February 7, 2022 • 40 mins
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Matt Boettger (00:00):
You're listening to the pandemic podcast.
We equip you to live the mostreal life possible.
And the host today's crises.
My name is Matt Boettger.
I'm joined once again every twoweeks.
I'm a good, good, good friend,Dr.
Stephen Kissler andepidemiologist, the Harvard
school of public health.
How are you doing in thiswonderful wintry weather?
You got blasted by storms or didyou do.
Stephen Kissler (00:18):
We did.
Yeah, we got buried.
It was it was pretty well therewas, it was about two, two and a
half feet of snow almost.
So, gosh.
Yeah, it was it's pretty wellmelted by now, amazingly, which
doesn't usually happen here.
Usually it kind of lingers andjust turns, you know, ugly
colors from all the cars goingby.
But yeah, it's so, so we'redoing better.
But it just, it's proper winterup here in, by.
Matt Boettger (00:41):
Oh, my gosh, I do not NVU or do not want to be
there.
I just want to be someplace forwarms.
So yeah, it's cold here.
We've had like negative 14waking up in the morning kind of
stuff, and it's just brutal.
And of course the boys, likelet's go outside and play and we
get them all jazzed up and getthem all clothed.
And I'm taking, they're going tolast like two minutes, but
(01:01):
somehow their resiliency and thenegative weather outside.
It's so inspiring.
So yeah, it's winter for most ofus here in the U S a lot of
storms going on, and it's been acouple of weeks and like usual,
there's a bunch of things on mymind.
So this episode might be alittle bit different now it's
probably the same, but justlike, I have a random questions
(01:22):
that I want to throw a pass.
So.
The he'll have brilliant, greatanswers to somebody which I
might catch him off guardbecause I don't know what to do
with some of this stuff, butbefore we get going the same
stuff.
So if you can't leave a review,we love it.
Now.
I can't believe we're almost intwo years of having this
podcast.
It's like mind boggling.
It's like, I like one year feltnormal two years for like, wait
(01:42):
a minute.
That's that went way too fast.
Second year went way, way, waytoo fast.
But nonetheless, the reason whyI mentioned.
It's because I think we havehope, gosh, I don't know how
many reviews.
We have a bunch of reviews, Ithink 180 some or something.
And I thought, man, if you guyswould all hop on and we could
cross the 200 threshold by ourtwo year anniversary would be
(02:02):
phenomenal.
So I was looking Stephen, I waslooking all all the random,
like, have you looked around atthe other random COVID
coronavirus podcasts.
I'm like, I didn't know.
We're kind of like a we're ahit, I didn't know this.
I was looking at the ratings andI'm like, oh, we've got like
4.8, most like 4.3 and a lotthem like 50 to a hundred
reviews.
And I was, I'm like, it'sreally, I was really surprised,
(02:23):
I think partly because you guysare incredible and we have like
a little family.
We're just not, so we don't getinto the politics.
We don't get into all thisstuff.
We're just here to help.
You know, do the best we can toserve.
And Stephen, you guys havetaught me so much about just
embracing complications and Ithink a lot of people love that
and so they dig it and want tolisten more.
So
Stephen Kissler (02:42):
thank you.
Appreciate it.
It's yeah, this has been a lotof fun and yeah, excited to
keep.
Yeah,
Matt Boettger (02:47):
absolutely.
So we've got another one fromJanuary on January 30th, just a
few days ago.
Five stars listener 1, 2 0, 2, 19 says this is the best of all
the COVID podcasts.
It sets the problem in contextso well, and I actually learned
something new and significanteach time, keep up the good
work.
So that's great.
Keeping appreciate that.
Love it.
So if you can't leave a review,do it apple podcasts as well.
(03:08):
If you wanna support usfinancially, we'd love that at
patrion.com/pandemic podcast, aslittle as$5 a month can help or
just a one-time gift.
Do you want to all in the shownotes, that'd be Venmo or PayPal
there's links there.
So let's get going.
I want to start with thisbecause I think let's just start
with experience.
It's been a wacky few weeks forme, Stephen, because outside of
(03:28):
you, which I kind of feel likeyou're kind of in some sense of
anchor of reality for me, I'm mycircles might not necessarily
reflect that.
And you know, what was it twoweeks ago?
We talked about my pediatricianand the thing that he talked
about for those of you whohaven't listened to the
episodes.
Basically, I love him.
We trust him dearly, but just,it was interesting how he was
really not really for the COVIDvaccine for our little ones.
(03:52):
But was for the flu shot.
And just, I was confused bythat.
We talked about this, I thinkthat was two weeks ago.
And just seeing how it's not assimple as things just consult
your primary care physician forthe rock solid answers seems
then my wife went to my primarycare physician and got a similar
answer of like, oh, you know,don't do it to the kids.
And I, you know, I'm justfollowing the data and all this
(04:15):
stuff.
Right.
And so the kids too, for two,it's just really weird.
And then last Friday, Stephen.
My mother-in-law goes to see heroncology.
And she's like, oh, see, youknow, she's like, oh, sorry for
waiting.
I just wanted to get my booster.
And the oncologists made thisvery quick, small response,
like, oh, you know, vaccinesdon't work anyway.
So forget about it.
Right.
So here I am, Stephen three forthree, an oncologist, a
(04:35):
pediatrician, and a familypractice person, all kind of
same, roughly the same thing.
And I'm just so I don't takeinfused.
Blown away by the, even in themedical field of just what's
going out there.
And maybe you will speak back toit.
We were talking about a littlebit about this off.
I know you mentioned the bestperson right now, be mark to
(04:56):
have on, because he's the one onthe ground doing this stuff, but
you've been helpful to kind ofgive the distinction of, you
know, possibly what two kind ofsides are looking at and how it
can get a little blurred attimes.
Stephen Kissler (05:07):
Yeah.
I mean, I think that, you know,the most important thing to
remember is that, you know, Dr.
Epidemiologist, whatever thatwe're, you know, we're people
who are bringing all our ownstuff to all our things.
And I think that it's easy tosort of see a person as the as
the role that they fill.
Especially when it's somebodywith some kind of expertise or
(05:29):
authority especially thinkingabout somebody like a doctor and
then just, you know, rememberingthat, like to some extent A
doctor will has the sameprobability of falling along any
one of the lines of opinion andconviction as anyone else.
And that's, you know, it, but Iunderstand how, you know,
especially with something likevaccination, you would expect
(05:51):
maybe a practicing doctor tohave a different opinion than
the ones that you that you heardfrom them.
And so to try to sort of breaksome of that open, I mean, I
think that Maybe it's easiest toseparate out the advice given to
your kids versus the commentabout vaccines not working.
I think that it's relativelyeasy to dismiss the idea that
that the vaccines areineffective for people who are
(06:12):
older.
I think that that's, you know,there, the evidence of.
Overwhelming that they are safe,effective, hugely valuable in
making sure that people who areadults and elderly are staying
out of the hospital and notdying from COVID-19.
And again they're not perfect,but they, boy, they are
extremely good at what they do.
(06:33):
And I think, you know, that is apretty solid scientific
consensus.
And so I'm not really sure wherethat information would have been
coming from, but that, that justisn't doesn't make sense to me.
Now we can think about kids.
So, there's been a lot ofconversation about Authorization
of vaccines for kidsrecommending vaccines for kids
and sort of what we should do inthis next stage.
And I think that there's alittle bit more latitude because
(06:55):
COVID-19 seems to be a lot lesssevere, generally on a case by
case basis for young kids thanit is for older people.
And there's Also seems like,vaccinating kids may not be a
super effective way atcontrolling spread because there
are so many breakthroughinfections happening.
Right?
So, so those are generally thetwo reasons you would want to
vaccinate somebody is to protectthem from severe disease or from
(07:16):
infection and to prevent thespread of disease.
So, you know, while I still, youknow, from all the evidence,
I've seen it, vaccinating kidsdoes seem to.
Reduce their risk of severedisease and illness as well.
Just bearing in mind that theirabsolute risk the baseline
probability that they end upwith severe disease is already
(07:36):
very low and lower than a lot ofother things, other risks that
they probably face in theirlives from day to day.
And so, you know, I think thatthere is a little bit more space
for complexity there.
You know, the thing is that I'vebeen thinking a lot about sort
of what I would recommend topeople who have young kids in
terms of getting vaccinated.
I'm a strong, strong supporterfor making sure that the
(07:56):
vaccines you know, assuming theycome back with Acceptable safety
and efficacy that they beapproved for use in kids.
And I think that's especiallyimportant for the many kids who
who have respiratory conditionsor who have other conditions
that put them at higher risk ofsevere disease.
I think, you know, and there area lot of.
Out there who areimmunocompromised or who have
(08:19):
asthma or who have downsyndrome, who are at higher risk
of certain respiratoryillnesses.
And for those kids, I think thatit makes an awful lot of sense
to get vaccinated.
Now, I am less certain as towhether it makes sense to have a
blanket vaccine recommendationfor all.
'cause there, I think the costand benefit I'm not really sure
yet how that's going to fall outand it's a lot less clear cut to
(08:42):
me than it is for older peopleand even kids over the age of
12.
And so there's, I do understandsome of the complexity there,
and while I would probablyrecommend.
People get their kidsvaccinated, you know, once, once
the vaccines are approved, I, I,I have a lot more understanding
for both physicians and parentsand guardians who may be less
(09:05):
onboard with that.
Matt Boettger (09:06):
That's great.
And we're going to talk aboutthis later, but Monza, bring it
up now in this, adding to thecomplexity.
So, you know, I just read abouthow the Pfizer vaccine is
getting FDA approved for thelittle ones, I think from two to
five or two to fours.
For at the data, but you know,adding to this thing is I saw
this, I don't know who thisdoctor is.
