of your
most concern, right?
Dr Keith Gagnon (16:07):
Yeah. How did it come out of that game? And
again, we're hoping we're allhoping it was just by accident.
Maybe it was by chance, maybegot lucky. But my my feeling is
there's something a little extrato it. That can't be completely
complained. Sorry, explained bychance. And so then, of course,
now you add on top of it, theseother mutations that we're
(16:28):
worried about, again, where doesthat leave us? Does that mean,
we have something even moreworrisome. That's homegrown, if
you will...
Raymond McAnally (16:35):
And it is uniquely American?
Dr Keith Gagnon (16:38):
Absolutely.
It's you born and raised in theUS.
Raymond McAnally (16:42):
So it exhibits a lot of freedom. It exhibits a
lot of like,
Dr Keith Gagnon (16:48):
it wants its guns rights. Yes. (laughing)
Raymond McAnally (16:53):
It's strong individualism. (laughing)
Caroline Amos (16:56):
Oh, my God.
(laughing) Now, when you talkabout mutations, and you talk
about the longevity of thisvirus, do you have any
predictions about where youthink this mutation might end
up?
Dr Keith Gagnon (17:14):
Yeah, so I mean, we can just speculate a
little bit. By the way, allbefore I jump into this, I'll
add that a lot of the stuff saidabout the different variants,
especially the variance ofconcern, a lot of it is
speculation, and even thoughthere's some science behind it,
it's really hard to prove someof the things like the media,
everybody wants us to prove thatit's more transmissible or prove
(17:35):
that it's more dangerous. It'sreally hard to do that. From a
scientific standpoint, all wecan do is look at this data set.
Look at that one, does it? Isthere some correlation or
connection, and it's just hardto do that. So keep that in
mind, I'll speculate a littlebit of what I think the future
might hold for us, I can imaginethat it's going to mutate, it's
(17:55):
continuing to grow. And it's ait's an ongoing, ongoing, and
it's a cumulative thing too,because it accumulates those
acquiring noon, noon, moremorning mutations. So um, a
couple of ways we could go here,let's talk about the 20 g
variant 20 cus variant, what'sthat going to do? Well, it's
(18:18):
currently the most prevalent anddominant form in the US. And it
is continuing to rise in somestates and some other states,
it's kind of plateaued, maybeeven going down. Looks like it's
going down a little bit inCalifornia. Again, it's hard to
tell because you need two orthree months of data to really
see which way it's going, youknow, it might drop a little bit
(18:39):
one month go back up, but likeit's going down in some places
up, but overall, it's continuingto rise. So I think it's going
to continue to be the dominantvariant. I've heard the CDC say
that the variant that was fromthe UK is probably going to take
over in the US by March, Idisagree, wholeheartedly, 100%,
(19:00):
that is not going to be thecase. It has to first battle
against if you will oroutcompete the entrenched,
incumbent variant that's alreadyhere. And the competition it had
in the UK is not the samecompetition it has here. About
the time of its introduction,we're starting to see now the
introduction of the variant thatwas first seen in Brazil, and
(19:22):
the one that was first seen inSouth Africa. So we're getting
some really different dynamicshere in the US. And on top of
that, as I mentioned, now, this20 G is also starting to
accumulate some of thosemutations that we see that are
the most concerning from theother variants, other
international variants. So Ithink it's going to be a bit
more of a complex interplay. Theother thing is, it's hard to say
(19:43):
if it's a if it's like acompetition really between
viruses, you know, no one persongets infected by two different
viruses or variants at the sametime or a very, very rare event,
right? So it's more likepopulation based competition,
which is the most fit virus thatcan keep going. So um, that's
what I think in the short term,I think the 20cus is going to
(20:06):
continue to persist, I thinkit's going to pick up and
acquire a couple new mutationsthat are going to accumulate.
And it's going to allow it tosort of compete with these
international ones. And I do youthink it's going to go down over
time, though, because there's somany new things that are gonna
pop up. And what we're dealingwith is some really uncharted
territory where the virus isgoing from almost a completely
(20:29):
naive population, like basicallyno one in the population before
the pandemic could ever reallyhad this virus. So it's just
free to, to rampage through thepopulation, in fact, sort of
freely, if you will, withouthaving to be forced to mutate,
and change in order to survive.
But now what we're seeing ismore and more people, we're
getting closer and closer,slowly to that herd immunity,
(20:50):
more people are gettingvaccinated. And so for this
virus to be persistent, and justsort of continue its lineage, if
you will, it has to mutate andit has to, or it has it the
mutations that help it have tohave to persist. And it has to
be able to reinfect people evadethe immune system a little bit
those sort of features. And so,we don't know, but all this is
(21:14):
going to start happening. Andit's a little bit of a foot race
between can we vaccinate quickenough?
Raymond McAnally (21:21):
Yeah, yeah.
Yeah, for lack of a betterGlossary of scientific terms. Is
it the nature of a virus tomutate for those reasons? It is
it is trying to do what virusesdo and is trying to stay alive,
I guess, in some way, shape, orform?
Dr Keith Gagnon (21:41):
Yes, you can think of it, you know, we often
don't think of viruses as beingliving but they possess many
features of a living organism.
And so mutation is sort of builtinto the virus, it has a low
level of mutation that ithappily allows to happen,
because that gives it thatlittle edge when I mean, when
everything's working great, andit doesn't have to mutate. It
doesn't have to evade immunesystem. Why would it change, so
(22:04):
it wants to maintain what worksreally well, but it has a small,
low level of mutation that itallows and to put in
perspective, the Coronavirus,you tastes a little slower than
the seasonal flu, you know, theseasonal flu that we get
influenza every year. But it'sstill mutates fast enough, and
especially with you know, thehuge number of cases worldwide,
(22:25):
to pick up enough mutations towhere we get these rare events
where you get a couple ofmutations that really give it a
jump in fitness, and ability tokeep going. And so that's kind
of so that's another part of theprediction, I would say is we're
going to continue to see novelvariants pop up all over the
world, especially in isolatedareas, because international
(22:45):
travels pretty restricted, whichexplains why this 20 g variant
really hasn't spread too muchbeyond the us because we're not
really allowing that. Butthere's no state there's no
state border controls in the US.
So people freely runintermingle. And it spreads very
quickly in the US. So weshouldn't be surprised to see
these pop up. But we we gotta beon the lookout for new ones that
(23:09):
could be problematic. If we'requick enough, we can catch it
and do contact tracing andtraditional epidemiology and
sort of kill that transmissionline. If you know what I mean.
Caroline Amos (23:21):
I'm really curious to know, how will the
vaccine be effective againstthis new this new mutation?
Dr Keith Gagnon (23:29):
Yeah, so it's so far it looks like the
vaccines are effective enoughagainst some of these new
mutations. I guess the concernis can the virus mutate enough
to get fully around the vaccine?
If it can, that's okay. Youknow, we'll make new vaccines
and give booster shots. And whoknows, maybe it'll become like a
seasonal thing. And I mean, youknow, where every year just like
(23:53):
the flu where they put out a newvaccine to try and keep up with
these mutations that Yeah, theyhave to do that with the
Coronavirus. I guess that's yetto be seen.
