0:00

Hi, I'm

0:00

Caroline Amos. And I'm Raymond

0:02

McAnally. And we are FATIGUED

0:02

(laughter).

0:13

All right, Dr.

0:13

Keith gagnant. Tell us a little

0:16

bit about yourself.

0:19

Well, I'm an

0:19

associate professor here at

0:21

Southern Illinois, Illinois

0:21

University in Carbondale. So

0:24

SEIU been here for six and a

0:24

half years, I grew up in New

0:29

England, went to college and did

0:29

my PhD in North Carolina, did

0:34

some postdoctoral work in

0:34

Dallas, Texas area, I have three

0:39

kids and beautiful wife. I play

0:39

basketball when the gym is open,

0:43

and there's not a pandemic going

0:43

on. I like to work on cars, with

0:48

my hands around the house. And I love my job because

0:51

science is a nice a merger or

0:56

marriage of working with your

0:56

hands, but also getting to think

0:59

critically.

0:59

Oh, I love that.

0:59

That's awesome. Yeah, man, many

1:02

facets then I guess. So.

1:02

Congratulation.

1:07

And for our

1:07

audience, what is what is your

1:09

area of expertise?

1:11

So I

1:11

traditionally trained as an RNA

1:14

biochemist. So RNA is the cousin

1:14

molecule to DNA doesn't quite

1:20

get as much fanfare, but it

1:20

performs many important roles in

1:24

the cell and in biology. So

1:24

that's what I learned when I was

1:28

an undergraduate graduate

1:28

student was how to work with RNA

1:31

and the many roles it plays in

1:31

biology. So that's my background

1:36

sort of RNA biology or on RNA

1:36

biochemistry. And the two major

1:40

areas we've worked on the most.

1:40

Before we started working on

1:44

SARS, COBie two was a disease

1:44

called Lou Gehrig's disease.

1:48

This is also known as a my

1:48

atrophic lateral sclerosis, or

1:52

ALS, was the devastating

1:52

neurological disorder. And so we

1:56

try to understand more about

1:56

what's going on at the molecular

1:59

cellular level, and are there

1:59

ways we could come up with

2:02

strategies to treat it. And the

2:02

other area is, like gene therapy

2:07

development, there is a type of

2:07

enzyme called CRISPR. And CRISPR

2:13

is being it's a bacterial enzyme

2:13

that's being co opted or

2:16

developed as a gene therapy

2:16

tool. very promising, but it's

2:20

got some it's got some problems,

2:20

it's not quite perfect, it

2:23

didn't evolve to work. And

2:23

people evolved to work in

2:25

bacteria to fight against, you

2:25

know, bacteria phages. So it

2:30

needs a little bit of engineering. And so that's kind of what my lab does is we do

2:32

some of the engineering of this

2:34

enzyme, so it can be hopefully

2:34

suitable for human gene therapy

2:38

or human use. That's very cool.

2:38

And of course, we started

2:42

sequencing, SARS, COVID, two

2:42

viruses this year, so yeah,

2:47

well, so that's the whole reason

2:47

we wanted to talk to you today.

2:51

As you can read in the news, Dr.

2:51

Keith, or Dr. G, as I like to

2:55

call him now has part of his lab

2:55

was important in discovering the

3:02

new mutation of COVID-19.

3:07

Tell us a little

3:07

bit more about what the process

3:09

of discovering a mutation of a

3:09

virus looks like?

3:15

Well, it starts

3:15

with a lot of painstaking

3:18

sequencing, a lot of called

3:18

molecular biology, you have to

3:23

get access to some of these

3:23

samples, that took a long time

3:26

to come up with an agreement

3:26

with the state where we could

3:29

access clinical samples. There's

3:29

some important equipment and

3:34

expertise. So we had to set all

3:34

that up. And then we were able

3:38

to eventually start sequencing

3:38

the genome of the virus. And for

3:44

those who are not really

3:44

hardcore scientists, what we're

3:47

talking about is, the genome is

3:47

all those sort of letters that

3:51

make up the the book of what the

3:51

virus is, you know, think of it

3:56

as a book with 30,000 letters in

3:56

it that make up words and

3:59

sentences and chapters and all

3:59

that. And so that's sort of like

4:04

what a genome is, it has all the

4:04

information to reproduce another

4:07

organism or, in this case,

4:07

another virus. And so what we do

4:11

is we look at every single one

4:11

of those letters to see if any

4:14

of them have changed. Now, we

4:14

don't do this manually. We have

4:18

computers, which we've trained

4:18

to screen through and scan

4:20

through this very, very quickly.

4:20

And we look for changes in that

4:25

sequence. And we compare this

4:25

these sequences of different

4:29

viruses all against each other,

4:29

essentially See, how much does

4:33

it change from maybe the first

4:33

Coronavirus in China? versus how

4:38

much does it change from one

4:38

that we sequenced last month,

4:41

you know, in Illinois, so we can

4:41

track all this. And by doing

4:45

this, we can determine if we're

4:45

getting any significant changes

4:48

or important changes, maybe a

4:48

recurring change that we see

4:52

over and over again and multiple

4:52

viruses, and then that sort of

4:55

constitutes a new family or a

4:55

new variant of the virus. That's

5:00

kind of the process that we go

5:00

through. And a lot of people are

5:04

working in this area around the

5:04

world looking for these variants

5:08

and trying to keep our finger on

5:08

the pulse, if you will, to make

5:11

sure we don't get caught with

5:11

our by surprise.

5:14

Yeah.