Zeke Emanuel person is, but youknow, mentioned vaccine children
(09:27):
five and above.
It seems like it's a no braineraccording to this doctor.
And it was a very short articleup in the show notes, but the,
the, the quote that kind ofcaught my attention was this
with the Omicron variant kidsare either going to get the
vaccine or they're likely to geta serious condition of.
It just seems like this is wherejust adds more confusion too.
(09:48):
I think the flames, because Idon't think is an accurate
reflection of what you're seeingand what globally we're seeing
with
Stephen Kissler (09:53):
kids and Alma.
Yeah, no, that's right.
It's and, and I was actuallyjust just as we were doing our
little minute long countdown, Iwas looking up this guy and it
sounds like he's recently justsaid that he misspoke that, that
I think what he was referring towith a severe case of COVID, it
was just a case of COVID thatlike, as opposed to a vaccine
where there's, you know, you're,you get the vaccine and you
(10:14):
might have side effects from thevaccine, you would get a case of
COVID and potentially showsymptoms of some variety.
But but, but I think, you know,all of what we just said stands,
but you're right.
I mean, I think what's, what'smore important here potentially
is just that there's what issaid.
Can't be unsaid in a way.
And so this does contribute to afair amount of confusion as
well.
And to a lack of trust, youknow, this this person is also a
(10:37):
doctor, I think an oncologist.
And and so it's like, you know,it sort of continues to sort of
build this kind of a sense of.
I don't know, just a caution andmaybe I'm lack of trust in the
medical establishment from allangles.
And I think that that's, that'sreally difficult.
That's sort of an even deeperproblem that we've we've got a
(10:58):
lot of work to figure out how tosort out in the coming years.
Absolutely.
Matt Boettger (11:02):
And we're not even needed.
We do a bookmark that as well.
Cause we're gonna talk aboutthat in a second, but just.
How science is under themicroscope by the public in so
many ways, because of justeither, you know, from a lot of
different reasons that we're a,because of our ignorance are not
understanding the field, thebeam, you know, and also just
the way it's communicated andhow it gets confused and those
(11:24):
kinds of things.
But before we get into that, onemore thing about this.
Maybe you can touch on thisbecause.
Pfizer striving to approvethrough the FDA.
The vaccine for the littlekiddos, you know, was weeks ago.
We were talking about how, oh,it looks like the two dose
didn't work.
It's going to go to a threedose.
I would imagine this is going tobe the talk of the town for a
(11:44):
number of months, because numberone, just, just at the baseline
of exposing your little kids toa vaccine is already going to
have a lot of questions behindit because you were in the
protective as much as.
Then when you get a narrativesaying, quote, you know, I'm
using my narrative, it didn'twork, whatever that means.
Right.
So we're gonna do a third shotand then we're ready to go.
(12:05):
And we're going to do two shots.
Wait a minute.
Now I'm confused.
You just told me it didn't work.
In other words.
And now, and part of this I readhere was this idea of looking
through two different, like amicro lens and a macro lens.
And initially it was the microlens.
Now it's the macro lens.
Now of course, now we're addingmore complications.
Of course can cause morehesitancy.
So I thought I knew.
(12:26):
Maybe you can at least helpstart the ball rolling on this
discussion of what's reallygoing on.
And as you were saying before weeven got on the podcast, this is
maybe a reflection of maybe eventhe development of vaccines in
general of how they're lookedupon and those kinds of things
in light of what we'veexperienced with other vaccines
with COVID.
Stephen Kissler (12:43):
Yeah.
So let's, that's great.
I think we can get into some ofthe nuts and bolts of the, the
vaccine approval for young kids.
So, as a, you know, as, as wetalk about.
A long time ago.
I mean, I think that we've,we've been anticipating it
taking a long time to get thevaccines approved for kids in
large part, you know, bothbecause as we were saying, they,
they face a lower, absolute riskof severe disease from COVID-19
(13:05):
and because it's just trickierall of, all of the ethics, all
of the approvals, everything isjust a lot harder, especially
when you start getting into theyoungest age groups.
So I think we're seeing some ofthat.
So, so, so I think a couple ofthings to just Review an
outline.
I'm most familiar with with thePfizer trials.
And and the first thing to noteis that the vaccine doses that
(13:26):
they've been testing in youngkids are quite a bit smaller
than the doses that they've beengiving to adults.
I think they're like on theorder of a 30th of the size so
much, much smaller doses thatthey're giving.
Which, you know, might, it mightalready lead you to suspect
that, you know, maybe they'renot going to have as strong of a
response because you're justgetting a lot less vaccine.
And so, and, and that seems tobe in part what they've seen.
(13:47):
So, these vaccine trials havebeen ongoing and.
Administered vaccines to youngkids.
And they've been trying tomeasure the effectiveness of the
vaccine through a couple ofdifferent ways.
You know, normally the goldstandard for measuring vaccine
efficacy is by.
Giving a control group, aplacebo and giving the
(14:09):
experimental group, the vaccine,and then comparing their risk of
clinical disease as you goforward in time.
And so early on in the pandemic,when we were recruiting the
vaccine efficacy numbers forMadrona and Pfizer and the
different vaccines, that's wherethose were coming from.
So when you see an 80% and 90%,95% vaccine efficacy, that means
that the, the, the experimentalgroup has a.
(14:33):
95% reduced risk relative to thecontrol group of something.
And in that case, it was usuallyshowing symptomatic disease or
symptomatic illness.
Now with kids, there's been abit of a different approach
taken.
And it's in large part again,because kids.
Don't show symptomatic diseaseas often.
(14:53):
And so to do these vaccinetrials in the traditional way
where you're measuringdifferences in the rate of
symptomatic disease you have tofollow a lot of kids and you may
have to follow them for a longperiod of time, simply because
the absolute risk of showingsymptoms is so low.
So to get any sort ofstatistical.
Accuracy around theeffectiveness of the vaccine.
You need a massive trial for along period of time and that's
(15:14):
difficult to do so they look forother proxies.
And one of those proxies islooking at immune response.
So the easiest immune responseto measure is your B cell immune
response.
And so, that does seem to be apretty good proxy for
protection, even though we knowthat other types of immune
response, especially our T cellresponse is the one that's most
effective at keeping us out ofthe hospital and from severe
disease illness.
(15:35):
But that's also much harder tobe.
And so my understanding is thatin these trials from the micro
perspective, what Pfizer hasbeen doing is looking at the B
cell response and they've beenfinding, well, actually it
doesn't seem like we have muchof a response from two doses of
the vaccine.
Maybe we'll try three and see ifwe get to get a better B cell
response.
But as that's been going,they've also been following the
kids in this macro trial.
(15:56):
And over time they've beencollecting more and more data.
And it actually seems like eventhe kids who have been dosed
twice, They do seem to be lesslikely to show up in the
hospital and have a severeoutcomes, even though the
baseline probability is so low,they've been able to distinguish
now finally, because enough timehas passed and enough kids have
been through this trial thatthere does seem to be a reduced
risk of severe disease for kidswho are doubly vaccinated.
(16:17):
And so I think that's part ofwhat's going on here is that
it's just taking some time towrap up.
Evidence.
And because, you know, becausekids face such a lower risk,
absolute risk of, you know,acute, severe illness it was
just a lot, they had to look forother ways to measure.
That
Matt Boettger (16:32):
makes sense.
That's really helpful.
And just shows a little, youknow, you just, I think unfolded
beautifully because it's somultilayered in its complexity,
because you just said that partat the end, which was like the
grand finale, but then youtouched on the other huge piece
at the beginning, which is justgetting these groups in general
is exceedingly difficult.
So you have to obtain the groupsincredibly difficult.
And then the measurementincredibly difficult that you
(16:54):
have a lot of creativecreativity is needed here.
And it just goes back to.
The first thing we talked aboutof pediatricians and physicians
having different responses andsaying, well, I look at the data
it's not working.
And I know we we've eaten thisto death in some regard of
always asking the question, whatis it like, what is the it
they're talking about?
Yep.
You're absolutely right.
When if you're really trying tocontrol the spread of the virus
(17:17):
and then that we're on the samepage, it's not even, it's not
that effective, but it is like,you don't want your kid or your
grandma.
Going to the hospital and thatit is very different, right?
Stephen Kissler (17:31):
Yeah.
Yep.
Matt Boettger (17:33):
Great.
Helpful in that let's, let'sswitch gears for a second and
let's come back to this variantof Omicron, just chat about the
updates.
It seems like nothing to beconcerned about.
I don't know if you could speakin as we didn't talk about this
before we started, but I foundit a little weird how, when the
first version of yeoman Cron,which apparently best these,
these both.
(17:54):
I guess sisters they've kind ofcame at the same time.
They're not really that, butjust one kind of dominated ones.
I don't know.
But anyway, nonetheless, I wasamazed how, when Omicron raised
its first ugly head, there was aseries of the case.
You know, we need to take sometime evaluate where, you know,
maybe week two, we'll kind ofhave this week four, we'll have
this week eight, we might havethis information.
It seemed as though.
(18:15):
As soon as Susan, it came intothe media outlets.
There's already information likeright away.
That was so much faster than thefirst Alma Cron variant, where
like I was hearing right away,like two weeks ago I saw an
article.
Like it looks like it's maybeone to 3% more infectious, like
that's a very quick conclusionafter the first article.
So maybe a couple of things.
(18:36):
I what's the status of this,this ugly.
And to how on earth did we getdata so quickly compare to the
first summit?
Stephen Kissler (18:44):
Yeah.
So, these are, these are great.
So, right.
So, so the, the Omicron that wenormally think of is also one of
the other ways that we've beenreferring to it as B a one.
And I think, you know, we cantalk, I think we've talked about
nomenclature on previousepisodes, so I won't, I won't
get into all of that.