Raymond McAnally (24:04):
Yeah, I was wondering about that. myself.
I'm glad to hear you bring thatup that it. So it is comparable
to what we go through withdifferent flu shots and
different strains of flu everyyear?
Dr Keith Gagnon (24:15):
Yeah, hopefully, because it mutates a
lot slower than the normal flu,the seasonal flu. We won't need,
you know, booster shots or newnew vaccines every year, it
might be every couple years. AndI guess the hope is that it will
die out. I have a feeling thoughit will stay at a low level of
persistence in the populationcalled this sort of becoming
(24:39):
endemic in the population. Soit's sort of always there at a
low level. So I think we couldprobably expect that to be the
case. I do think though with thevaccines really rolling out and
we've really got a lot ofmomentum with the vaccines. I do
think that by the time thesummer comes, as was predicted
early on that the vaccines willallow us to return most of the
(24:59):
normal life, I really thinkthat's gonna be the case. But
there could be a couple bumps inthe road with some new variants
as we go. But I don't think Ithink ultimately we, you know,
the vaccinations should shouldhelp us tremendously.
Raymond McAnally (25:13):
I cannot tell you how much hope just ran
through my body just becausesomeone with your with your
level of expertise andunderstanding of this could
could say that that's what theyfeel. And that's - It was just
my, I just had a visceralreaction to that. So thank you.
Yeah. Well, because right now,it's hard to know.
Dr Keith Gagnon (25:38):
Exactly. I mean, I'm not the only one who
has the same feeling. I thinkyou have people who are more
optimistic and people who aremore pessimistic. I tend to be a
more optimistic person. But I'malso kind of a realist, but I
think I'm optimistic. But Ithink the reality is matching
that is the vaccine some so forexample, the vaccines, a couple
(25:59):
of them have been tested againstthe variants that are of the
most concern right now, which isthe one that was first found in
South Africa and Brazil. Ithink, I think the Brazil ones
been testing test, I can'trecall. And then the one that
was found in the UK, so and itappears that they work well
enough, and they seem to almostcompletely 100% block death,
(26:19):
which is a really importantthing. And then severe cases
that require hospitalization areway, way lower. And so that's
the key. I mean, if we canconvert this to something where
Yeah, you get a nasty cold, butyou don't feel the hospital, you
don't worry about dying. If wecan at least get there. That's
That's good. I think we candefinitely get there by the, by
the summertime or the end of thesummer.
Caroline Amos (26:41):
Oh, that's so great.
Raymond McAnally (26:42):
Is that typically, on a scientific
level? The best case scenariofor any pandemic type virus, for
example? How do you know, in inyour education and study, what
happened to the influenza virusthat hit in, you know, the
(27:06):
1918/1919 timeframe?
Dr Keith Gagnon (27:10):
Yeah, I mean, I'm certainly not the authority
on this. But I mean, I've readsome things as a leisure
reading, like sort of you guys,you know,
Caroline Amos (27:18):
leisure reading, I love that!
Dr Keith Gagnon (27:20):
leisure reading, but it was a
scientific, scientific, youknow, angled paper article I
read. And the the, the argumentwas that the 1918 pandemic had
multiple waves. And then it cameback the next year, and then the
year after, but each year it wasweakened and then largely
disappeared, and sort of diedout because it was really just
(27:44):
too virulent. It just was, itjust killed people too, too
much. But we had but but then Ialso saw that same article, the
argument that some of the annualor seasonal influenza a has the
remnants of that virus. And soOkay, yeah, and so the influenza
virus can recombine with otherinfluenza viruses a lot more
Raymond McAnally (28:05):
So they don't really - in our brains, you
readily. And I think it's alittle more common for two
influenza viruses to be in thesame person. So pieces of it
have somehow persisted for 100years. But but the the major one
that drove it apparently diedout. And so you may also know,
though, on top of that,intriguingly is that the common
(28:28):
cold is a lot of common colds orcoronaviruses. I'm not an expert
in this area, too. So it's kindof tempting to think while some
fragment or remnants of thissource code could persist for a
long time, either it justevolves to become highly
transmissible, but very nontoxic or non virulent to the
(28:50):
host. So it survives better orsort of at some point recombines
with another common Coronavirus,and you know, so
know, they they can beeradicated but it sounds like
they they lessen and degree andare somehow, but somehow do
(29:13):
stick around and in a remnantform.
Caroline Amos (29:15):
It was interesting to think of it as
like, you know, the Spanish Fluhas had grandbabies. And the
grandbabies are colds that weexperience every day and someday
Coronavirus is going to havegrandbabies, too.
Dr Keith Gagnon (29:26):
That may be the case. And you know, it's
important to remember too thatCoronavirus is a very common in
nature and and lots of animalsand what we've had here what
what appears to be is the jumpfrom bats to humans, there was
enough mutations and it seems tobe the case. There could have
been some intermediate inbetween but lots of Coronavirus
(29:47):
is out there in the world. Mostof them don't infect us, I don't
do so very efficiently. So, atleast if this ever happens
again, maybe it will be a lotmore prepared.
Caroline Amos (29:59):
Let's hope! How does it feel to be the bearer of
such trepidatious news?
trepidations might not be theright word, but it looks like
came to mind.
Dr Keith Gagnon (30:11):
Yeah.
Caroline Amos (30:11):
What does it feel like to be the bearer of bad
news?
Dr Keith Gagnon (30:13):
Well, the question is, is it good news or
bad news? Right? Because a wewere very hesitant about this.
When we first made theobservation of this variant. It
was kind of, well, it's beenhere for a long time. So maybe
it's not a big deal. Butnobody's ever said anything
about we can find anything inthe literature even on even on
on Google nothing about thisvariant or and these mutations
(30:34):
we were finding, and we thought,well, we need to say something.
But, you know, so it was like,this is important, but how
important and we've gotten thesame feeling from the scientific
community. Some people like, Oh,this is fantastic, I'm glad you
characterized it, you know, thiscreates the backdrop for any new
variants that would emerge inthe US. So it's important to
study this, this variant. Andother people. Well, it's not the
(30:57):
UK variants, not the variantthat we saw in South Africa
doesn't have those mutations. Soit's not must not be important.
So I get both of that, and it'skind of have mixed feelings. And
I don't know, that's bad news,because it's been here for
months. And we don't have adramatically higher death rate,
or hospitalization, or, youknow, it sort of came on
(31:19):
quietly, you know, didn't make abig racket. And so even even
possible that it might be lessvirulent, or as transmissible
but not any more dangerous thanthe original one. So who knows,
maybe after we do enough studiesand characterize us better,
maybe it turns out that it's,it's, it's, it's a good variant
(31:40):
that is very transmissible, butyeah, dangerous. Who knows?
Caroline Amos (31:43):
Yeah.
Raymond McAnally (31:44):
That's interesting to think about,
that. That mutation can alsomean that it mutates down and
weakens or it it, it gets easierto combat in some way.
Unknown (31:56):
Or maybe maybe I found the good variant that we
shouldn't be concerned with.
Caroline Amos (32:01):
Yeah. I'm really, I'm more anecdotally, what are
you really looking forward todoing once the world returns to
some semblance of normalcy? Whatdo you miss?