5:17

What, um, when

5:17

you say viruses, you're Are you

5:21

referring to the these

5:21

individual samples that you're

5:23

able to obtain?

5:26

That's correct.

5:26

So these are samples that were

5:28

basically mouth swabs are called

5:28

nasal pharyngeal swabs, the NP

5:32

swabs from patients. And so

5:32

that's what's collected during

5:36

the time of testing. And then,

5:36

if the test comes up positive,

5:41

those samples typically get

5:41

archived in the freezer. And

5:44

then my lab later gets access to

5:44

those and we can sequence those

5:48

positive samples to see what

5:48

kind of variant that virus was.

5:53

What kind of mutations it had

5:53

its genome.

5:55

Wow,

5:56

are you?

5:56

Are you

5:56

limited to the samples that you

5:59

have physical access to? Or are

5:59

there labs like you're sharing

6:03

the genome information?

6:06

That's a great

6:06

question. So, so the types of

6:10

some analyses are limited to

6:10

what we have on hand that we

6:13

generate, but but the vast

6:13

majority of the analyses we do

6:17

can be done with lots of data by

6:17

other groups. And so my lab,

6:21

we've only sequenced about maybe

6:21

close to 600 genomes so far. But

6:26

there is about 450,000 that have

6:26

been sequenced globally around

6:32

the world. And these are all

6:32

actually, I think there's more

6:34

than that. But they're all

6:34

deposited in these databases,

6:37

where then researchers like me,

6:37

we can go, we can pull those

6:40

out. And so this is how we sort

6:40

of identified this one variant

6:44

that my lab recently sort of

6:44

reported, is, we were looking at

6:49

our Illinois data, our local

6:49

data, and we saw some trends.

6:53

And then we just simply want to

6:53

ask, Is this trend true in the

6:56

United States? How does this

6:56

trend look around the world? And

7:01

so we were able to pull that

7:01

data and analyze that at larger

7:04

scale? And so your answer is

7:04

yes, the answer to your question

7:07

is yes, there's a lot of people

7:07

we're all sharing our data. And

7:10

that's, that's sort of key to

7:10

catching these new variants.

7:13

So...

7:13

Yeah, I can

7:13

only imagine is it? Is it a

7:16

situation where that has that

7:16

sharing has improved? We've

7:21

heard, you know, you hear in the

7:21

news, or, to be honest, I

7:25

imagine, we think we know it

7:25

from movies and TV shows more

7:29

than anything that that labs,

7:29

kind of, for reasons for funding

7:35

and, and research and kind of

7:35

their own r&d. Stay a little bit

7:40

siloed. Is that is that true of

7:40

the real science world? Or is

7:45

this something that new that's

7:45

happening, that that all this

7:49

information is being shared globally?

7:52

So, so yes, and

7:52

no to that question, let me pick

7:56

this apart a little bit, because

7:56

I know I asked about three

7:59

questions. I mean, they're all

7:59

very related, it's a great

8:02

question, to see if we can

8:02

unpack a little bit. So

8:07

traditionally, yes, academic

8:07

scientists were a little bit

8:09

protective of our of our data,

8:09

you know, we put a lot of blood

8:12

sweat and tears into collecting

8:12

this data, trying to make sense

8:15

of it. And then, you know, we

8:15

have to publish and disseminate

8:19

that. And unfortunately, for

8:19

better or worse, our careers,

8:22

whether we get funding or we can

8:22

certain things depends on what

8:26

we publish and, and what

8:26

journals we publish in. And so

8:29

sort of naturally, people are a

8:29

little protective. Buta couple

8:34

of these databases in particular

8:34

one called, it's pronounced, he

8:37

said, er g said, it's sort of

8:37

the one of the big major

8:41

databases out there for putting

8:41

these genomes into. And they

8:45

have, then they were around

8:45

before the pandemic, and but

8:49

they, they've been heavily used

8:49

during the pandemic. And they

8:52

have tried to go out of the way

8:52

to sort of share openly, but at

8:56

the same time, protect the

8:56

rights, if you will, scientists

9:00

with their data. So when we

9:00

pulled all that data from the

9:04

gisa, database, we, we have to

9:04

make sure we cite the people who

9:09

contributed that data. And so we

9:09

made sure we had, you know, gave

9:12

them credit for all for sharing

9:12

their data with us. And the same

9:16

goes for my lab, we, we submit

9:16

it on there, and it's shared

9:20

with others. So there is a

9:20

little bit of a protectiveness

9:23

naturally, but during the

9:23

pandemic, people have let our

9:26

we've let our guard down a

9:26

little bit for the better good

9:29

of you know, the world really

9:29

well. That's good. Yeah. And the

9:32

data sharing is much is getting

9:32

better and better. And it

9:37

doesn't go as fast as it could.

9:37

And there's still some groups or

9:40

places around the world that a

9:40

little hesitant to share with

9:45

share their data. But I think in

9:45

general, it's very open and it's

9:49

getting better. And one of the

9:49

few silver linings of the

9:52

pandemic is just how do we come

9:52

together to tackle these big

9:55

problems? data sharing,

9:55

important part.

9:58

Yeah, that's

9:58

really encouraging to hear. Nice

10:01

to see everybody work together.

10:01

And yeah, for a change. Yeah,

10:04

that's great. I'm really curious

10:04

to know, in this new mutation

10:14

that you've discovered, the one

10:14

that was, I was doing some

10:18

research before we talk to you

10:18

today. And it was discovered,

10:22

the earliest known case of it

10:22

was in Houston, Texas?