But this, as you said, is aclosely related lineage that
we've been referring to as Andand yeah, so it's, it's not
(19:08):
totally clear where this thingemerged from.
There's been a lot of Andconversation going on to try to
sort of clarify this and try tounderstand sort of like how
these two related lineagesemerged that were actually, you
know, very distantly related towhat we had seen before.
So that's still a bit of apuzzle, but we do know that
they're closely related to oneanother.
Part of the reason we know somuch about it is because it's
actually been circulating for aslong as BA one has been
(19:29):
circulating too.
And so we've, we've had cases ofBA two in the U S since
December.
But they've been sort ofbubbling along at relatively
low.
It's a bit of a mystery rightnow.
Why hasn't taken off and why itdidn't take.
Before BA one did.
Because it does seem to be maybea little bit more infectious.
We're starting to see a BA orsorry, a BA to wave in South
(19:51):
Africa, you know, which was thefirst place to see a major
documented BA one wave.
And so that's interestingbecause it suggests that BA two
can spread in places where BIone has just had a huge impact.
So that's a little bit puzzling,but why is it taking off there?
Here.
So there's a lot, we're nottotally sure about, but one of
the reasons we've gotteninformation relatively early is
(20:12):
because again, within we've beenactually tracking it for a long
period of time, but it's onlystarted now to emerge as
something that is starting tocause an increasing number of
cases.
And also because it's growthrate is.
Relatively slow compared to BAone, even though both are very
fast that also gives us a littlebit more time to sort of track
it because of its growth or itwas explosive than relative to
(20:34):
epidemiological time.
Then we wouldn't be gettinginformation very quickly at all.
But since its growth isrelatively slow compared to BA
one, that also gives us a littlebit more time in terms of the
spread of the pandemic itself toget information about BA too.
So.
The couple of things about BAtoo.
They some of you may rememberhearing I think the guardian had
an article about stealth Omicronawhile ago.
(20:56):
And so I think this is what theywere referring to.
It it's this it's this otherlineage of Omicron.
And the reason they called itstealth Omicron is because boy.
Alright, so, so Omicron.
Like alpha had this strangething that caused one of the
three PCR primers to drop out.
So that means that when you gottested with PCR with both alpha
(21:17):
or Omicron, you would light upas positive on two of the, sort
of two of the, the redundanttags, but negative on the third.
And that's actually reallyuseful for surveillance because
that, you know, that that helps,you know, if it's something
that's likely to be Omicronversus Delta, where just Delta
had all three adults to lit upall three.
Omicron BA one only lit up too,but now BA two lights up all
(21:38):
three again.
And so the reason it was calledstealth Omicron in that sense is
because it on a PCR test, itmight look like Delta, but was
actually related to Omicron.
And so it was a little bitharder to keep track of.
And so, so that's one of thecharacteristics of BA two is
that it's.
It it's lacking this S genetarget failure which is what
that dropout is called.
So that's one thing that thatdifferentiates it.
(22:00):
There are a couple of otherthings, too.
It seems like there's maybeheightened resistance to some of
the monoclonal antibodytherapies.
Maybe one in particular thatstill worked against BI one, but
it seems to have reducedefficacy against BA two.
So there's maybe a higher degreeof immune evasion for BA two
than there was for BA one.
But in terms of, as far as wecan tell clinical severity risk
(22:21):
of reinfection early datasuggests that it's really
actually pretty similar to whatwe've seen with Omicron so far.
Which I don't know if that's, Idon't know if that's good news
or bad news or what kind ofnews, but it's news.
And so, yeah, so there'sthere's, there's roughly what we
know.
I think, you know, once again,South Africa is probably the
place where we're going to get.
The most new information aboutVA two from, because again, they
(22:43):
had such a strong wave of andnow they're seeing a lot of BA
too, and more than many otherplaces in the world, actually,
Denmark has a pretty big BA twowave right now.
And one of the things that we'veseen there actually is that it
seems to be actually trackingthe relative severity of Omicron
pretty closely where it doesn'tseem to be any more severe to
(23:04):
people who are vaccinated.
Then overcrowd was so, so that'sall, that's all I, that I think
is generally good.
Okay.
Matt Boettger (23:10):
Good.
Good.
Well, you know, I don't know ifyou can predict this, this
early, but you know, having theSouth Africa, maybe starting to
have its own way with BA too,what do you think about, is this
something you think is going tohappen to the U S or because of
the inundation of Omicron herethat the first one may not
compete?
Or what do you see the next twomonths?
Stephen Kissler (23:31):
Yeah.
You know, I don't know this is,this is really puzzling it's.
You know, I I've been joiningthese weekly calls with
colleagues about the variantsand then this one has had us
puzzled for a little while.
We're, we're starting to see BAto picking up in the
Northeastern us and in a lot ofplaces that have just seen the
spread of BA one.
And.
So, you know, that that mightlead you to think that you
almost need a BA one wave beforeyou see a BA too, but that also
(23:54):
doesn't seem to be the casebecause Denmark is seeing a big
BA two wave and they reallydidn't get much original Loma
Cron at all.
So that's a long way of sayingwe really have no idea what's
what's going to happen.
And to what extent this is goingto cause continued infections.
I think, you know, it'simportant to note that in South
Africa, the BA two has sort oflengthened the tail of their own
McCrone wave, but it actuallyhasn't really caused much of an
(24:16):
increase yet.
So hopefully Omicron crown stillprovides good protection against
BA too.
That would be my hunch becausethey're so closely related.
But we'll see.
Matt Boettger (24:25):
Okay, let's keep it.
I just saw a comment here fromCatherine.
She's watching live.
Thanks for watching.
She's one of our long timelisteners.
And so, let's continue on.
Cause I want to put a bookmarkon you have no clue because I
think this is because it'sreally going to be an important
piece of our conversation inabout maybe seven minutes or so.
Two more big things I want tochat about.
Related to maybe I have no clue,but this, you do have a clue
(24:48):
about because you actuallyhelped publish this article.
So Harvard medical professorssays it's time to move on from
the pandemic.
Now that's not
Stephen Kissler (24:56):
what we published.
Matt Boettger (25:02):
Yeah, sorry.
Yeah, that was totally twoconnected.
Right?
A Harvard professor.
I just said that.
Yeah.
So that's not what you publish,but this is a medical professor
saying this what caught myattention?
Not so much the article, I guessit did.
Cause I read it.
But this quote that came fromthis, that this is from Dr.
Stephanos kales.
If I said the name, right?
He says once a macaron peaks,subsequent variants are likely
(25:24):
to be even more mild than.
Totally threw me off becausedaddy have likely to see, oh,
wow.
Okay.
This is pretty confident thatcoming from Harvard, that we're,
this is all downhill from here,so we can kind of be in the
coast and you kind of gave anexcellent explanation off the
podcast now.
And to bring it back on thepodcast, explain it.
Cause then we can bring in Dr.
Fowchee as well, and kind ofjuxtapose these two and show
(25:47):
that where these nuances comefrom.
Stephen Kissler (25:50):
Yeah.
Yeah.
So this idea that, that future.
Variance of SARS, cov two willbe less severe is is a common
one and it's not entirelyincorrect.
But I think it's important toknow where it's coming from so
we can put it in the propercontext.
Right.
So, part of the reason why thisdoctor and many other people, I
(26:11):
think rightly believe that it'slikely that future SARS COVID
two variants will be less severeis simply because our immune
systems.
Good at doing what they do thatwith repeated exposures to a
pathogen either throughinfection or through vaccination
our immune systems learn andthey learn better and better.
The more they're exposed,generally speaking, that's often
the case.
And it seems to be the case withSARS COVID.
(26:33):
Were repeated exposures.
You know, that's why the threedose vaccine series is helping
keep people out of the hospital.
That's why people who have beenpreviously infected and
vaccinated are better thanpeople who've just been
previously infected in terms oftheir protection from being, you
know, going to the hospital.
And that's likely to continuethat that as we move forward,
Higher and higher proportions ofthe population will be
vaccinated or previouslyexposed.
(26:55):
So that will reduce, you know,people going to the hospital,
which will help reduce burden onthe healthcare system.
And, and, and I think that's,that is likely to be the case
for sure.
The place where I've also seenarguments for this, that I don't
think are accurate is withrespect to the inherent severity
of the virus itself.
There is some belief thatpathogens naturally evolve to be
(27:15):
less severe and from sort of apop site from a pop evolutionary
perspective.
That kind of makes sense becauseyou know, the idea is that if a
pathogen kills its host, that'snot beneficial to the pathogens.
So a pathogen will evolve to beless severe.
So it doesn't kill its host.
So it has opportunities totrain.
It's true, but only true for apathogen that can only transmit
(27:35):
after it's caused a severedisease, but that's not true for
SARS.
COVID two, most of SARS COVIDtwo transmission happens before
you even realized you've beeninfected.
So there's no selection pressurefor it to become less severe
because it's already done it'stransmitting by the time it
causes any sort of severedisease.
So, so the severity, theinherent severity of SARS, cov
two is just totally decoupledfrom its transmissibility.
Maybe not totally, you know,nothing in biology is totally
(27:57):
disconnected, but you know, forour purposes here, we can say
that.
So, so, so is that statementright?
Well, yes and no.
I, I think that, you know,generally speaking where our
experienced impact with COVID-19is likely to be less severe with
future variants because ourimmune systems are good.
But you know, one of the areaswhere this really matters is for
people who can't mountain mean agood immune response, right.
For people who areimmunocompromised for you know,
(28:18):
that for them future variants ofSARS, COVID two are likely to
be.
Just as severe, maybe notjustice severe, but much more so
than the population level datasuggests.
And I think that's really worthbearing in mind that there are
going to be a lot of peoplestill living around us that
when, for whom, you know, this,this isn't just another, you
know, Mine are cold.
And, and won't be for a verylong time if ever.