Dr Keith Gagnon (32:12):
Gosh, you know, I've got three kids, and like,
they can't go see their friends.
I'll just be happy when they cango to school. My wife is mostly
staying home with the kids and,you know, helps mediate,
they're, they're learning,they're learning at a distance.
And it's just hard on her, Ithink she has a much harder job
than I do. So I'm just lookingforward to normal life for my
(32:34):
kids. And then, like I said, I'dlove to go to the gym and play
basketball again, that would bewithout ask. Yeah, you know, we
haven't taken any familyvacations. I've been working
harder since the pandemic thanany other time because we're
trying to maintain our normalprojects, but now take on this
(32:55):
new COVID-19 project. So I thinkI think it would be nice to just
be able to take some vacations,just do the normal go to the
restaurant, you know, I justlooking forward to the things
really nothing more.
Raymond McAnally (33:08):
Yeah, it's it's amazing how just those
little things that the feelingof being able to spontaneously
go somewhere, grab something or,you know, whether it's a
restaurant or the post office,or whatnot. We were just talking
my wife and I last night aboutthe fact that we're, we're
(33:28):
coming up on what will be hersecond birthday in the pandemic.
And we're, we're both very, youknow, we we try to understand
the science of it, and we do ourpart. But she was like, Can we
please do something a little bitspecial for my birthday? It just
(33:51):
last time, you know, we had justbeen shut down. Everything was
closed. And, you know, we didsomething quiet at home. So
we're trying to figure out whatthat is. Because it's not like
things have improved enough(laughter).
Caroline Amos (34:07):
Can we it's gonna be like a walk down the street
today? That'd be so nice.
Dr Keith Gagnon (34:12):
Yeah, I've got I agree. We've got a two and a
half year old and she's trainednow she wants when we go on
public, she wears her mask. Ifher mask comes off. She freaks
out, like, what kind of worldare is my portrait growing up?
And you know, our masks arenormal. But yeah. And in fact,
(34:33):
earlier today, I'm sitting in myoffice working on my computer,
and I'm wearing my mask. And I'mlike, why am I wearing my mask?
That was like, when I left myoffice 20 minutes ago, and I
came I didn't take it off. It'slike, we're so trained now. I
never would have I mean, youknow, imagine when we first
started the pandemic, peoplewere so resistant to wearing
masks. Yeah, it's, it'scommonplace. Yeah, you just
(34:55):
accept it as normal life.
Caroline Amos (34:57):
Yeah, I fell asleep with mine on actually
Last night, yeah, I wentdownstairs to pick up a package
came back in, realized I wastired and fell asleep. And it
took like halfway through thenight for me to be like, what is
on my face? What is going on,which is also really gross,
because yeah, just breathe andmore of my own air for a long
time. We usually love to sort ofround out these interview
(35:21):
conversations with a morepositive note. And honestly,
frankly, this conversation was alot more hopeful and positive
than I was sort of expecting itto be. So thank you for that.
Yes. I'm curious to know what,what gives you hope right now?
Dr Keith Gagnon (35:37):
Well, um, I got, I think the vaccines are
huge. And unfortunately, nomatter what happens, the
pandemic will run its course,and you know, you can only
infect people so many times. Andeven if we had no intervention,
viruses are at some pointnaturally going to become less
virulent, because, you know, youcan't kill every host. So those
(36:01):
simple, simple, you know,biology, things I think, are, I
feel like, you know, eventually,you know, things will change,
just like in the 1918 pandemic,eventually, people's immune
systems adapted, or the viruscouldn't adapt further. But
realistically, the vaccine, Ithink, has been important to
help push things along. And Ithink it was a big deal at the
(36:22):
beginning of the pandemic, weput a lot of stress on it. And
I'm glad we did, because itallowed things to move quickly.
And I think it's living up toits promise, so to speak. So
that gives me hope. You know,and also what I've seen is a lot
of, at least in my laboratory,we've come together to solve
some hard problems. sequencingthe viruses genome was not a
(36:45):
simple task, it requiredeverybody in my lab to come in,
during the pandemic, and risksthemselves, you know, and put on
all the the PP you know, themasks and the gear. Yeah. And
there was a lot of unknownsearly in the pandemic. So we
didn't know how much of a riskwe were taking. And, but so I
got to see people come together.
And I think that's, that alwaysbrings a little bit of hope to
(37:07):
situations when we can bandtogether and solve problems. And
we see that in the world and inthe science world, and in
medicine, and hopefully, withgeneral everyday people were
very supportive of like, comingtogether and solving this.
Caroline Amos (37:20):
Yeah, gosh, that gives me so much hope. Thank
you. Yeah, yay, science, listento science, everybody listened
to it? Well, awesome. Thank you.
Thank you so much. I know thatyou don't know us at all, and
that we just reached out on awhim. And I know you've got the
busiest schedule in the world.
So we just appreciate the factthat you took a little bit of
(37:40):
your time to talk to us, itmeans so much.
Dr Keith Gagnon (37:42):
Well, no, I appreciate it. I feel like I
know, you guys know. So weshould keep in touch. And don't
forget to reach out and maybe ina couple weeks or a few months,
we'll have some updates, andwe'll probably be good to
update. You know, well, a lot oflike unknowns, we don't know
what the next couple months aregonna bring. So again,
Caroline Amos (38:00):
yeah, man,
Raymond McAnally (38:01):
We'd love that!
Caroline Amos (38:02):
We'll reach out for follow up soon.
Dr Keith Gagnon (38:04):
And I like these sort of interactions,
because I've done a lot ofinterviews with, you know, at
least recently regarding thiswith different types of media,
and, you know, sometimes the,they only have two minutes, you
know, and they rapid fire and,and this is much more relaxed
and enjoyable, we can actuallyhave conversation. Soit gives me
(38:25):
more time to go into teachermode and, and explain things a
little bit better to, you know,with our listeners and stuff out
there that, you know,
Caroline Amos (38:35):
You really spell it for two people. I mean, we're
both actors. I hate to admitthis, but I got terrible grades
and science.
Raymond McAnally (38:41):
I've never ever been hired to play a
scientist yet. So I don't thinkI'd be good at it.
Caroline Amos (38:48):
But it's really great to have you. It's like
explaining things in layman'sterms. I feel like I know. I
feel like I've learned somethingtoday. And hopefully whoever's
listening to this will have alot to learn as well.
Dr Keith Gagnon (38:59):
Yeah. So yeah, Everybody stay safe. Get the
vaccine if you can. Keep wearingyour mask for now. Stay six feet
apart. Hang in there, it's gonnaget better. And see how things
go.
Caroline Raymond (39:23):
Hey, this is Caroline. Raymond, we wanted to
say thank you for listening tothis episode and let you know
that there will be more everyweek from now until we get
fatigued by it. We're buildingout this podcast as we go. So
stay tuned for improvements onour website, our graphics, video
clips and just everything else.
The time was now to tell ourstories so we're learning as we
go. We really do appreciate yourinterest in support. We truly
(39:45):
hope that the personal storiesthat come out in each episode
can help build a betterunderstanding of COVID-19 how it
spreads and how it affects us.