10:27

Yeah, that's

10:27

correct. Using the global

10:30

database, where we could

10:30

download sequences from

10:32

everybody else, we look for the

10:32

earliest case, the earliest

10:37

genome sequence that had the key

10:37

key signature, or Hallmark

10:41

Hallmark mutations of this

10:41

variant, and we traced it back

10:45

to may 20, in the Houston, Texas

10:45

area.

10:48

Now, what makes

10:48

this mutation different than

10:52

what we have been experiencing

10:52

in the United States as a whole

10:55

over this time?

10:57

So this variant

10:57

that we found, we call it 20cUS.

11:01

Is there a

11:01

media term for it that people

11:05

would be more familiar with?

11:07

No 20cUS - it's

11:07

not like the quote unquote, UK

11:10

variant. Brazil is a variant

11:10

that was first observed in South

11:16

Africa. So it doesn't have one

11:16

of those names. There are some

11:20

different naming schemes that

11:20

are used, for example, the

11:24

variant that was first found in

11:24

the UK, they call it some people

11:27

just call it colloquially the UK

11:27

variant. It's also known as B

11:31

117.

11:32

That sounds

11:32

like a Star Wars character.

11:36

Yep. Yep. I

11:36

think it's, there's another one

11:39

it's called 20I or 501YV1. So

11:39

there's there and they're trying

11:44

to work out the the naming

11:44

system so that it's more we have

11:47

a single one to use. But yeah,

11:47

so ours is B12, is one naming

11:53

system for us also often called

11:53

20G, because it matches really

11:57

closely with a with one that's

11:57

called 20G.

12:00

20G is like a

12:00

really fun name. I like that.

12:02

Yeah. So we can

12:02

call it 20 G, we can go with

12:04

that. You got 20 G's.

12:09

Yeah. 20G's

12:09

albums gonna drop next fall.

12:12

Yeah!

12:13

So tell us more about 20 G.

12:15

Yeah, so. it's

12:15

actually picked up a couple

12:18

mutations really, either really

12:18

rapidly or almost at the same

12:21

time. And so that set of

12:21

mutations is what defines is not

12:25

a single one, but a group. And

12:25

so same with the variant that

12:29

first was found in the UK, it

12:29

has a set of mutations which

12:33

distinguish it clearly from all

12:33

the other virus variants out

12:37

there. And so this set of

12:37

mutations for the 20cus or the

12:42

20g variant, it looks a little

12:42

bit vanilla, or mundane on the

12:46

surface, it doesn't have the

12:46

mutations that some of the other

12:49

variants in the world have. And

12:49

so we've actually been kind of,

12:52

I don't want to say brushed off,

12:52

but a little bit, you know, not

12:56

taken very seriously, because it

12:56

doesn't have those telltale

13:00

mutations that everybody's

13:00

looking for, which is number

13:04

one, why it got missed in the

13:04

first place, and it grew. In the

13:08

US, it's now the the probably

13:08

the most dominant one, it's

13:11

right around between 40 to 50%

13:11

of all the variants are derived

13:15

from this particular 20 G. And

13:15

so it basically took over our

13:20

backyard without us even knowing

13:20

Oh, and of course, it doesn't

13:23

have those telltale mutations.

13:23

So everybody's like, well, it

13:26

can't be that big of a deal. Or

13:26

is it is the point I'm trying to

13:30

make? And I'm saying how did

13:30

this thing, gain prevalence and

13:35

gain dominance in the US with

13:35

all the other variants floating

13:38

around, especially during a

13:38

massive third pandemic wave? And

13:41

there's so many other variants

13:41

that that could have taken over.

13:44

But this one did. So I'm arguing

13:44

it's not entirely by chance.

13:48

This is not by accident, I do

13:48

believe and we're working on

13:52

experiments to sort of

13:52

demonstrate that, that this

13:55

variant has some unique features

13:55

to it. So the good news is,

13:59

though, when you look at and you

13:59

do some correlations and you

14:02

say, okay, our case, our deaths

14:02

per cases, they call case

14:07

fatality rate, has that changed

14:07

dramatically? In the US? No, it

14:11

hasn't. It's actually gone down.

14:11

So and there's a lot of factors

14:16

that feed into that. The other

14:16

end we looked at is what about

14:19

hospitalization rates? Have

14:19

those gone up per patients with

14:22

COVID-19? And no, they're both

14:22

that sort of a little, a little

14:26

wavy pattern to them, but that

14:26

hasn't really changed. So we

14:31

don't think this variants

14:31

necessarily more dangerous, but

14:34

it's it may be it may be more

14:34

transmissible it, that means it

14:37

may spread a little faster. We

14:37

may have some other advantages

14:40

that other viruses other

14:40

variants don't have. So we're

14:45

going to watch that carefully.

14:45

The last thing I'll say about

14:48

its mutations is that it's now

14:48

starting to pick up and acquire

14:53

some of the mutations that the

14:53

UK variant, the South African

14:56

variant, the Brazilian variant

14:56

have and these are the ones who

14:59

call variants of concern that

14:59

everybody's worried about,

15:02

because those particular

15:02

mutations have been up not

15:06

proven, but highly linked to

15:06

evading the immune system,

15:11

reducing the effectiveness of

15:11

the vaccine. And the point I

15:14

want to make is that this, this

15:14

variant that's in the US that

15:18

gained dominance without any of

15:18

those mutations, is now

15:21

acquiring those mutations. And

15:21

so my question is, what does

15:25

that leave us with? What What

15:25

happened? about what's in our

15:28

what's in our own backyard?