(28:40):
And so I think, you know, Ithink that that is worth bearing
in mind.
Now the other thing that we weretalking about at the beginning
that relates to this is thatwhile I agree that the most
likely scenario that our averagelived experience with COVID-19
is going to become less severewith future variants as our
immune systems get their.
Exposure.
That's not to say that we canrule out the less likely, but
still possible scenario that wewill end up with a variant that
(29:02):
is more severe.
And so while I don't thinkthat's something that like we,
as a.
Nation and world need to benecessarily concerned about all
the time.
That is something that we asepidemiologists, if we, as
doctors are going to beconcerned about thinking about
all the time, because there'sthis trade-off between
likelihood and hazard that weconstantly need to be bearing in
(29:24):
mind where we, even, ifsomething is a rare scenario, If
it's a really bad scenario, westill want to be prepared for
it.
And so that's one of the thingsthat we'll be thinking about a
lot.
And so, you know, all of that isto say that I don't, I don't
anticipate that we're going tohave a variant that totally
escapes our immunity and bringsus all the way back to square
one with COVID-19.
(29:45):
Is it a real remote possibility?
Yes.
I mean, it's also a remotepossibility that we end up with
a flu pandemic next year.
And we, you know, we have anentirely different pandemic to
deal with as well.
I'm sorry.
I know I have probably half ofour listeners shifts hearts just
dropped out of their chests,but, you know, and, and again, I
want to emphasize the rare, youknow, this is, this is not
likely, but it is a possibilityand something that we're
(30:06):
thinking about as well.
So yes, I think with thispandemic, as in my own life and
our own lives, we're always sortof seeking after this certainty
and reassurance and believe me,I know this as well as anyone
I'm constantly trying to find.
Comfort and reassurance and, youknow, certainty that things are
going to be okay, whether it'swith this pandemic or with
anything else in life.
(30:28):
And so I think it's a reallynatural thing to really
gravitate towards these kinds ofthings that like, oh yeah,
future variants are going to beless severe.
We can sort of be done withthis.
And I think that that isprobably operationally a
reasonable way to live one'slife going forward.
But I think the most accuratestatement is that yes, that's
probably true, but we're also.
Keep bearing in mind that therethere still remains some risk
(30:48):
and and, and that risk is goingto be why I keep doing what I
do.
Matt Boettger (30:52):
That's perfect.
I love it.
Cause you know what number onefull, I need to make a, an
apology.
This is not the article thatyou're talking about.
This.
I, my eyes went to a differentwhole different article.
So when I mentioned aboutStephen publishing article, it
has nothing to do with this one.
It's the next one we'll talkabout, but I think this is a
great.
Like place of discussion note,because here's where I am at.
(31:13):
Like, I have a, tends to be alittle too optimistic.
Ah, it'll be fine.
Right.
That's my thing.
It'll be fine.
It'll be fine.
So I would make an, a terribleepidemiologist.
Like it would be literally wouldnot want to put the world's fate
in my hands because you wouldhear, oh, plague.
Ah, I think would be fine, youknow, and we just, we just
stopped there.
Right.
So, so this is where the.
(31:34):
Yeah, like the eternaloptimists, whatever.
And they knew where you internaltestaments, whatever those are
kind of pigeonholed people, butlike, it takes both to really be
able to cope with life becausewe need people who, and this is
where I say you have like theStefanos kales.
Well, I'm not gonna, I'm notgonna put him in a box, but
like, Maybe I'm going to putthem in a box just for a second,
but just for the caricature,not, not for any, just to try to
(31:54):
make this kind of this dichotomyof like, okay, I'm optimistic,
it'll be fine.
No big deal.
It should be less.
And then you have someone likeFowchee, he was being criticized
nonstop, like a fearmonger.
And I think this is, I thinkStephen, you just really helped
to show the nuance.
It's not being a fearmonger it'sdoing his job.
Like, I mean, he's, you know,this quote, it was in the same
article.
He says.
(32:14):
Though he were talking aboutFowchee.
He's cautiously optimistic aboutthe pandemic.
Dr.
Anthony Fowchee said anothervariant could arise.
That alludes current immunity.
I hope that's not the case.
He said, I don't think it willbe, but we, but we have to be
prepared.
Right.
So I think you just, you hitthat were Fowchee is not a
fearmonger he's doing his job.
He's not going to overlook thedata that there's a possibility
(32:35):
of.
Ah, you know what?
I'm a really good scientist, butlet's just forget about, let's
just focus on the optimism.
Right.
You know?
The we who's the, we, I think Iwant to take myself out of that
week and be like, that's youStephen?
That's you Dr.
Fowchee.
You guys think about that.
You guys make sure we're okay.
I'm going to focus on theoptimism, but be also cautious
as well.
So I like that.
(32:56):
Thanks Stephen, for bringingthat to the attention.
Now, let's go to the lastarticle here, and this is when
we're at.
An article that was grounded inyour research and somebody took
it and did again, not the,probably the best articles, very
short from nature, nature,magazine, or nature, the nature
article and the, the, the, thetitle of this one is how does
Omicron spread so fast, a highviral load?
(33:17):
Isn't the answer?
And so I wanted you to talkabout, because I read it, it was
very short.
Three minutes long to read.
And I got no conclusion aboutit.
It basically just said, Hey,look, there's the viral loads
the same, in fact Delta, maybe alittle bit higher, but then it's
landed the plane somewhere.
I'm like, okay.
So then how does on God's greenearth does this thing spread way
faster than Delta?
If it, if the viral loads thesame.
Stephen Kissler (33:37):
Yeah.
Yeah.
So this is, I mean, in a way,this is interesting, cause it's
like a message that we've sortof been repeatedly sort of
putting out.
But I think that it bearsrepeating, you know, with each
new variant because there's thisreally sort of strongly
entrenched and actually wellfounded idea.
In epidemiology.
And I think even more broadlythat that if something is more
(33:58):
transmissible, that means thatthere's, it's, it's generating
more virus because.
You know, that's is more virusmeans more likely to spread in
that kind of thing.
And, and that's true for manyviruses.
I mean, we know that a lot ofour understanding of the
relationship betweentransmission and viral
production comes from HIV wherethe two are very tightly.
And the, to the point where, youknow, there's, there's a very
(34:21):
common phrase in the HIVpositive community.
That undetectable meansuntranslatable right.
So like, if you can't detect thevirus, that means that you can't
spread it.
And, and to detect the virus,they're using things like PCR,
right?
Like the same things that we'reusing to detect stars.
And so, so yeah, from, from ourprevious experience with
viruses, we really expectedthere to be a tight relationship
between the amount of virus thata person produced and how
(34:42):
infectious the virus was.
Based off of what we've foundboth for Delta and for Omicron,
that really doesn't seem to bevery much the case.
Definitely I've had a slightlypeak a slightly higher peak
viral load relative to previousvariants.
But as you said, I'm a chronic.
A lower peak.
And so that doesn't seem to beable to explain why it's more
(35:04):
infectious.
No, some of this has confounded,right?
Because not only were wecomparing Delta against Omicron,
but also more people werevaccinated and.
Between the Delta and theunderground waves.
And so there's a little bit ofconfounding there too, where
we're vaccinated.
People may be less likely toshow peak viral loads, but, but
the conclusion is still thesame, right?
Like, even so Omicron is able tospread explosively.
(35:25):
Why?
So I think there are a couple oflikely reasons for this.
And the most obvious thing is,is, is that there's an increased
infectiousness on a per viralper, per viral particle basis.
And that can happen for a numberof reasons.
One of them is that maybethere's a differences in Omicron
that allow it to be more stableand aerosols.
And that's something that hasbeen studied by a lot of Aerosol
(35:46):
engineers and experts, you know,people who study fluid dynamics
and such.
And, and that, that's a reallyinteresting thing because it
actually does seem like,Sometimes the more transmissible
variants on their viral surfacesactually have different sort of
electrical charges in a way.
Like they have differentproteins that have different
electrical charges that attractdifferent kinds of molecules to
them when they're suspended andaerosols.
(36:08):
Could potentially protect themas they move around from being
sort of denatured and dehydratedin the air.
So that's one possibility.
The other that I think is alsovery likely is that it's better
at binding to ourselves.
It's just better able to A thirdpossibility is that it actually
binds slightly different typesof cells or cells in different
parts of the body.
And that may actually be part ofthe difference in severity as
(36:30):
well.
That it seems like Omicron ismaybe less detectable in the
nose, but more detectable in thethroat.
At different stages ofinfection.
And so maybe that's just the waythat it's getting into our
bodies is a little bit differentand that sort of gives it an
edge for transmission too, butwe don't observe any of that in
the raw amount of virus that'sbeing produced.
So, so I think that's, you know,that that's one of the key
takeaways from the study.
(36:51):
The second thing you know, isthat we, we found that people
remain positive at potentiallyinfectious levels of virus for.
Generally well over five days.
And so w w when we posted thispre-print and we're working on
sort of the full submission nowfor a peer reviewed article, but
this pre-print, we were, we weresort of reviewing that in light
of the CDC has updated guidancethat after five days you could
essentially end isolation.
(37:12):
I, yes, but you should also beaware that like, if you end up
isolation after five days, thereis a good chance that you're
still infectious.
So you still, you know, try todistance and mask and all of
those things.
And I think the best strategy isto use a rapid test to detect.
That you're negative before youleave.
So that would be myrecommendation, but that's sort
of the other thing that we weretrying to evaluate with this
study is just how long are youpositive with Omicron?
(37:36):
And it seems like you can bepositive with Alma crown for
just as long as you werepositive with the other viruses,
the other variants as well.
Matt Boettger (37:41):
Okay, great.
Super helpful.
It seems like Kate measuringviral loads because you, one of
the easiest things to do as ascientist.
Right?