If you have a story or aquestion that you'd like us to
address in an episode. pleaseemail us at
fatiguepodcast@gmail.com that'sfat igu ed podcast@gmail.com
(40:07):
Thanks for listening bye
Hi, I'm Caroline Amos. And I'm Raymond
(00:02):
McAnally. And we are FATIGUED(laughter).
Caroline Amos (00:13):
All right, Dr.
Keith gagnant. Tell us a littlebit about yourself.
Dr Keith Gagnon (00:19):
Well, I'm an associate professor here at
Southern Illinois, IllinoisUniversity in Carbondale. So
SEIU been here for six and ahalf years, I grew up in New
England, went to college and didmy PhD in North Carolina, did
some postdoctoral work inDallas, Texas area, I have three
(00:39):
kids and beautiful wife. I playbasketball when the gym is open,
and there's not a pandemic goingon. I like to work on cars, with
my hands around the house.
And I love my job becausescience is a nice a merger or
marriage of working with yourhands, but also getting to think
critically.
Caroline Amos (00:59):
Oh, I love that.
That's awesome. Yeah, man, manyfacets then I guess. So.
Congratulation.
Raymond McAnally (01:07):
And for our audience, what is what is your
area of expertise?
Dr Keith Gagnon (01:11):
So I traditionally trained as an RNA
biochemist. So RNA is the cousinmolecule to DNA doesn't quite
get as much fanfare, but itperforms many important roles in
the cell and in biology. Sothat's what I learned when I was
an undergraduate graduatestudent was how to work with RNA
and the many roles it plays inbiology. So that's my background
(01:36):
sort of RNA biology or on RNAbiochemistry. And the two major
areas we've worked on the most.
Before we started working onSARS, COBie two was a disease
called Lou Gehrig's disease.
This is also known as a myatrophic lateral sclerosis, or
ALS, was the devastatingneurological disorder. And so we
(01:56):
try to understand more aboutwhat's going on at the molecular
cellular level, and are thereways we could come up with
strategies to treat it. And theother area is, like gene therapy
development, there is a type ofenzyme called CRISPR. And CRISPR
is being it's a bacterial enzymethat's being co opted or
developed as a gene therapytool. very promising, but it's
(02:20):
got some it's got some problems,it's not quite perfect, it
didn't evolve to work. Andpeople evolved to work in
bacteria to fight against, youknow, bacteria phages. So it
needs a little bit ofengineering. And so that's kind
of what my lab does is we dosome of the engineering of this
enzyme, so it can be hopefullysuitable for human gene therapy
or human use. That's very cool.
And of course, we startedsequencing, SARS, COVID, two
(02:42):
viruses this year, so yeah,well, so that's the whole reason
we wanted to talk to you today.
As you can read in the news, Dr.
Keith, or Dr. G, as I like tocall him now has part of his lab
was important in discovering thenew mutation of COVID-19.
Caroline Amos (03:07):
Tell us a little bit more about what the process
of discovering a mutation of avirus looks like?
Dr Keith Gagnon (03:15):
Well, it starts with a lot of painstaking
sequencing, a lot of calledmolecular biology, you have to
get access to some of thesesamples, that took a long time
to come up with an agreementwith the state where we could
access clinical samples. There'ssome important equipment and
expertise. So we had to set allthat up. And then we were able
(03:38):
to eventually start sequencingthe genome of the virus. And for
those who are not reallyhardcore scientists, what we're
talking about is, the genome isall those sort of letters that
make up the the book of what thevirus is, you know, think of it
as a book with 30,000 letters init that make up words and
(03:59):
sentences and chapters and allthat. And so that's sort of like
what a genome is, it has all theinformation to reproduce another
organism or, in this case,another virus. And so what we do
is we look at every single oneof those letters to see if any
of them have changed. Now, wedon't do this manually. We have
computers, which we've trainedto screen through and scan
(04:20):
through this very, very quickly.
And we look for changes in thatsequence. And we compare this
these sequences of differentviruses all against each other,
essentially See, how much doesit change from maybe the first
Coronavirus in China? versus howmuch does it change from one
that we sequenced last month,you know, in Illinois, so we can
(04:41):
track all this. And by doingthis, we can determine if we're
getting any significant changesor important changes, maybe a
recurring change that we seeover and over again and multiple
viruses, and then that sort ofconstitutes a new family or a
new variant of the virus. That'skind of the process that we go
through. And a lot of people areworking in this area around the
(05:04):
world looking for these variantsand trying to keep our finger on
the pulse, if you will, to makesure we don't get caught with
our by surprise.
Caroline Amos (05:14):
Yeah.
Raymond McAnally (05:17):
What, um, when you say viruses, you're Are you
referring to the theseindividual samples that you're
able to obtain?
Dr Keith Gagnon (05:26):
That's correct.
So these are samples that werebasically mouth swabs are called
nasal pharyngeal swabs, the NPswabs from patients. And so
that's what's collected duringthe time of testing. And then,
if the test comes up positive,those samples typically get
archived in the freezer. Andthen my lab later gets access to
those and we can sequence thosepositive samples to see what
(05:48):
kind of variant that virus was.
What kind of mutations it hadits genome.
Caroline Amos (05:55):
Wow,
Unknown (05:56):
are you?
Raymond McAnally (05:56):
Are you limited to the samples that you
have physical access to? Or arethere labs like you're sharing
the genome information?
Dr Keith Gagnon (06:06):
That's a great question. So, so the types of
some analyses are limited towhat we have on hand that we
generate, but but the vastmajority of the analyses we do
can be done with lots of data byother groups. And so my lab,
we've only sequenced about maybeclose to 600 genomes so far. But
(06:26):
there is about 450,000 that havebeen sequenced globally around
the world. And these are allactually, I think there's more
than that. But they're alldeposited in these databases,
where then researchers like me,we can go, we can pull those
out. And so this is how we sortof identified this one variant
that my lab recently sort ofreported, is, we were looking at
(06:49):
our Illinois data, our localdata, and we saw some trends.
And then we just simply want toask, Is this trend true in the
United States? How does thistrend look around the world? And
so we were able to pull thatdata and analyze that at larger
scale? And so your answer isyes, the answer to your question
is yes, there's a lot of peoplewe're all sharing our data. And
(07:10):
that's, that's sort of key tocatching these new variants.
So...
Raymond McAnally (07:13):
Yeah, I can only imagine is it? Is it a
situation where that has thatsharing has improved? We've
heard, you know, you hear in thenews, or, to be honest, I
imagine, we think we know itfrom movies and TV shows more
than anything that that labs,kind of, for reasons for funding
(07:35):
and, and research and kind oftheir own r&d. Stay a little bit
siloed. Is that is that true ofthe real science world? Or is
this something that new that'shappening, that that all this
information is being sharedglobally?