15:28

Yeah. And the answer is, Yes, we

15:31

should. And that's kind of where

15:31

I feel like the role my lab is

15:34

playing is everybody's looking

15:34

for the other variants, as they

15:38

should be. What I'm more

15:38

concerned with what's already

15:40

here, and what we have to deal

15:40

with, if we're not watching

15:43

carefully. So sorry, I talked a

15:43

lot. But...

15:46

No, no, this is

15:46

the reason we wanted to bring

15:50

you on this is this stuff that

15:50

we're really interested to learn

15:52

a lot more about.

15:53

I would

15:53

imagine, because it has taken

15:56

over so much - that that its

15:56

ability to do so is kind of your

16:05

most concern, right?

16:07

Yeah. How did

16:07

it come out of that game? And

16:09

again, we're hoping we're all

16:09

hoping it was just by accident.

16:13

Maybe it was by chance, maybe

16:13

got lucky. But my my feeling is

16:17

there's something a little extra

16:17

to it. That can't be completely

16:20

complained. Sorry, explained by

16:20

chance. And so then, of course,

16:25

now you add on top of it, these

16:25

other mutations that we're

16:28

worried about, again, where does

16:28

that leave us? Does that mean,

16:30

we have something even more

16:30

worrisome. That's homegrown, if

16:35

you will...

16:35

And it is uniquely American?

16:38

Absolutely.

16:38

It's you born and raised in the

16:40

US.

16:42

So it exhibits

16:42

a lot of freedom. It exhibits a

16:45

lot of like,

16:48

it wants its

16:48

guns rights. Yes. (laughing)

16:53

It's strong individualism. (laughing)

16:56

Oh, my God.

16:56

(laughing) Now, when you talk

17:03

about mutations, and you talk

17:03

about the longevity of this

17:06

virus, do you have any

17:06

predictions about where you

17:09

think this mutation might end up?

17:14

Yeah, so I

17:14

mean, we can just speculate a

17:17

little bit. By the way, all

17:17

before I jump into this, I'll

17:21

add that a lot of the stuff said

17:21

about the different variants,

17:24

especially the variance of concern, a lot of it is speculation, and even though

17:26

there's some science behind it,

17:29

it's really hard to prove some

17:29

of the things like the media,

17:32

everybody wants us to prove that

17:32

it's more transmissible or prove

17:35

that it's more dangerous. It's

17:35

really hard to do that. From a

17:38

scientific standpoint, all we

17:38

can do is look at this data set.

17:41

Look at that one, does it? Is

17:41

there some correlation or

17:44

connection, and it's just hard

17:44

to do that. So keep that in

17:48

mind, I'll speculate a little

17:48

bit of what I think the future

17:51

might hold for us, I can imagine

17:51

that it's going to mutate, it's

17:55

continuing to grow. And it's a

17:55

it's an ongoing, ongoing, and

18:01

it's a cumulative thing too,

18:01

because it accumulates those

18:05

acquiring noon, noon, more

18:05

morning mutations. So um, a

18:11

couple of ways we could go here,

18:11

let's talk about the 20 g

18:14

variant 20 cus variant, what's

18:14

that going to do? Well, it's

18:18

currently the most prevalent and

18:18

dominant form in the US. And it

18:22

is continuing to rise in some

18:22

states and some other states,

18:26

it's kind of plateaued, maybe

18:26

even going down. Looks like it's

18:31

going down a little bit in

18:31

California. Again, it's hard to

18:34

tell because you need two or

18:34

three months of data to really

18:37

see which way it's going, you

18:37

know, it might drop a little bit

18:39

one month go back up, but like

18:39

it's going down in some places

18:42

up, but overall, it's continuing

18:42

to rise. So I think it's going

18:48

to continue to be the dominant

18:48

variant. I've heard the CDC say

18:52

that the variant that was from

18:52

the UK is probably going to take

18:56

over in the US by March, I

18:56

disagree, wholeheartedly, 100%,

19:00

that is not going to be the

19:00

case. It has to first battle

19:04

against if you will or

19:04

outcompete the entrenched,

19:08

incumbent variant that's already

19:08

here. And the competition it had

19:12

in the UK is not the same

19:12

competition it has here. About

19:17

the time of its introduction,

19:17

we're starting to see now the

19:19

introduction of the variant that

19:19

was first seen in Brazil, and

19:22

the one that was first seen in

19:22

South Africa. So we're getting

19:25

some really different dynamics

19:25

here in the US. And on top of

19:28

that, as I mentioned, now, this

19:28

20 G is also starting to

19:32

accumulate some of those

19:32

mutations that we see that are

19:35

the most concerning from the other variants, other international variants. So I

19:37

think it's going to be a bit

19:40

more of a complex interplay. The

19:40

other thing is, it's hard to say

19:43

if it's a if it's like a

19:43

competition really between

19:46

viruses, you know, no one person

19:46

gets infected by two different

19:52

viruses or variants at the same

19:52

time or a very, very rare event,

19:55

right? So it's more like

19:55

population based competition,

19:58

which is the most fit virus that

19:58

can keep going. So um, that's

20:03

what I think in the short term,

20:03

I think the 20cus is going to

20:06

continue to persist, I think

20:06

it's going to pick up and

20:09

acquire a couple new mutations

20:09

that are going to accumulate.