So these other things I'mguessing are these kind of like
more like just Intuit, likeintuitive theories, because I
would imagine.
How would you study a viralproduct called a virus, a virus
(38:02):
particle to see whether it'squalitatively more infectious
than a non I'm?
Sure.
That's a whole other level oflike, I don't even know if it's
even, you can even do that.
If this is just like theoriesof, well, it's not this, and
it's probably this, this, this,or this.
How do we actually define.
We have no clue or maybe you dohave glues.
I have no idea.
Stephen Kissler (38:17):
Yeah.
So, so there are, there arestudies you can run to, to sort
of get closer and closer to thatinformation.
I think probably the next stepand something that we're
thinking about doing is what arecalled viral culture studies.
So then what you can do is for agiven viral load, you can
isolate that virus and spirit ona plate and see if it grows.
And so, so one way.
(38:38):
Of of measuring infectiousnessis to just to see if the virus
is viable on a plate that isseated with the types of human
cells that we have in our noseand whatever.
And so, so that's one way youcan also measure with much
larger epidemiological studies.
You can actually see, you know,you can try to compare very into
variant how many new infectionsare caused.
If you're tracking people veryclosely, then you can maybe
(38:59):
reconstruct.
How infectious, they were atdifferent points in their viral
load trajectory, but that that'sreally difficult and haven't
seen many studies of that typeat all.
But those are really, probablythe two best ways to go about
it.
The other way potentially isusing animal models.
But that's also not very goodbecause.
Our animals, one animal toanother differs, a ton in immune
response and the cells that weuse and such, so that that's a
(39:22):
very rough proxy, but it'ssomething people have tried.
Okay,
Matt Boettger (39:25):
great.
Thanks buddy.
I appreciate the answering allmy questions.
I hope this was helpful to allthe listeners here to get a
little information about.
Totally keep you on your game.
Little newbie mat, trying to gettheir simple questions answered.
All right, well that wraps upthis episode.
Thank you all for listening.
Again, you want to support us.
You can do that atpatrion.com/pandemic podcast or
(39:46):
one-time gift to PayPal Venmo inthe show notes, please leave a
review and leave some comments.
I'd love to get over 200 by.
I think the first week of Marchwould be our two year
anniversary.
It'd be an awesome little giftto us.
And I think that wraps it up.
Of course follow Stephen S T E PH E N K I S S L E R on Twitter.
I did that more and more everyweek now, as my main focus of
(40:10):
updates.
If you want to get ahold of us,matt@livingthereal.com, just an
email, and I will forward itdirectly to Stephen and mark.
Those of you who are newlisteners in the past few
months, you probably thinkingwho in the heck is mark.
I've never heard of this dude.
He used to be a part of ourshow.
He still is, but he's been verybusy at home with a lot of
stuff, but I would imagine he'llreport back sometime soon.
I have a wonderful two weeks.
(40:30):
We'll see you in two weeks.
Take care.
And bye-bye.
You're listening to the pandemic podcast.
We equip you to live the mostreal life possible.
And the host today's crises.
My name is Matt Boettger.
I'm joined once again every twoweeks.
I'm a good, good, good friend,Dr.
Stephen Kissler andepidemiologist, the Harvard
school of public health.
How are you doing in thiswonderful wintry weather?
You got blasted by storms or didyou do.
Stephen Kissler (00:18):
We did.
Yeah, we got buried.
It was it was pretty well therewas, it was about two, two and a
half feet of snow almost.
So, gosh.
Yeah, it was it's pretty wellmelted by now, amazingly, which
doesn't usually happen here.
Usually it kind of lingers andjust turns, you know, ugly
colors from all the cars goingby.
But yeah, it's so, so we'redoing better.
But it just, it's proper winterup here in, by.
Matt Boettger (00:41):
Oh, my gosh, I do not NVU or do not want to be
there.
I just want to be someplace forwarms.
So yeah, it's cold here.
We've had like negative 14waking up in the morning kind of
stuff, and it's just brutal.
And of course the boys, likelet's go outside and play and we
get them all jazzed up and getthem all clothed.
And I'm taking, they're going tolast like two minutes, but
(01:01):
somehow their resiliency and thenegative weather outside.
It's so inspiring.
So yeah, it's winter for most ofus here in the U S a lot of
storms going on, and it's been acouple of weeks and like usual,
there's a bunch of things on mymind.
So this episode might be alittle bit different now it's
probably the same, but justlike, I have a random questions
(01:22):
that I want to throw a pass.
So.
The he'll have brilliant, greatanswers to somebody which I
might catch him off guardbecause I don't know what to do
with some of this stuff, butbefore we get going the same
stuff.
So if you can't leave a review,we love it.
Now.
I can't believe we're almost intwo years of having this
podcast.
It's like mind boggling.
It's like, I like one year feltnormal two years for like, wait
(01:42):
a minute.
That's that went way too fast.
Second year went way, way, waytoo fast.
But nonetheless, the reason whyI mentioned.
It's because I think we havehope, gosh, I don't know how
many reviews.
We have a bunch of reviews, Ithink 180 some or something.
And I thought, man, if you guyswould all hop on and we could
cross the 200 threshold by ourtwo year anniversary would be
(02:02):
phenomenal.
So I was looking Stephen, I waslooking all all the random,
like, have you looked around atthe other random COVID
coronavirus podcasts.
I'm like, I didn't know.
We're kind of like a we're ahit, I didn't know this.
I was looking at the ratings andI'm like, oh, we've got like
4.8, most like 4.3 and a lotthem like 50 to a hundred
reviews.
And I was, I'm like, it'sreally, I was really surprised,
(02:23):
I think partly because you guysare incredible and we have like
a little family.
We're just not, so we don't getinto the politics.
We don't get into all thisstuff.
We're just here to help.
You know, do the best we can toserve.
And Stephen, you guys havetaught me so much about just
embracing complications and Ithink a lot of people love that
and so they dig it and want tolisten more.
So
Stephen Kissler (02:42):
thank you.
Appreciate it.
It's yeah, this has been a lotof fun and yeah, excited to
keep.
Yeah,
Matt Boettger (02:47):
absolutely.
So we've got another one fromJanuary on January 30th, just a
few days ago.
Five stars listener 1, 2 0, 2, 19 says this is the best of all
the COVID podcasts.
It sets the problem in contextso well, and I actually learned
something new and significanteach time, keep up the good
work.
So that's great.
Keeping appreciate that.
Love it.
So if you can't leave a review,do it apple podcasts as well.
(03:08):
If you wanna support usfinancially, we'd love that at
patrion.com/pandemic podcast, aslittle as$5 a month can help or
just a one-time gift.
Do you want to all in the shownotes, that'd be Venmo or PayPal
there's links there.
So let's get going.
I want to start with thisbecause I think let's just start
with experience.
It's been a wacky few weeks forme, Stephen, because outside of
(03:28):
you, which I kind of feel likeyou're kind of in some sense of
anchor of reality for me, I'm mycircles might not necessarily
reflect that.
And you know, what was it twoweeks ago?
We talked about my pediatricianand the thing that he talked
about for those of you whohaven't listened to the
episodes.
Basically, I love him.
We trust him dearly, but just,it was interesting how he was
really not really for the COVIDvaccine for our little ones.
(03:52):
But was for the flu shot.
And just, I was confused bythat.
We talked about this, I thinkthat was two weeks ago.
And just seeing how it's not assimple as things just consult
your primary care physician forthe rock solid answers seems
then my wife went to my primarycare physician and got a similar
answer of like, oh, you know,don't do it to the kids.
And I, you know, I'm justfollowing the data and all this
(04:15):
stuff.
Right.
And so the kids too, for two,it's just really weird.
And then last Friday, Stephen.
My mother-in-law goes to see heroncology.
And she's like, oh, see, youknow, she's like, oh, sorry for
waiting.
I just wanted to get my booster.
And the oncologists made thisvery quick, small response,
like, oh, you know, vaccinesdon't work anyway.
So forget about it.
Right.
So here I am, Stephen three forthree, an oncologist, a
(04:35):
pediatrician, and a familypractice person, all kind of
same, roughly the same thing.
And I'm just so I don't takeinfused.
Blown away by the, even in themedical field of just what's
going out there.
And maybe you will speak back toit.
We were talking about a littlebit about this off.
I know you mentioned the bestperson right now, be mark to
(04:56):
have on, because he's the one onthe ground doing this stuff, but
you've been helpful to kind ofgive the distinction of, you
know, possibly what two kind ofsides are looking at and how it
can get a little blurred attimes.
Stephen Kissler (05:07):
Yeah.
I mean, I think that, you know,the most important thing to
remember is that, you know, Dr.
Epidemiologist, whatever thatwe're, you know, we're people
who are bringing all our ownstuff to all our things.
And I think that it's easy tosort of see a person as the as
the role that they fill.
Especially when it's somebodywith some kind of expertise or
(05:29):
authority especially thinkingabout somebody like a doctor and
then just, you know, rememberingthat, like to some extent A
doctor will has the sameprobability of falling along any
one of the lines of opinion andconviction as anyone else.
And that's, you know, it, but Iunderstand how, you know,
especially with something likevaccination, you would expect
(05:51):
maybe a practicing doctor tohave a different opinion than
the ones that you that you heardfrom them.
And so to try to sort of breaksome of that open, I mean, I
think that Maybe it's easiest toseparate out the advice given to
your kids versus the commentabout vaccines not working.
I think that it's relativelyeasy to dismiss the idea that
that the vaccines areineffective for people who are
(06:12):
older.
I think that that's, you know,there, the evidence of.
Overwhelming that they are safe,effective, hugely valuable in
making sure that people who areadults and elderly are staying
out of the hospital and notdying from COVID-19.
And again they're not perfect,but they, boy, they are
extremely good at what they do.