Dr Keith Gagnon (07:52):
So, so yes, and no to that question, let me pick
this apart a little bit, becauseI know I asked about three
questions. I mean, they're allvery related, it's a great
question, to see if we canunpack a little bit. So
traditionally, yes, academicscientists were a little bit
protective of our of our data,you know, we put a lot of blood
sweat and tears into collectingthis data, trying to make sense
(08:15):
of it. And then, you know, wehave to publish and disseminate
that. And unfortunately, forbetter or worse, our careers,
whether we get funding or we cancertain things depends on what
we publish and, and whatjournals we publish in. And so
sort of naturally, people are alittle protective. Buta couple
of these databases in particularone called, it's pronounced, he
(08:37):
said, er g said, it's sort ofthe one of the big major
databases out there for puttingthese genomes into. And they
have, then they were aroundbefore the pandemic, and but
they, they've been heavily usedduring the pandemic. And they
have tried to go out of the wayto sort of share openly, but at
the same time, protect therights, if you will, scientists
(09:00):
with their data. So when wepulled all that data from the
gisa, database, we, we have tomake sure we cite the people who
contributed that data. And so wemade sure we had, you know, gave
them credit for all for sharingtheir data with us. And the same
goes for my lab, we, we submitit on there, and it's shared
with others. So there is alittle bit of a protectiveness
(09:23):
naturally, but during thepandemic, people have let our
we've let our guard down alittle bit for the better good
of you know, the world reallywell. That's good. Yeah. And the
data sharing is much is gettingbetter and better. And it
doesn't go as fast as it could.
And there's still some groups orplaces around the world that a
little hesitant to share withshare their data. But I think in
(09:45):
general, it's very open and it'sgetting better. And one of the
few silver linings of thepandemic is just how do we come
together to tackle these bigproblems? data sharing,
important part.
Caroline Amos (09:58):
Yeah, that's really encouraging to hear. Nice
to see everybody work together.
And yeah, for a change. Yeah,that's great. I'm really curious
to know, in this new mutationthat you've discovered, the one
that was, I was doing someresearch before we talk to you
today. And it was discovered,the earliest known case of it
(10:22):
was in Houston, Texas?
Dr Keith Gagnon (10:27):
Yeah, that's correct. Using the global
database, where we coulddownload sequences from
everybody else, we look for theearliest case, the earliest
genome sequence that had the keykey signature, or Hallmark
Hallmark mutations of thisvariant, and we traced it back
to may 20, in the Houston, Texasarea.
Caroline Amos (10:48):
Now, what makes this mutation different than
what we have been experiencingin the United States as a whole
over this time?
Dr Keith Gagnon (10:57):
So this variant that we found, we call it 20cUS.
Raymond McAnally (11:01):
Is there a media term for it that people
would be more familiar with?
Dr Keith Gagnon (11:07):
No 20cUS - it's not like the quote unquote, UK
variant. Brazil is a variantthat was first observed in South
Africa. So it doesn't have oneof those names. There are some
different naming schemes thatare used, for example, the
variant that was first found inthe UK, they call it some people
just call it colloquially the UKvariant. It's also known as B
(11:31):
117.
Raymond McAnally (11:32):
That sounds like a Star Wars character.
Dr Keith Gagnon (11:36):
Yep. Yep. I think it's, there's another one
it's called 20I or 501YV1. Sothere's there and they're trying
to work out the the namingsystem so that it's more we have
a single one to use. But yeah,so ours is B12, is one naming
system for us also often called20G, because it matches really
(11:57):
closely with a with one that'scalled 20G.
Caroline Amos (12:00):
20G is like a really fun name. I like that.
Dr Keith Gagnon (12:02):
Yeah. So we can call it 20 G, we can go with
that. You got 20 G's.
Raymond McAnally (12:09):
Yeah. 20G's albums gonna drop next fall.
Dr Keith Gagnon (12:12):
Yeah!
Caroline Amos (12:13):
So tell us more about 20 G.
Dr Keith Gagnon (12:15):
Yeah, so. it's actually picked up a couple
mutations really, either reallyrapidly or almost at the same
time. And so that set ofmutations is what defines is not
a single one, but a group. Andso same with the variant that
first was found in the UK, ithas a set of mutations which
distinguish it clearly from allthe other virus variants out
(12:37):
there. And so this set ofmutations for the 20cus or the
20g variant, it looks a littlebit vanilla, or mundane on the
surface, it doesn't have themutations that some of the other
variants in the world have. Andso we've actually been kind of,
I don't want to say brushed off,but a little bit, you know, not
taken very seriously, because itdoesn't have those telltale
(13:00):
mutations that everybody'slooking for, which is number
one, why it got missed in thefirst place, and it grew. In the
US, it's now the the probablythe most dominant one, it's
right around between 40 to 50%of all the variants are derived
from this particular 20 G. Andso it basically took over our
backyard without us even knowingOh, and of course, it doesn't
(13:23):
have those telltale mutations.
So everybody's like, well, itcan't be that big of a deal. Or
is it is the point I'm trying tomake? And I'm saying how did
this thing, gain prevalence andgain dominance in the US with
all the other variants floatingaround, especially during a
massive third pandemic wave? Andthere's so many other variants
that that could have taken over.
(13:44):
But this one did. So I'm arguingit's not entirely by chance.
This is not by accident, I dobelieve and we're working on
experiments to sort ofdemonstrate that, that this
variant has some unique featuresto it. So the good news is,
though, when you look at and youdo some correlations and you
say, okay, our case, our deathsper cases, they call case
(14:07):
fatality rate, has that changeddramatically? In the US? No, it
hasn't. It's actually gone down.
So and there's a lot of factorsthat feed into that. The other
end we looked at is what abouthospitalization rates? Have
those gone up per patients withCOVID-19? And no, they're both
that sort of a little, a littlewavy pattern to them, but that
hasn't really changed. So wedon't think this variants
(14:31):
necessarily more dangerous, butit's it may be it may be more
transmissible it, that means itmay spread a little faster. We
may have some other advantagesthat other viruses other
variants don't have. So we'regoing to watch that carefully.
The last thing I'll say aboutits mutations is that it's now
starting to pick up and acquiresome of the mutations that the
(14:53):
UK variant, the South Africanvariant, the Brazilian variant
have and these are the ones whocall variants of concern that
everybody's worried about,because those particular
mutations have been up notproven, but highly linked to
evading the immune system,reducing the effectiveness of
the vaccine. And the point Iwant to make is that this, this
(15:14):
variant that's in the US thatgained dominance without any of
those mutations, is nowacquiring those mutations. And
so my question is, what doesthat leave us with? What What
happened? about what's in ourwhat's in our own backyard?
Yeah. And the answer is, Yes, weshould. And that's kind of where
I feel like the role my lab isplaying is everybody's looking
for the other variants, as theyshould be. What I'm more
(15:38):
concerned with what's alreadyhere, and what we have to deal
with, if we're not watchingcarefully. So sorry, I talked a
lot. But...
Caroline Amos (15:46):
No, no, this is the reason we wanted to bring
you on this is this stuff thatwe're really interested to learn
a lot more about.
Raymond McAnally (15:53):
I would imagine, because it has taken
over so much - that that itsability to do so is kind of your
most concern, right?
Dr Keith Gagnon (16:07):
Yeah. How did it come out of that game? And
again, we're hoping we're allhoping it was just by accident.