20:13

And it's going to allow it to

20:13

sort of compete with these

20:16

international ones. And I do you

20:16

think it's going to go down over

20:19

time, though, because there's so

20:19

many new things that are gonna

20:22

pop up. And what we're dealing

20:22

with is some really uncharted

20:25

territory where the virus is

20:25

going from almost a completely

20:29

naive population, like basically

20:29

no one in the population before

20:32

the pandemic could ever really

20:32

had this virus. So it's just

20:35

free to, to rampage through the

20:35

population, in fact, sort of

20:39

freely, if you will, without

20:39

having to be forced to mutate,

20:44

and change in order to survive.

20:44

But now what we're seeing is

20:48

more and more people, we're

20:48

getting closer and closer,

20:50

slowly to that herd immunity,

20:50

more people are getting

20:53

vaccinated. And so for this

20:53

virus to be persistent, and just

20:57

sort of continue its lineage, if

20:57

you will, it has to mutate and

21:01

it has to, or it has it the

21:01

mutations that help it have to

21:05

have to persist. And it has to

21:05

be able to reinfect people evade

21:10

the immune system a little bit

21:10

those sort of features. And so,

21:14

we don't know, but all this is

21:14

going to start happening. And

21:17

it's a little bit of a foot race

21:17

between can we vaccinate quick

21:19

enough?

21:21

Yeah, yeah.

21:21

Yeah, for lack of a better

21:26

Glossary of scientific terms. Is

21:26

it the nature of a virus to

21:31

mutate for those reasons? It is

21:31

it is trying to do what viruses

21:35

do and is trying to stay alive,

21:35

I guess, in some way, shape, or

21:40

form?

21:41

Yes, you can think of it, you know, we often don't think of viruses as being

21:43

living but they possess many

21:45

features of a living organism.

21:45

And so mutation is sort of built

21:50

into the virus, it has a low

21:50

level of mutation that it

21:53

happily allows to happen,

21:53

because that gives it that

21:57

little edge when I mean, when

21:57

everything's working great, and

22:00

it doesn't have to mutate. It

22:00

doesn't have to evade immune

22:04

system. Why would it change, so

22:04

it wants to maintain what works

22:07

really well, but it has a small,

22:07

low level of mutation that it

22:11

allows and to put in

22:11

perspective, the Coronavirus,

22:14

you tastes a little slower than

22:14

the seasonal flu, you know, the

22:19

seasonal flu that we get

22:19

influenza every year. But it's

22:22

still mutates fast enough, and

22:22

especially with you know, the

22:25

huge number of cases worldwide,

22:25

to pick up enough mutations to

22:30

where we get these rare events

22:30

where you get a couple of

22:32

mutations that really give it a

22:32

jump in fitness, and ability to

22:35

keep going. And so that's kind

22:35

of so that's another part of the

22:38

prediction, I would say is we're

22:38

going to continue to see novel

22:40

variants pop up all over the

22:40

world, especially in isolated

22:45

areas, because international

22:45

travels pretty restricted, which

22:48

explains why this 20 g variant

22:48

really hasn't spread too much

22:52

beyond the us because we're not

22:52

really allowing that. But

22:55

there's no state there's no

22:55

state border controls in the US.

22:58

So people freely run

22:58

intermingle. And it spreads very

23:01

quickly in the US. So we

23:01

shouldn't be surprised to see

23:05

these pop up. But we we gotta be

23:05

on the lookout for new ones that

23:09

could be problematic. If we're

23:09

quick enough, we can catch it

23:13

and do contact tracing and

23:13

traditional epidemiology and

23:15

sort of kill that transmission

23:15

line. If you know what I mean.

23:21

I'm really

23:21

curious to know, how will the

23:24

vaccine be effective against

23:24

this new this new mutation?

23:29

Yeah, so it's

23:29

so far it looks like the

23:31

vaccines are effective enough

23:31

against some of these new

23:36

mutations. I guess the concern

23:36

is can the virus mutate enough

23:40

to get fully around the vaccine?

23:40

If it can, that's okay. You

23:44

know, we'll make new vaccines

23:44

and give booster shots. And who

23:49

knows, maybe it'll become like a

23:49

seasonal thing. And I mean, you

23:53

know, where every year just like

23:53

the flu where they put out a new

23:56

vaccine to try and keep up with

23:56

these mutations that Yeah, they

23:59

have to do that with the

23:59

Coronavirus. I guess that's yet

24:03

to be seen.

24:04

Yeah, I was

24:04

wondering about that. myself.

24:06

I'm glad to hear you bring that

24:06

up that it. So it is comparable

24:10

to what we go through with

24:10

different flu shots and

24:13

different strains of flu every year?

24:15

Yeah,

24:15

hopefully, because it mutates a

24:18

lot slower than the normal flu,

24:18

the seasonal flu. We won't need,

24:23

you know, booster shots or new

24:23

new vaccines every year, it

24:27

might be every couple years. And

24:27

I guess the hope is that it will

24:32

die out. I have a feeling though

24:32

it will stay at a low level of

24:35

persistence in the population

24:35

called this sort of becoming

24:39

endemic in the population. So

24:39

it's sort of always there at a

24:42

low level. So I think we could

24:42

probably expect that to be the

24:46

case. I do think though with the

24:46

vaccines really rolling out and

24:49

we've really got a lot of

24:49

momentum with the vaccines. I do

24:53

think that by the time the

24:53

summer comes, as was predicted

24:56

early on that the vaccines will

24:56

allow us to return most of the

24:59

normal life, I really think

24:59

that's gonna be the case. But

25:03

there could be a couple bumps in

25:03

the road with some new variants

25:05

as we go. But I don't think I

25:05

think ultimately we, you know,

25:09

the vaccinations should should

25:09

help us tremendously.