(06:33):
And I think, you know, that is apretty solid scientific
consensus.
And so I'm not really sure wherethat information would have been
coming from, but that, that justisn't doesn't make sense to me.
Now we can think about kids.
So, there's been a lot ofconversation about Authorization
of vaccines for kidsrecommending vaccines for kids
and sort of what we should do inthis next stage.
And I think that there's alittle bit more latitude because
(06:55):
COVID-19 seems to be a lot lesssevere, generally on a case by
case basis for young kids thanit is for older people.
And there's Also seems like,vaccinating kids may not be a
super effective way atcontrolling spread because there
are so many breakthroughinfections happening.
Right?
So, so those are generally thetwo reasons you would want to
vaccinate somebody is to protectthem from severe disease or from
(07:16):
infection and to prevent thespread of disease.
So, you know, while I still, youknow, from all the evidence,
I've seen it, vaccinating kidsdoes seem to.
Reduce their risk of severedisease and illness as well.
Just bearing in mind that theirabsolute risk the baseline
probability that they end upwith severe disease is already
(07:36):
very low and lower than a lot ofother things, other risks that
they probably face in theirlives from day to day.
And so, you know, I think thatthere is a little bit more space
for complexity there.
You know, the thing is that I'vebeen thinking a lot about sort
of what I would recommend topeople who have young kids in
terms of getting vaccinated.
I'm a strong, strong supporterfor making sure that the
(07:56):
vaccines you know, assuming theycome back with Acceptable safety
and efficacy that they beapproved for use in kids.
And I think that's especiallyimportant for the many kids who
who have respiratory conditionsor who have other conditions
that put them at higher risk ofsevere disease.
I think, you know, and there area lot of.
Out there who areimmunocompromised or who have
(08:19):
asthma or who have downsyndrome, who are at higher risk
of certain respiratoryillnesses.
And for those kids, I think thatit makes an awful lot of sense
to get vaccinated.
Now, I am less certain as towhether it makes sense to have a
blanket vaccine recommendationfor all.
'cause there, I think the costand benefit I'm not really sure
yet how that's going to fall outand it's a lot less clear cut to
(08:42):
me than it is for older peopleand even kids over the age of
12.
And so there's, I do understandsome of the complexity there,
and while I would probablyrecommend.
People get their kidsvaccinated, you know, once, once
the vaccines are approved, I, I,I have a lot more understanding
for both physicians and parentsand guardians who may be less
(09:05):
onboard with that.
Matt Boettger (09:06):
That's great.
And we're going to talk aboutthis later, but Monza, bring it
up now in this, adding to thecomplexity.
So, you know, I just read abouthow the Pfizer vaccine is
getting FDA approved for thelittle ones, I think from two to
five or two to fours.
For at the data, but you know,adding to this thing is I saw
this, I don't know who thisdoctor is.
Zeke Emanuel person is, but youknow, mentioned vaccine children
(09:27):
five and above.
It seems like it's a no braineraccording to this doctor.
And it was a very short articleup in the show notes, but the,
the, the quote that kind ofcaught my attention was this
with the Omicron variant kidsare either going to get the
vaccine or they're likely to geta serious condition of.
It just seems like this is wherejust adds more confusion too.
(09:48):
I think the flames, because Idon't think is an accurate
reflection of what you're seeingand what globally we're seeing
with
Stephen Kissler (09:53):
kids and Alma.
Yeah, no, that's right.
It's and, and I was actuallyjust just as we were doing our
little minute long countdown, Iwas looking up this guy and it
sounds like he's recently justsaid that he misspoke that, that
I think what he was referring towith a severe case of COVID, it
was just a case of COVID thatlike, as opposed to a vaccine
where there's, you know, you're,you get the vaccine and you
(10:14):
might have side effects from thevaccine, you would get a case of
COVID and potentially showsymptoms of some variety.
But but, but I think, you know,all of what we just said stands,
but you're right.
I mean, I think what's, what'smore important here potentially
is just that there's what issaid.
Can't be unsaid in a way.
And so this does contribute to afair amount of confusion as
well.
And to a lack of trust, youknow, this this person is also a
(10:37):
doctor, I think an oncologist.
And and so it's like, you know,it sort of continues to sort of
build this kind of a sense of.
I don't know, just a caution andmaybe I'm lack of trust in the
medical establishment from allangles.
And I think that that's, that'sreally difficult.
That's sort of an even deeperproblem that we've we've got a
(10:58):
lot of work to figure out how tosort out in the coming years.
Absolutely.
Matt Boettger (11:02):
And we're not even needed.
We do a bookmark that as well.
Cause we're gonna talk aboutthat in a second, but just.
How science is under themicroscope by the public in so
many ways, because of justeither, you know, from a lot of
different reasons that we're a,because of our ignorance are not
understanding the field, thebeam, you know, and also just
the way it's communicated andhow it gets confused and those
(11:24):
kinds of things.
But before we get into that, onemore thing about this.
Maybe you can touch on thisbecause.
Pfizer striving to approvethrough the FDA.
The vaccine for the littlekiddos, you know, was weeks ago.
We were talking about how, oh,it looks like the two dose
didn't work.
It's going to go to a threedose.
I would imagine this is going tobe the talk of the town for a
(11:44):
number of months, because numberone, just, just at the baseline
of exposing your little kids toa vaccine is already going to
have a lot of questions behindit because you were in the
protective as much as.
Then when you get a narrativesaying, quote, you know, I'm
using my narrative, it didn'twork, whatever that means.
Right.
So we're gonna do a third shotand then we're ready to go.
(12:05):
And we're going to do two shots.
Wait a minute.
Now I'm confused.
You just told me it didn't work.
In other words.
And now, and part of this I readhere was this idea of looking
through two different, like amicro lens and a macro lens.
And initially it was the microlens.
Now it's the macro lens.
Now of course, now we're addingmore complications.
Of course can cause morehesitancy.
So I thought I knew.
(12:26):
Maybe you can at least helpstart the ball rolling on this
discussion of what's reallygoing on.
And as you were saying before weeven got on the podcast, this is
maybe a reflection of maybe eventhe development of vaccines in
general of how they're lookedupon and those kinds of things
in light of what we'veexperienced with other vaccines
with COVID.
Stephen Kissler (12:43):
Yeah.
So let's, that's great.
I think we can get into some ofthe nuts and bolts of the, the
vaccine approval for young kids.
So, as a, you know, as, as wetalk about.
A long time ago.
I mean, I think that we've,we've been anticipating it
taking a long time to get thevaccines approved for kids in
large part, you know, bothbecause as we were saying, they,
they face a lower, absolute riskof severe disease from COVID-19
(13:05):
and because it's just trickierall of, all of the ethics, all
of the approvals, everything isjust a lot harder, especially
when you start getting into theyoungest age groups.
So I think we're seeing some ofthat.
So, so, so I think a couple ofthings to just Review an
outline.
I'm most familiar with with thePfizer trials.
And and the first thing to noteis that the vaccine doses that
(13:26):
they've been testing in youngkids are quite a bit smaller
than the doses that they've beengiving to adults.
I think they're like on theorder of a 30th of the size so
much, much smaller doses thatthey're giving.
Which, you know, might, it mightalready lead you to suspect
that, you know, maybe they'renot going to have as strong of a
response because you're justgetting a lot less vaccine.
And so, and, and that seems tobe in part what they've seen.
(13:47):
So, these vaccine trials havebeen ongoing and.
Administered vaccines to youngkids.
And they've been trying tomeasure the effectiveness of the
vaccine through a couple ofdifferent ways.
You know, normally the goldstandard for measuring vaccine
efficacy is by.
Giving a control group, aplacebo and giving the
(14:09):
experimental group, the vaccine,and then comparing their risk of
clinical disease as you goforward in time.
And so early on in the pandemic,when we were recruiting the
vaccine efficacy numbers forMadrona and Pfizer and the
different vaccines, that's wherethose were coming from.
So when you see an 80% and 90%,95% vaccine efficacy, that means
that the, the, the experimentalgroup has a.
(14:33):
95% reduced risk relative to thecontrol group of something.
And in that case, it was usuallyshowing symptomatic disease or
symptomatic illness.
Now with kids, there's been abit of a different approach
taken.
And it's in large part again,because kids.
Don't show symptomatic diseaseas often.
(14:53):
And so to do these vaccinetrials in the traditional way
where you're measuringdifferences in the rate of
symptomatic disease you have tofollow a lot of kids and you may
have to follow them for a longperiod of time, simply because
the absolute risk of showingsymptoms is so low.
So to get any sort ofstatistical.
Accuracy around theeffectiveness of the vaccine.
You need a massive trial for along period of time and that's
(15:14):
difficult to do so they look forother proxies.
And one of those proxies islooking at immune response.
So the easiest immune responseto measure is your B cell immune
response.
And so, that does seem to be apretty good proxy for
protection, even though we knowthat other types of immune
response, especially our T cellresponse is the one that's most
effective at keeping us out ofthe hospital and from severe
disease illness.
(15:35):
But that's also much harder tobe.
And so my understanding is thatin these trials from the micro
perspective, what Pfizer hasbeen doing is looking at the B
cell response and they've beenfinding, well, actually it
doesn't seem like we have muchof a response from two doses of
the vaccine.
Maybe we'll try three and see ifwe get to get a better B cell
response.
But as that's been going,they've also been following the
kids in this macro trial.
(15:56):
And over time they've beencollecting more and more data.
And it actually seems like eventhe kids who have been dosed
twice, They do seem to be lesslikely to show up in the
hospital and have a severeoutcomes, even though the
baseline probability is so low,they've been able to distinguish
now finally, because enough timehas passed and enough kids have
been through this trial thatthere does seem to be a reduced
risk of severe disease for kidswho are doubly vaccinated.