Maybe it was by chance, maybegot lucky. But my my feeling is
there's something a little extrato it. That can't be completely
complained. Sorry, explained bychance. And so then, of course,
now you add on top of it, theseother mutations that we're
(16:28):
worried about, again, where doesthat leave us? Does that mean,
we have something even moreworrisome. That's homegrown, if
you will...
Raymond McAnally (16:35):
And it is uniquely American?
Dr Keith Gagnon (16:38):
Absolutely.
It's you born and raised in theUS.
Raymond McAnally (16:42):
So it exhibits a lot of freedom. It exhibits a
lot of like,
Dr Keith Gagnon (16:48):
it wants its guns rights. Yes. (laughing)
Raymond McAnally (16:53):
It's strong individualism. (laughing)
Caroline Amos (16:56):
Oh, my God.
(laughing) Now, when you talkabout mutations, and you talk
about the longevity of thisvirus, do you have any
predictions about where youthink this mutation might end
up?
Dr Keith Gagnon (17:14):
Yeah, so I mean, we can just speculate a
little bit. By the way, allbefore I jump into this, I'll
add that a lot of the stuff saidabout the different variants,
especially the variance ofconcern, a lot of it is
speculation, and even thoughthere's some science behind it,
it's really hard to prove someof the things like the media,
everybody wants us to prove thatit's more transmissible or prove
(17:35):
that it's more dangerous. It'sreally hard to do that. From a
scientific standpoint, all wecan do is look at this data set.
Look at that one, does it? Isthere some correlation or
connection, and it's just hardto do that. So keep that in
mind, I'll speculate a littlebit of what I think the future
might hold for us, I can imaginethat it's going to mutate, it's
(17:55):
continuing to grow. And it's ait's an ongoing, ongoing, and
it's a cumulative thing too,because it accumulates those
acquiring noon, noon, moremorning mutations. So um, a
couple of ways we could go here,let's talk about the 20 g
variant 20 cus variant, what'sthat going to do? Well, it's
(18:18):
currently the most prevalent anddominant form in the US. And it
is continuing to rise in somestates and some other states,
it's kind of plateaued, maybeeven going down. Looks like it's
going down a little bit inCalifornia. Again, it's hard to
tell because you need two orthree months of data to really
see which way it's going, youknow, it might drop a little bit
(18:39):
one month go back up, but likeit's going down in some places
up, but overall, it's continuingto rise. So I think it's going
to continue to be the dominantvariant. I've heard the CDC say
that the variant that was fromthe UK is probably going to take
over in the US by March, Idisagree, wholeheartedly, 100%,
(19:00):
that is not going to be thecase. It has to first battle
against if you will oroutcompete the entrenched,
incumbent variant that's alreadyhere. And the competition it had
in the UK is not the samecompetition it has here. About
the time of its introduction,we're starting to see now the
introduction of the variant thatwas first seen in Brazil, and
(19:22):
the one that was first seen inSouth Africa. So we're getting
some really different dynamicshere in the US. And on top of
that, as I mentioned, now, this20 G is also starting to
accumulate some of thosemutations that we see that are
the most concerning from theother variants, other
international variants. So Ithink it's going to be a bit
more of a complex interplay. Theother thing is, it's hard to say
(19:43):
if it's a if it's like acompetition really between
viruses, you know, no one persongets infected by two different
viruses or variants at the sametime or a very, very rare event,
right? So it's more likepopulation based competition,
which is the most fit virus thatcan keep going. So um, that's
what I think in the short term,I think the 20cus is going to
(20:06):
continue to persist, I thinkit's going to pick up and
acquire a couple new mutationsthat are going to accumulate.
And it's going to allow it tosort of compete with these
international ones. And I do youthink it's going to go down over
time, though, because there's somany new things that are gonna
pop up. And what we're dealingwith is some really uncharted
territory where the virus isgoing from almost a completely
(20:29):
naive population, like basicallyno one in the population before
the pandemic could ever reallyhad this virus. So it's just
free to, to rampage through thepopulation, in fact, sort of
freely, if you will, withouthaving to be forced to mutate,
and change in order to survive.
But now what we're seeing ismore and more people, we're
getting closer and closer,slowly to that herd immunity,
(20:50):
more people are gettingvaccinated. And so for this
virus to be persistent, and justsort of continue its lineage, if
you will, it has to mutate andit has to, or it has it the
mutations that help it have tohave to persist. And it has to
be able to reinfect people evadethe immune system a little bit
those sort of features. And so,we don't know, but all this is
(21:14):
going to start happening. Andit's a little bit of a foot race
between can we vaccinate quickenough?
Raymond McAnally (21:21):
Yeah, yeah.
Yeah, for lack of a betterGlossary of scientific terms. Is
it the nature of a virus tomutate for those reasons? It is
it is trying to do what virusesdo and is trying to stay alive,
I guess, in some way, shape, orform?
Dr Keith Gagnon (21:41):
Yes, you can think of it, you know, we often
don't think of viruses as beingliving but they possess many
features of a living organism.
And so mutation is sort of builtinto the virus, it has a low
level of mutation that ithappily allows to happen,
because that gives it thatlittle edge when I mean, when
everything's working great, andit doesn't have to mutate. It
doesn't have to evade immunesystem. Why would it change, so
(22:04):
it wants to maintain what worksreally well, but it has a small,
low level of mutation that itallows and to put in
perspective, the Coronavirus,you tastes a little slower than
the seasonal flu, you know, theseasonal flu that we get
influenza every year. But it'sstill mutates fast enough, and
especially with you know, thehuge number of cases worldwide,
(22:25):
to pick up enough mutations towhere we get these rare events
where you get a couple ofmutations that really give it a
jump in fitness, and ability tokeep going. And so that's kind
of so that's another part of theprediction, I would say is we're
going to continue to see novelvariants pop up all over the
world, especially in isolatedareas, because international
(22:45):
travels pretty restricted, whichexplains why this 20 g variant
really hasn't spread too muchbeyond the us because we're not
really allowing that. Butthere's no state there's no
state border controls in the US.
So people freely runintermingle. And it spreads very
quickly in the US. So weshouldn't be surprised to see
these pop up. But we we gotta beon the lookout for new ones that
(23:09):
could be problematic. If we'requick enough, we can catch it
and do contact tracing andtraditional epidemiology and
sort of kill that transmissionline. If you know what I mean.
Caroline Amos (23:21):
I'm really curious to know, how will the
vaccine be effective againstthis new this new mutation?
Dr Keith Gagnon (23:29):
Yeah, so it's so far it looks like the
vaccines are effective enoughagainst some of these new
mutations. I guess the concernis can the virus mutate enough
to get fully around the vaccine?
If it can, that's okay. Youknow, we'll make new vaccines
and give booster shots. And whoknows, maybe it'll become like a
seasonal thing. And I mean, youknow, where every year just like
(23:53):
the flu where they put out a newvaccine to try and keep up with
these mutations that Yeah, theyhave to do that with the
Coronavirus. I guess that's yetto be seen.
Raymond McAnally (24:04):
Yeah, I was wondering about that. myself.
I'm glad to hear you bring thatup that it. So it is comparable
to what we go through withdifferent flu shots and
different strains of flu everyyear?