25:13

I cannot tell

25:13

you how much hope just ran

25:17

through my body just because

25:17

someone with your with your

25:20

level of expertise and

25:20

understanding of this could

25:24

could say that that's what they

25:24

feel. And that's - It was just

25:29

my, I just had a visceral

25:29

reaction to that. So thank you.

25:33

Yeah. Well, because right now,

25:33

it's hard to know.

25:38

Exactly. I

25:38

mean, I'm not the only one who

25:42

has the same feeling. I think

25:42

you have people who are more

25:44

optimistic and people who are

25:44

more pessimistic. I tend to be a

25:47

more optimistic person. But I'm

25:47

also kind of a realist, but I

25:50

think I'm optimistic. But I

25:50

think the reality is matching

25:53

that is the vaccine some so for

25:53

example, the vaccines, a couple

25:59

of them have been tested against

25:59

the variants that are of the

26:01

most concern right now, which is

26:01

the one that was first found in

26:05

South Africa and Brazil. I

26:05

think, I think the Brazil ones

26:08

been testing test, I can't

26:08

recall. And then the one that

26:11

was found in the UK, so and it

26:11

appears that they work well

26:14

enough, and they seem to almost

26:14

completely 100% block death,

26:19

which is a really important

26:19

thing. And then severe cases

26:23

that require hospitalization are

26:23

way, way lower. And so that's

26:27

the key. I mean, if we can

26:27

convert this to something where

26:29

Yeah, you get a nasty cold, but

26:29

you don't feel the hospital, you

26:33

don't worry about dying. If we

26:33

can at least get there. That's

26:36

That's good. I think we can

26:36

definitely get there by the, by

26:38

the summertime or the end of the summer.

26:41

Oh, that's so great.

26:42

Is that

26:42

typically, on a scientific

26:45

level? The best case scenario

26:45

for any pandemic type virus, for

26:50

example? How do you know, in in

26:50

your education and study, what

26:58

happened to the influenza virus

26:58

that hit in, you know, the

27:06

1918/1919 timeframe?

27:10

Yeah, I mean, I'm certainly not the authority on this. But I mean, I've read

27:11

some things as a leisure

27:16

reading, like sort of you guys,

27:16

you know,

27:18

leisure reading, I love that!

27:20

leisure

27:20

reading, but it was a

27:22

scientific, scientific, you

27:22

know, angled paper article I

27:26

read. And the the, the argument

27:26

was that the 1918 pandemic had

27:30

multiple waves. And then it came

27:30

back the next year, and then the

27:35

year after, but each year it was

27:35

weakened and then largely

27:40

disappeared, and sort of died

27:40

out because it was really just

27:44

too virulent. It just was, it

27:44

just killed people too, too

27:48

much. But we had but but then I

27:48

also saw that same article, the

27:53

argument that some of the annual

27:53

or seasonal influenza a has the

27:58

remnants of that virus. And so

27:58

Okay, yeah, and so the influenza

28:02

virus can recombine with other

28:02

influenza viruses a lot more

28:05

So they don't

28:05

really - in our brains, you

28:07

readily. And I think it's a

28:07

little more common for two

28:11

influenza viruses to be in the

28:11

same person. So pieces of it

28:15

have somehow persisted for 100

28:15

years. But but the the major one

28:20

that drove it apparently died

28:20

out. And so you may also know,

28:24

though, on top of that,

28:24

intriguingly is that the common

28:28

cold is a lot of common colds or

28:28

coronaviruses. I'm not an expert

28:33

in this area, too. So it's kind

28:33

of tempting to think while some

28:38

fragment or remnants of this

28:38

source code could persist for a

28:42

long time, either it just

28:42

evolves to become highly

28:46

transmissible, but very non

28:46

toxic or non virulent to the

28:50

host. So it survives better or

28:50

sort of at some point recombines

28:55

with another common Coronavirus,

28:55

and you know, so

29:02

know, they they can be

29:02

eradicated but it sounds like

29:05

they they lessen and degree and

29:05

are somehow, but somehow do

29:13

stick around and in a remnant

29:13

form.

29:15

It was interesting to think of it as like, you know, the Spanish Flu

29:17

has had grandbabies. And the

29:20

grandbabies are colds that we

29:20

experience every day and someday

29:24

Coronavirus is going to have

29:24

grandbabies, too.

29:26

That may be the

29:26

case. And you know, it's

29:29

important to remember too that

29:29

Coronavirus is a very common in

29:32

nature and and lots of animals

29:32

and what we've had here what

29:36

what appears to be is the jump

29:36

from bats to humans, there was

29:39

enough mutations and it seems to

29:39

be the case. There could have

29:43

been some intermediate in

29:43

between but lots of Coronavirus

29:47

is out there in the world. Most

29:47

of them don't infect us, I don't

29:50

do so very efficiently. So, at

29:50

least if this ever happens

29:56

again, maybe it will be a lot more prepared.

29:59

Let's hope! How

29:59

does it feel to be the bearer of

30:05

such trepidatious news?

30:05

trepidations might not be the

30:09

right word, but it looks like came to mind.

30:11

Yeah.

30:11

What does it feel like to be the bearer of bad news?

30:13

Well, the question is, is it good news or bad news? Right? Because a we

30:15

were very hesitant about this.