(16:17):
And so I think that's part ofwhat's going on here is that
it's just taking some time towrap up.
Evidence.
And because, you know, becausekids face such a lower risk,
absolute risk of, you know,acute, severe illness it was
just a lot, they had to look forother ways to measure.
That
Matt Boettger (16:32):
makes sense.
That's really helpful.
And just shows a little, youknow, you just, I think unfolded
beautifully because it's somultilayered in its complexity,
because you just said that partat the end, which was like the
grand finale, but then youtouched on the other huge piece
at the beginning, which is justgetting these groups in general
is exceedingly difficult.
So you have to obtain the groupsincredibly difficult.
And then the measurementincredibly difficult that you
(16:54):
have a lot of creativecreativity is needed here.
And it just goes back to.
The first thing we talked aboutof pediatricians and physicians
having different responses andsaying, well, I look at the data
it's not working.
And I know we we've eaten thisto death in some regard of
always asking the question, whatis it like, what is the it
they're talking about?
Yep.
You're absolutely right.
When if you're really trying tocontrol the spread of the virus
(17:17):
and then that we're on the samepage, it's not even, it's not
that effective, but it is like,you don't want your kid or your
grandma.
Going to the hospital and thatit is very different, right?
Stephen Kissler (17:31):
Yeah.
Yep.
Matt Boettger (17:33):
Great.
Helpful in that let's, let'sswitch gears for a second and
let's come back to this variantof Omicron, just chat about the
updates.
It seems like nothing to beconcerned about.
I don't know if you could speakin as we didn't talk about this
before we started, but I foundit a little weird how, when the
first version of yeoman Cron,which apparently best these,
these both.
(17:54):
I guess sisters they've kind ofcame at the same time.
They're not really that, butjust one kind of dominated ones.
I don't know.
But anyway, nonetheless, I wasamazed how, when Omicron raised
its first ugly head, there was aseries of the case.
You know, we need to take sometime evaluate where, you know,
maybe week two, we'll kind ofhave this week four, we'll have
this week eight, we might havethis information.
It seemed as though.
(18:15):
As soon as Susan, it came intothe media outlets.
There's already information likeright away.
That was so much faster than thefirst Alma Cron variant, where
like I was hearing right away,like two weeks ago I saw an
article.
Like it looks like it's maybeone to 3% more infectious, like
that's a very quick conclusionafter the first article.
So maybe a couple of things.
(18:36):
I what's the status of this,this ugly.
And to how on earth did we getdata so quickly compare to the
first summit?
Stephen Kissler (18:44):
Yeah.
So, these are, these are great.
So, right.
So, so the, the Omicron that wenormally think of is also one of
the other ways that we've beenreferring to it as B a one.
And I think, you know, we cantalk, I think we've talked about
nomenclature on previousepisodes, so I won't, I won't
get into all of that.
But this, as you said, is aclosely related lineage that
we've been referring to as Andand yeah, so it's, it's not
(19:08):
totally clear where this thingemerged from.
There's been a lot of Andconversation going on to try to
sort of clarify this and try tounderstand sort of like how
these two related lineagesemerged that were actually, you
know, very distantly related towhat we had seen before.
So that's still a bit of apuzzle, but we do know that
they're closely related to oneanother.
Part of the reason we know somuch about it is because it's
actually been circulating for aslong as BA one has been
(19:29):
circulating too.
And so we've, we've had cases ofBA two in the U S since
December.
But they've been sort ofbubbling along at relatively
low.
It's a bit of a mystery rightnow.
Why hasn't taken off and why itdidn't take.
Before BA one did.
Because it does seem to be maybea little bit more infectious.
We're starting to see a BA orsorry, a BA to wave in South
(19:51):
Africa, you know, which was thefirst place to see a major
documented BA one wave.
And so that's interestingbecause it suggests that BA two
can spread in places where BIone has just had a huge impact.
So that's a little bit puzzling,but why is it taking off there?
Here.
So there's a lot, we're nottotally sure about, but one of
the reasons we've gotteninformation relatively early is
(20:12):
because again, within we've beenactually tracking it for a long
period of time, but it's onlystarted now to emerge as
something that is starting tocause an increasing number of
cases.
And also because it's growthrate is.
Relatively slow compared to BAone, even though both are very
fast that also gives us a littlebit more time to sort of track
it because of its growth or itwas explosive than relative to
(20:34):
epidemiological time.
Then we wouldn't be gettinginformation very quickly at all.
But since its growth isrelatively slow compared to BA
one, that also gives us a littlebit more time in terms of the
spread of the pandemic itself toget information about BA too.
So.
The couple of things about BAtoo.
They some of you may rememberhearing I think the guardian had
an article about stealth Omicronawhile ago.
(20:56):
And so I think this is what theywere referring to.
It it's this it's this otherlineage of Omicron.
And the reason they called itstealth Omicron is because boy.
Alright, so, so Omicron.
Like alpha had this strangething that caused one of the
three PCR primers to drop out.
So that means that when you gottested with PCR with both alpha
(21:17):
or Omicron, you would light upas positive on two of the, sort
of two of the, the redundanttags, but negative on the third.
And that's actually reallyuseful for surveillance because
that, you know, that that helps,you know, if it's something
that's likely to be Omicronversus Delta, where just Delta
had all three adults to lit upall three.
Omicron BA one only lit up too,but now BA two lights up all
(21:38):
three again.
And so the reason it was calledstealth Omicron in that sense is
because it on a PCR test, itmight look like Delta, but was
actually related to Omicron.
And so it was a little bitharder to keep track of.
And so, so that's one of thecharacteristics of BA two is
that it's.
It it's lacking this S genetarget failure which is what
that dropout is called.
So that's one thing that thatdifferentiates it.
(22:00):
There are a couple of otherthings, too.
It seems like there's maybeheightened resistance to some of
the monoclonal antibodytherapies.
Maybe one in particular thatstill worked against BI one, but
it seems to have reducedefficacy against BA two.
So there's maybe a higher degreeof immune evasion for BA two
than there was for BA one.
But in terms of, as far as wecan tell clinical severity risk
(22:21):
of reinfection early datasuggests that it's really
actually pretty similar to whatwe've seen with Omicron so far.
Which I don't know if that's, Idon't know if that's good news
or bad news or what kind ofnews, but it's news.
And so, yeah, so there'sthere's, there's roughly what we
know.
I think, you know, once again,South Africa is probably the
place where we're going to get.
The most new information aboutVA two from, because again, they
(22:43):
had such a strong wave of andnow they're seeing a lot of BA
too, and more than many otherplaces in the world, actually,
Denmark has a pretty big BA twowave right now.
And one of the things that we'veseen there actually is that it
seems to be actually trackingthe relative severity of Omicron
pretty closely where it doesn'tseem to be any more severe to
(23:04):
people who are vaccinated.
Then overcrowd was so, so that'sall, that's all I, that I think
is generally good.
Okay.
Matt Boettger (23:10):
Good.
Good.
Well, you know, I don't know ifyou can predict this, this
early, but you know, having theSouth Africa, maybe starting to
have its own way with BA too,what do you think about, is this
something you think is going tohappen to the U S or because of
the inundation of Omicron herethat the first one may not
compete?
Or what do you see the next twomonths?
Stephen Kissler (23:31):
Yeah.
You know, I don't know this is,this is really puzzling it's.
You know, I I've been joiningthese weekly calls with
colleagues about the variantsand then this one has had us
puzzled for a little while.
We're, we're starting to see BAto picking up in the
Northeastern us and in a lot ofplaces that have just seen the
spread of BA one.
And.
So, you know, that that mightlead you to think that you
almost need a BA one wave beforeyou see a BA too, but that also
(23:54):
doesn't seem to be the casebecause Denmark is seeing a big
BA two wave and they reallydidn't get much original Loma
Cron at all.
So that's a long way of sayingwe really have no idea what's
what's going to happen.
And to what extent this is goingto cause continued infections.
I think, you know, it'simportant to note that in South
Africa, the BA two has sort oflengthened the tail of their own
McCrone wave, but it actuallyhasn't really caused much of an
(24:16):
increase yet.
So hopefully Omicron crown stillprovides good protection against
BA too.
That would be my hunch becausethey're so closely related.
But we'll see.
Matt Boettger (24:25):
Okay, let's keep it.
I just saw a comment here fromCatherine.
She's watching live.
Thanks for watching.
She's one of our long timelisteners.
And so, let's continue on.
Cause I want to put a bookmarkon you have no clue because I
think this is because it'sreally going to be an important
piece of our conversation inabout maybe seven minutes or so.
Two more big things I want tochat about.
Related to maybe I have no clue,but this, you do have a clue
(24:48):
about because you actuallyhelped publish this article.
So Harvard medical professorssays it's time to move on from
the pandemic.
Now that's not
Stephen Kissler (24:56):
what we published.
Matt Boettger (25:02):
Yeah, sorry.
Yeah, that was totally twoconnected.
Right?
A Harvard professor.
I just said that.
Yeah.
So that's not what you publish,but this is a medical professor
saying this what caught myattention?
Not so much the article, I guessit did.
Cause I read it.
But this quote that came fromthis, that this is from Dr.
Stephanos kales.
If I said the name, right?
He says once a macaron peaks,subsequent variants are likely
(25:24):
to be even more mild than.
Totally threw me off becausedaddy have likely to see, oh,
wow.
Okay.
This is pretty confident thatcoming from Harvard, that we're,
this is all downhill from here,so we can kind of be in the
coast and you kind of gave anexcellent explanation off the
podcast now.
And to bring it back on thepodcast, explain it.
Cause then we can bring in Dr.
Fowchee as well, and kind ofjuxtapose these two and show
(25:47):
that where these nuances comefrom.
Stephen Kissler (25:50):
Yeah.
Yeah.
So this idea that, that future.