Dr Keith Gagnon (24:15):
Yeah, hopefully, because it mutates a
lot slower than the normal flu,the seasonal flu. We won't need,
you know, booster shots or newnew vaccines every year, it
might be every couple years. AndI guess the hope is that it will
die out. I have a feeling thoughit will stay at a low level of
persistence in the populationcalled this sort of becoming
(24:39):
endemic in the population. Soit's sort of always there at a
low level. So I think we couldprobably expect that to be the
case. I do think though with thevaccines really rolling out and
we've really got a lot ofmomentum with the vaccines. I do
think that by the time thesummer comes, as was predicted
early on that the vaccines willallow us to return most of the
(24:59):
normal life, I really thinkthat's gonna be the case. But
there could be a couple bumps inthe road with some new variants
as we go. But I don't think Ithink ultimately we, you know,
the vaccinations should shouldhelp us tremendously.
Raymond McAnally (25:13):
I cannot tell you how much hope just ran
through my body just becausesomeone with your with your
level of expertise andunderstanding of this could
could say that that's what theyfeel. And that's - It was just
my, I just had a visceralreaction to that. So thank you.
Yeah. Well, because right now,it's hard to know.
Dr Keith Gagnon (25:38):
Exactly. I mean, I'm not the only one who
has the same feeling. I thinkyou have people who are more
optimistic and people who aremore pessimistic. I tend to be a
more optimistic person. But I'malso kind of a realist, but I
think I'm optimistic. But Ithink the reality is matching
that is the vaccine some so forexample, the vaccines, a couple
(25:59):
of them have been tested againstthe variants that are of the
most concern right now, which isthe one that was first found in
South Africa and Brazil. Ithink, I think the Brazil ones
been testing test, I can'trecall. And then the one that
was found in the UK, so and itappears that they work well
enough, and they seem to almostcompletely 100% block death,
(26:19):
which is a really importantthing. And then severe cases
that require hospitalization areway, way lower. And so that's
the key. I mean, if we canconvert this to something where
Yeah, you get a nasty cold, butyou don't feel the hospital, you
don't worry about dying. If wecan at least get there. That's
That's good. I think we candefinitely get there by the, by
the summertime or the end of thesummer.
Caroline Amos (26:41):
Oh, that's so great.
Raymond McAnally (26:42):
Is that typically, on a scientific
level? The best case scenariofor any pandemic type virus, for
example? How do you know, in inyour education and study, what
happened to the influenza virusthat hit in, you know, the
(27:06):
1918/1919 timeframe?
Dr Keith Gagnon (27:10):
Yeah, I mean, I'm certainly not the authority
on this. But I mean, I've readsome things as a leisure
reading, like sort of you guys,you know,
Caroline Amos (27:18):
leisure reading, I love that!
Dr Keith Gagnon (27:20):
leisure reading, but it was a
scientific, scientific, youknow, angled paper article I
read. And the the, the argumentwas that the 1918 pandemic had
multiple waves. And then it cameback the next year, and then the
year after, but each year it wasweakened and then largely
disappeared, and sort of diedout because it was really just
(27:44):
too virulent. It just was, itjust killed people too, too
much. But we had but but then Ialso saw that same article, the
argument that some of the annualor seasonal influenza a has the
remnants of that virus. And soOkay, yeah, and so the influenza
virus can recombine with otherinfluenza viruses a lot more
Raymond McAnally (28:05):
So they don't really - in our brains, you
readily. And I think it's alittle more common for two
influenza viruses to be in thesame person. So pieces of it
have somehow persisted for 100years. But but the the major one
that drove it apparently diedout. And so you may also know,
though, on top of that,intriguingly is that the common
(28:28):
cold is a lot of common colds orcoronaviruses. I'm not an expert
in this area, too. So it's kindof tempting to think while some
fragment or remnants of thissource code could persist for a
long time, either it justevolves to become highly
transmissible, but very nontoxic or non virulent to the
(28:50):
host. So it survives better orsort of at some point recombines
with another common Coronavirus,and you know, so
know, they they can beeradicated but it sounds like
they they lessen and degree andare somehow, but somehow do
(29:13):
stick around and in a remnantform.
Caroline Amos (29:15):
It was interesting to think of it as
like, you know, the Spanish Fluhas had grandbabies. And the
grandbabies are colds that weexperience every day and someday
Coronavirus is going to havegrandbabies, too.
Dr Keith Gagnon (29:26):
That may be the case. And you know, it's
important to remember too thatCoronavirus is a very common in
nature and and lots of animalsand what we've had here what
what appears to be is the jumpfrom bats to humans, there was
enough mutations and it seems tobe the case. There could have
been some intermediate inbetween but lots of Coronavirus
(29:47):
is out there in the world. Mostof them don't infect us, I don't
do so very efficiently. So, atleast if this ever happens
again, maybe it will be a lotmore prepared.
Caroline Amos (29:59):
Let's hope! How does it feel to be the bearer of
such trepidatious news?
trepidations might not be theright word, but it looks like
came to mind.
Dr Keith Gagnon (30:11):
Yeah.
Caroline Amos (30:11):
What does it feel like to be the bearer of bad
news?
Dr Keith Gagnon (30:13):
Well, the question is, is it good news or
bad news? Right? Because a wewere very hesitant about this.
When we first made theobservation of this variant. It
was kind of, well, it's beenhere for a long time. So maybe
it's not a big deal. Butnobody's ever said anything
about we can find anything inthe literature even on even on
on Google nothing about thisvariant or and these mutations
(30:34):
we were finding, and we thought,well, we need to say something.
But, you know, so it was like,this is important, but how
important and we've gotten thesame feeling from the scientific
community. Some people like, Oh,this is fantastic, I'm glad you
characterized it, you know, thiscreates the backdrop for any new
variants that would emerge inthe US. So it's important to
study this, this variant. Andother people. Well, it's not the
(30:57):
UK variants, not the variantthat we saw in South Africa
doesn't have those mutations. Soit's not must not be important.
So I get both of that, and it'skind of have mixed feelings. And
I don't know, that's bad news,because it's been here for
months. And we don't have adramatically higher death rate,
or hospitalization, or, youknow, it sort of came on
(31:19):
quietly, you know, didn't make abig racket. And so even even
possible that it might be lessvirulent, or as transmissible
but not any more dangerous thanthe original one. So who knows,
maybe after we do enough studiesand characterize us better,
maybe it turns out that it's,it's, it's, it's a good variant
(31:40):
that is very transmissible, butyeah, dangerous. Who knows?
Caroline Amos (31:43):
Yeah.
Raymond McAnally (31:44):
That's interesting to think about,
that. That mutation can alsomean that it mutates down and
weakens or it it, it gets easierto combat in some way.
Unknown (31:56):
Or maybe maybe I found the good variant that we
shouldn't be concerned with.
Caroline Amos (32:01):
Yeah. I'm really, I'm more anecdotally, what are
you really looking forward todoing once the world returns to
some semblance of normalcy? Whatdo you miss?
Dr Keith Gagnon (32:12):
Gosh, you know, I've got three kids, and like,
they can't go see their friends.