30:18

When we first made the

30:18

observation of this variant. It

30:22

was kind of, well, it's been

30:22

here for a long time. So maybe

30:25

it's not a big deal. But

30:25

nobody's ever said anything

30:28

about we can find anything in

30:28

the literature even on even on

30:31

on Google nothing about this

30:31

variant or and these mutations

30:34

we were finding, and we thought,

30:34

well, we need to say something.

30:37

But, you know, so it was like,

30:37

this is important, but how

30:40

important and we've gotten the

30:40

same feeling from the scientific

30:43

community. Some people like, Oh,

30:43

this is fantastic, I'm glad you

30:46

characterized it, you know, this

30:46

creates the backdrop for any new

30:50

variants that would emerge in

30:50

the US. So it's important to

30:53

study this, this variant. And

30:53

other people. Well, it's not the

30:57

UK variants, not the variant

30:57

that we saw in South Africa

30:59

doesn't have those mutations. So

30:59

it's not must not be important.

31:02

So I get both of that, and it's

31:02

kind of have mixed feelings. And

31:08

I don't know, that's bad news,

31:08

because it's been here for

31:11

months. And we don't have a

31:11

dramatically higher death rate,

31:15

or hospitalization, or, you

31:15

know, it sort of came on

31:19

quietly, you know, didn't make a

31:19

big racket. And so even even

31:24

possible that it might be less

31:24

virulent, or as transmissible

31:28

but not any more dangerous than

31:28

the original one. So who knows,

31:32

maybe after we do enough studies

31:32

and characterize us better,

31:35

maybe it turns out that it's,

31:35

it's, it's, it's a good variant

31:40

that is very transmissible, but

31:40

yeah, dangerous. Who knows?

31:43

Yeah.

31:44

That's interesting to think about, that. That mutation can also

31:46

mean that it mutates down and

31:50

weakens or it it, it gets easier

31:50

to combat in some way.

31:56

Or maybe maybe I found

31:56

the good variant that we

31:59

shouldn't be concerned with.

32:01

Yeah. I'm really,

32:01

I'm more anecdotally, what are

32:07

you really looking forward to

32:07

doing once the world returns to

32:10

some semblance of normalcy? What

32:10

do you miss?

32:12

Gosh, you know,

32:12

I've got three kids, and like,

32:16

they can't go see their friends.

32:16

I'll just be happy when they can

32:19

go to school. My wife is mostly

32:19

staying home with the kids and,

32:25

you know, helps mediate,

32:25

they're, they're learning,

32:27

they're learning at a distance.

32:27

And it's just hard on her, I

32:32

think she has a much harder job

32:32

than I do. So I'm just looking

32:34

forward to normal life for my

32:34

kids. And then, like I said, I'd

32:38

love to go to the gym and play

32:38

basketball again, that would be

32:42

without ask. Yeah, you know, we

32:42

haven't taken any family

32:47

vacations. I've been working

32:47

harder since the pandemic than

32:52

any other time because we're

32:52

trying to maintain our normal

32:55

projects, but now take on this

32:55

new COVID-19 project. So I think

33:01

I think it would be nice to just

33:01

be able to take some vacations,

33:04

just do the normal go to the

33:04

restaurant, you know, I just

33:06

looking forward to the things

33:06

really nothing more.

33:08

Yeah, it's

33:08

it's amazing how just those

33:11

little things that the feeling

33:11

of being able to spontaneously

33:16

go somewhere, grab something or,

33:16

you know, whether it's a

33:21

restaurant or the post office,

33:21

or whatnot. We were just talking

33:25

my wife and I last night about

33:25

the fact that we're, we're

33:28

coming up on what will be her

33:28

second birthday in the pandemic.

33:35

And we're, we're both very, you

33:35

know, we we try to understand

33:40

the science of it, and we do our

33:40

part. But she was like, Can we

33:46

please do something a little bit

33:46

special for my birthday? It just

33:51

last time, you know, we had just

33:51

been shut down. Everything was

33:55

closed. And, you know, we did

33:55

something quiet at home. So

33:59

we're trying to figure out what

33:59

that is. Because it's not like

34:03

things have improved enough

34:03

(laughter).

34:07

Can we it's gonna

34:07

be like a walk down the street

34:10

today? That'd be so nice.

34:12

Yeah, I've got

34:12

I agree. We've got a two and a

34:16

half year old and she's trained

34:16

now she wants when we go on

34:20

public, she wears her mask. If

34:20

her mask comes off. She freaks

34:24

out, like, what kind of world

34:24

are is my portrait growing up?

34:28

And you know, our masks are

34:28

normal. But yeah. And in fact,

34:33

earlier today, I'm sitting in my

34:33

office working on my computer,

34:36

and I'm wearing my mask. And I'm

34:36

like, why am I wearing my mask?

34:40

That was like, when I left my

34:40

office 20 minutes ago, and I

34:43

came I didn't take it off. It's

34:43

like, we're so trained now. I

34:47

never would have I mean, you

34:47

know, imagine when we first

34:49

started the pandemic, people

34:49

were so resistant to wearing

34:51

masks. Yeah, it's, it's

34:51

commonplace. Yeah, you just

34:55

accept it as normal life.

34:57

Yeah, I fell

34:57

asleep with mine on actually

34:59

Last night, yeah, I went

34:59

downstairs to pick up a package

35:03

came back in, realized I was

35:03

tired and fell asleep. And it

35:06

took like halfway through the

35:06

night for me to be like, what is

35:09

on my face? What is going on,

35:09

which is also really gross,

35:13

because yeah, just breathe and

35:13

more of my own air for a long

35:16

time. We usually love to sort of

35:16

round out these interview

35:21

conversations with a more

35:21

positive note. And honestly,

35:25

frankly, this conversation was a

35:25

lot more hopeful and positive

35:29

than I was sort of expecting it

35:29

to be. So thank you for that.

35:31

Yes. I'm curious to know what,

35:31

what gives you hope right now?

35:37

Well, um, I

35:37

got, I think the vaccines are

35:39

huge. And unfortunately, no

35:39

matter what happens, the

35:42

pandemic will run its course,

35:42

and you know, you can only

35:47

infect people so many times. And

35:47

even if we had no intervention,

35:52

viruses are at some point

35:52

naturally going to become less

35:55

virulent, because, you know, you

35:55

can't kill every host. So those

36:01

simple, simple, you know,

36:01

biology, things I think, are, I

36:05

feel like, you know, eventually,

36:05

you know, things will change,

36:07

just like in the 1918 pandemic,

36:07

eventually, people's immune

36:10

systems adapted, or the virus

36:10

couldn't adapt further. But

36:15

realistically, the vaccine, I

36:15

think, has been important to

36:18

help push things along. And I

36:18

think it was a big deal at the

36:22

beginning of the pandemic, we

36:22

put a lot of stress on it. And

36:24

I'm glad we did, because it

36:24

allowed things to move quickly.

36:27

And I think it's living up to

36:27

its promise, so to speak. So

36:31

that gives me hope. You know,

36:31

and also what I've seen is a lot

36:37

of, at least in my laboratory,

36:37

we've come together to solve

36:41

some hard problems. sequencing

36:41

the viruses genome was not a

36:45

simple task, it required

36:45

everybody in my lab to come in,

36:49

during the pandemic, and risks

36:49

themselves, you know, and put on

36:53

all the the PP you know, the

36:53

masks and the gear. Yeah. And

36:56

there was a lot of unknowns

36:56

early in the pandemic. So we

36:59

didn't know how much of a risk

36:59

we were taking. And, but so I

37:03

got to see people come together.

37:03

And I think that's, that always

37:07

brings a little bit of hope to

37:07

situations when we can band

37:09

together and solve problems. And

37:09

we see that in the world and in

37:12

the science world, and in

37:12

medicine, and hopefully, with

37:15

general everyday people were

37:15

very supportive of like, coming

37:18

together and solving this.

37:20

Yeah, gosh, that

37:20

gives me so much hope. Thank

37:22

you. Yeah, yay, science, listen

37:22

to science, everybody listened

37:28

to it? Well, awesome. Thank you.

37:28

Thank you so much. I know that

37:32

you don't know us at all, and

37:32

that we just reached out on a

37:35

whim. And I know you've got the

37:35

busiest schedule in the world.

37:38

So we just appreciate the fact

37:38

that you took a little bit of

37:40

your time to talk to us, it

37:40

means so much.

37:42

Well, no, I appreciate it. I feel like I know, you guys know. So we

37:44

should keep in touch. And don't

37:46

forget to reach out and maybe in

37:46

a couple weeks or a few months,

37:50

we'll have some updates, and

37:50

we'll probably be good to

37:53

update. You know, well, a lot of

37:53

like unknowns, we don't know

37:56

what the next couple months are

37:56

gonna bring. So again,

38:00

yeah, man,

38:01

We'd love that!

38:02

We'll reach out for follow up soon.

38:04

And I like these sort of interactions, because I've done a lot of

38:06

interviews with, you know, at

38:10

least recently regarding this

38:10

with different types of media,

38:13

and, you know, sometimes the,

38:13

they only have two minutes, you

38:16

know, and they rapid fire and,

38:16

and this is much more relaxed

38:21

and enjoyable, we can actually

38:21

have conversation. Soit gives me

38:25

more time to go into teacher

38:25

mode and, and explain things a

38:29

little bit better to, you know,

38:29

with our listeners and stuff out

38:32

there that, you know,

38:35

You really spell it for two people. I mean, we're both actors. I hate to admit

38:37

this, but I got terrible grades

38:41

and science.

38:41

I've never ever been hired to play a scientist yet. So I don't think

38:43

I'd be good at it.

38:48

But it's really great to have you. It's like explaining things in layman's

38:50

terms. I feel like I know. I

38:53

feel like I've learned something

38:53

today. And hopefully whoever's

38:56

listening to this will have a

38:56

lot to learn as well.

38:59

Yeah. So yeah,

38:59

Everybody stay safe. Get the

39:03

vaccine if you can. Keep wearing

39:03

your mask for now. Stay six feet

39:08

apart. Hang in there, it's gonna

39:08

get better. And see how things

39:15

go.

39:23

Hey, this is

39:23

Caroline. Raymond, we wanted to

39:25

say thank you for listening to

39:25

this episode and let you know

39:28

that there will be more every

39:28

week from now until we get

39:31

fatigued by it. We're building

39:31

out this podcast as we go. So

39:35

stay tuned for improvements on

39:35

our website, our graphics, video

39:38

clips and just everything else.

39:38

The time was now to tell our

39:41

stories so we're learning as we

39:41

go. We really do appreciate your

39:45

interest in support. We truly

39:45

hope that the personal stories

39:48

that come out in each episode

39:48

can help build a better

39:50

understanding of COVID-19 how it

39:50

spreads and how it affects us.

39:54

If you have a story or a

39:54

question that you'd like us to

39:57

address in an episode. please

39:57

email us at

39:59

[email protected] that's

39:59

fat igu ed [email protected]

40:07

Thanks for listening bye