I'll just be happy when they cango to school. My wife is mostly
staying home with the kids and,you know, helps mediate,
they're, they're learning,they're learning at a distance.
And it's just hard on her, Ithink she has a much harder job
than I do. So I'm just lookingforward to normal life for my
(32:34):
kids. And then, like I said, I'dlove to go to the gym and play
basketball again, that would bewithout ask. Yeah, you know, we
haven't taken any familyvacations. I've been working
harder since the pandemic thanany other time because we're
trying to maintain our normalprojects, but now take on this
(32:55):
new COVID-19 project. So I thinkI think it would be nice to just
be able to take some vacations,just do the normal go to the
restaurant, you know, I justlooking forward to the things
really nothing more.
Raymond McAnally (33:08):
Yeah, it's it's amazing how just those
little things that the feelingof being able to spontaneously
go somewhere, grab something or,you know, whether it's a
restaurant or the post office,or whatnot. We were just talking
my wife and I last night aboutthe fact that we're, we're
(33:28):
coming up on what will be hersecond birthday in the pandemic.
And we're, we're both very, youknow, we we try to understand
the science of it, and we do ourpart. But she was like, Can we
please do something a little bitspecial for my birthday? It just
(33:51):
last time, you know, we had justbeen shut down. Everything was
closed. And, you know, we didsomething quiet at home. So
we're trying to figure out whatthat is. Because it's not like
things have improved enough(laughter).
Caroline Amos (34:07):
Can we it's gonna be like a walk down the street
today? That'd be so nice.
Dr Keith Gagnon (34:12):
Yeah, I've got I agree. We've got a two and a
half year old and she's trainednow she wants when we go on
public, she wears her mask. Ifher mask comes off. She freaks
out, like, what kind of worldare is my portrait growing up?
And you know, our masks arenormal. But yeah. And in fact,
(34:33):
earlier today, I'm sitting in myoffice working on my computer,
and I'm wearing my mask. And I'mlike, why am I wearing my mask?
That was like, when I left myoffice 20 minutes ago, and I
came I didn't take it off. It'slike, we're so trained now. I
never would have I mean, youknow, imagine when we first
started the pandemic, peoplewere so resistant to wearing
masks. Yeah, it's, it'scommonplace. Yeah, you just
(34:55):
accept it as normal life.
Caroline Amos (34:57):
Yeah, I fell asleep with mine on actually
Last night, yeah, I wentdownstairs to pick up a package
came back in, realized I wastired and fell asleep. And it
took like halfway through thenight for me to be like, what is
on my face? What is going on,which is also really gross,
because yeah, just breathe andmore of my own air for a long
time. We usually love to sort ofround out these interview
(35:21):
conversations with a morepositive note. And honestly,
frankly, this conversation was alot more hopeful and positive
than I was sort of expecting itto be. So thank you for that.
Yes. I'm curious to know what,what gives you hope right now?
Dr Keith Gagnon (35:37):
Well, um, I got, I think the vaccines are
huge. And unfortunately, nomatter what happens, the
pandemic will run its course,and you know, you can only
infect people so many times. Andeven if we had no intervention,
viruses are at some pointnaturally going to become less
virulent, because, you know, youcan't kill every host. So those
(36:01):
simple, simple, you know,biology, things I think, are, I
feel like, you know, eventually,you know, things will change,
just like in the 1918 pandemic,eventually, people's immune
systems adapted, or the viruscouldn't adapt further. But
realistically, the vaccine, Ithink, has been important to
help push things along. And Ithink it was a big deal at the
(36:22):
beginning of the pandemic, weput a lot of stress on it. And
I'm glad we did, because itallowed things to move quickly.
And I think it's living up toits promise, so to speak. So
that gives me hope. You know,and also what I've seen is a lot
of, at least in my laboratory,we've come together to solve
some hard problems. sequencingthe viruses genome was not a
(36:45):
simple task, it requiredeverybody in my lab to come in,
during the pandemic, and risksthemselves, you know, and put on
all the the PP you know, themasks and the gear. Yeah. And
there was a lot of unknownsearly in the pandemic. So we
didn't know how much of a riskwe were taking. And, but so I
got to see people come together.
And I think that's, that alwaysbrings a little bit of hope to
(37:07):
situations when we can bandtogether and solve problems. And
we see that in the world and inthe science world, and in
medicine, and hopefully, withgeneral everyday people were
very supportive of like, comingtogether and solving this.
Caroline Amos (37:20):
Yeah, gosh, that gives me so much hope. Thank
you. Yeah, yay, science, listento science, everybody listened
to it? Well, awesome. Thank you.
Thank you so much. I know thatyou don't know us at all, and
that we just reached out on awhim. And I know you've got the
busiest schedule in the world.
So we just appreciate the factthat you took a little bit of
(37:40):
your time to talk to us, itmeans so much.
Dr Keith Gagnon (37:42):
Well, no, I appreciate it. I feel like I
know, you guys know. So weshould keep in touch. And don't
forget to reach out and maybe ina couple weeks or a few months,
we'll have some updates, andwe'll probably be good to
update. You know, well, a lot oflike unknowns, we don't know
what the next couple months aregonna bring. So again,
Caroline Amos (38:00):
yeah, man,
Raymond McAnally (38:01):
We'd love that!
Caroline Amos (38:02):
We'll reach out for follow up soon.
Dr Keith Gagnon (38:04):
And I like these sort of interactions,
because I've done a lot ofinterviews with, you know, at
least recently regarding thiswith different types of media,
and, you know, sometimes the,they only have two minutes, you
know, and they rapid fire and,and this is much more relaxed
and enjoyable, we can actuallyhave conversation. Soit gives me
(38:25):
more time to go into teachermode and, and explain things a
little bit better to, you know,with our listeners and stuff out
there that, you know,
Caroline Amos (38:35):
You really spell it for two people. I mean, we're
both actors. I hate to admitthis, but I got terrible grades
and science.
Raymond McAnally (38:41):
I've never ever been hired to play a
scientist yet. So I don't thinkI'd be good at it.
Caroline Amos (38:48):
But it's really great to have you. It's like
explaining things in layman'sterms. I feel like I know. I
feel like I've learned somethingtoday. And hopefully whoever's
listening to this will have alot to learn as well.
Dr Keith Gagnon (38:59):
Yeah. So yeah, Everybody stay safe. Get the
vaccine if you can. Keep wearingyour mask for now. Stay six feet
apart. Hang in there, it's gonnaget better. And see how things
go.
Caroline Raymond (39:23):
Hey, this is Caroline. Raymond, we wanted to
say thank you for listening tothis episode and let you know
that there will be more everyweek from now until we get
fatigued by it. We're buildingout this podcast as we go. So
stay tuned for improvements onour website, our graphics, video
clips and just everything else.
The time was now to tell ourstories so we're learning as we
go. We really do appreciate yourinterest in support. We truly
(39:45):
hope that the personal storiesthat come out in each episode
can help build a betterunderstanding of COVID-19 how it
spreads and how it affects us.
If you have a story or aquestion that you'd like us to
address in an episode. pleaseemail us at
fatiguepodcast@gmail.com that'sfat igu ed podcast@gmail.com
(40:07):
Thanks for listening bye
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