Variance of SARS, cov two willbe less severe is is a common
one and it's not entirelyincorrect.
But I think it's important toknow where it's coming from so
we can put it in the propercontext.
Right.
So, part of the reason why thisdoctor and many other people, I
(26:11):
think rightly believe that it'slikely that future SARS COVID
two variants will be less severeis simply because our immune
systems.
Good at doing what they do thatwith repeated exposures to a
pathogen either throughinfection or through vaccination
our immune systems learn andthey learn better and better.
The more they're exposed,generally speaking, that's often
the case.
And it seems to be the case withSARS COVID.
(26:33):
Were repeated exposures.
You know, that's why the threedose vaccine series is helping
keep people out of the hospital.
That's why people who have beenpreviously infected and
vaccinated are better thanpeople who've just been
previously infected in terms oftheir protection from being, you
know, going to the hospital.
And that's likely to continuethat that as we move forward,
Higher and higher proportions ofthe population will be
vaccinated or previouslyexposed.
(26:55):
So that will reduce, you know,people going to the hospital,
which will help reduce burden onthe healthcare system.
And, and, and I think that's,that is likely to be the case
for sure.
The place where I've also seenarguments for this, that I don't
think are accurate is withrespect to the inherent severity
of the virus itself.
There is some belief thatpathogens naturally evolve to be
(27:15):
less severe and from sort of apop site from a pop evolutionary
perspective.
That kind of makes sense becauseyou know, the idea is that if a
pathogen kills its host, that'snot beneficial to the pathogens.
So a pathogen will evolve to beless severe.
So it doesn't kill its host.
So it has opportunities totrain.
It's true, but only true for apathogen that can only transmit
(27:35):
after it's caused a severedisease, but that's not true for
SARS.
COVID two, most of SARS COVIDtwo transmission happens before
you even realized you've beeninfected.
So there's no selection pressurefor it to become less severe
because it's already done it'stransmitting by the time it
causes any sort of severedisease.
So, so the severity, theinherent severity of SARS, cov
two is just totally decoupledfrom its transmissibility.
Maybe not totally, you know,nothing in biology is totally
(27:57):
disconnected, but you know, forour purposes here, we can say
that.
So, so, so is that statementright?
Well, yes and no.
I, I think that, you know,generally speaking where our
experienced impact with COVID-19is likely to be less severe with
future variants because ourimmune systems are good.
But you know, one of the areaswhere this really matters is for
people who can't mountain mean agood immune response, right.
For people who areimmunocompromised for you know,
(28:18):
that for them future variants ofSARS, COVID two are likely to
be.
Just as severe, maybe notjustice severe, but much more so
than the population level datasuggests.
And I think that's really worthbearing in mind that there are
going to be a lot of peoplestill living around us that
when, for whom, you know, this,this isn't just another, you
know, Mine are cold.
And, and won't be for a verylong time if ever.
(28:40):
And so I think, you know, Ithink that that is worth bearing
in mind.
Now the other thing that we weretalking about at the beginning
that relates to this is thatwhile I agree that the most
likely scenario that our averagelived experience with COVID-19
is going to become less severewith future variants as our
immune systems get their.
Exposure.
That's not to say that we canrule out the less likely, but
still possible scenario that wewill end up with a variant that
(29:02):
is more severe.
And so while I don't thinkthat's something that like we,
as a.
Nation and world need to benecessarily concerned about all
the time.
That is something that we asepidemiologists, if we, as
doctors are going to beconcerned about thinking about
all the time, because there'sthis trade-off between
likelihood and hazard that weconstantly need to be bearing in
(29:24):
mind where we, even, ifsomething is a rare scenario, If
it's a really bad scenario, westill want to be prepared for
it.
And so that's one of the thingsthat we'll be thinking about a
lot.
And so, you know, all of that isto say that I don't, I don't
anticipate that we're going tohave a variant that totally
escapes our immunity and bringsus all the way back to square
one with COVID-19.
(29:45):
Is it a real remote possibility?
Yes.
I mean, it's also a remotepossibility that we end up with
a flu pandemic next year.
And we, you know, we have anentirely different pandemic to
deal with as well.
I'm sorry.
I know I have probably half ofour listeners shifts hearts just
dropped out of their chests,but, you know, and, and again, I
want to emphasize the rare, youknow, this is, this is not
likely, but it is a possibilityand something that we're
(30:06):
thinking about as well.
So yes, I think with thispandemic, as in my own life and
our own lives, we're always sortof seeking after this certainty
and reassurance and believe me,I know this as well as anyone
I'm constantly trying to find.
Comfort and reassurance and, youknow, certainty that things are
going to be okay, whether it'swith this pandemic or with
anything else in life.
(30:28):
And so I think it's a reallynatural thing to really
gravitate towards these kinds ofthings that like, oh yeah,
future variants are going to beless severe.
We can sort of be done withthis.
And I think that that isprobably operationally a
reasonable way to live one'slife going forward.
But I think the most accuratestatement is that yes, that's
probably true, but we're also.
Keep bearing in mind that therethere still remains some risk
(30:48):
and and, and that risk is goingto be why I keep doing what I
do.
Matt Boettger (30:52):
That's perfect.
I love it.
Cause you know what number onefull, I need to make a, an
apology.
This is not the article thatyou're talking about.
This.
I, my eyes went to a differentwhole different article.
So when I mentioned aboutStephen publishing article, it
has nothing to do with this one.
It's the next one we'll talkabout, but I think this is a
great.
Like place of discussion note,because here's where I am at.
(31:13):
Like, I have a, tends to be alittle too optimistic.
Ah, it'll be fine.
Right.
That's my thing.
It'll be fine.
It'll be fine.
So I would make an, a terribleepidemiologist.
Like it would be literally wouldnot want to put the world's fate
in my hands because you wouldhear, oh, plague.
Ah, I think would be fine, youknow, and we just, we just
stopped there.
Right.
So, so this is where the.
(31:34):
Yeah, like the eternaloptimists, whatever.
And they knew where you internaltestaments, whatever those are
kind of pigeonholed people, butlike, it takes both to really be
able to cope with life becausewe need people who, and this is
where I say you have like theStefanos kales.
Well, I'm not gonna, I'm notgonna put him in a box, but
like, Maybe I'm going to putthem in a box just for a second,
but just for the caricature,not, not for any, just to try to
(31:54):
make this kind of this dichotomyof like, okay, I'm optimistic,
it'll be fine.
No big deal.
It should be less.
And then you have someone likeFowchee, he was being criticized
nonstop, like a fearmonger.
And I think this is, I thinkStephen, you just really helped
to show the nuance.
It's not being a fearmonger it'sdoing his job.
Like, I mean, he's, you know,this quote, it was in the same
article.
He says.
(32:14):
Though he were talking aboutFowchee.
He's cautiously optimistic aboutthe pandemic.
Dr.
Anthony Fowchee said anothervariant could arise.
That alludes current immunity.
I hope that's not the case.
He said, I don't think it willbe, but we, but we have to be
prepared.
Right.
So I think you just, you hitthat were Fowchee is not a
fearmonger he's doing his job.
He's not going to overlook thedata that there's a possibility
(32:35):
of.
Ah, you know what?
I'm a really good scientist, butlet's just forget about, let's
just focus on the optimism.
Right.
You know?
The we who's the, we, I think Iwant to take myself out of that
week and be like, that's youStephen?
That's you Dr.
Fowchee.
You guys think about that.
You guys make sure we're okay.
I'm going to focus on theoptimism, but be also cautious
as well.
So I like that.
(32:56):
Thanks Stephen, for bringingthat to the attention.
Now, let's go to the lastarticle here, and this is when
we're at.
An article that was grounded inyour research and somebody took
it and did again, not the,probably the best articles, very
short from nature, nature,magazine, or nature, the nature
article and the, the, the, thetitle of this one is how does
Omicron spread so fast, a highviral load?
(33:17):
Isn't the answer?
And so I wanted you to talkabout, because I read it, it was
very short.
Three minutes long to read.
And I got no conclusion aboutit.
It basically just said, Hey,look, there's the viral loads
the same, in fact Delta, maybe alittle bit higher, but then it's
landed the plane somewhere.
I'm like, okay.
So then how does on God's greenearth does this thing spread way
faster than Delta?
If it, if the viral loads thesame.
Stephen Kissler (33:37):
Yeah.
Yeah.
So this is, I mean, in a way,this is interesting, cause it's
like a message that we've sortof been repeatedly sort of
putting out.
But I think that it bearsrepeating, you know, with each
new variant because there's thisreally sort of strongly
entrenched and actually wellfounded idea.
In epidemiology.
And I think even more broadlythat that if something is more
(33:58):
transmissible, that means thatthere's, it's, it's generating
more virus because.
You know, that's is more virusmeans more likely to spread in
that kind of thing.
And, and that's true for manyviruses.
I mean, we know that a lot ofour understanding of the
relationship betweentransmission and viral
production comes from HIV wherethe two are very tightly.
And the, to the point where, youknow, there's, there's a very
(34:21):
common phrase in the HIVpositive community.
That undetectable meansuntranslatable right.
So like, if you can't detect thevirus, that means that you can't
spread it.
And, and to detect the virus,they're using things like PCR,
right?
Like the same things that we'reusing to detect stars.
And so, so yeah, from, from ourprevious experience with
viruses, we really expectedthere to be a tight relationship
between the amount of virus thata person produced and how
(34:42):
infectious the virus was.
Based off of what we've foundboth for Delta and for Omicron,
that really doesn't seem to bevery much the case.
Definitely I've had a slightlypeak a slightly higher peak
viral load relative to previousvariants.
But as you said, I'm a chronic.
A lower peak.
And so that doesn't seem to beable to explain why it's more
(35:04):
infectious.
No, some of this has confounded,right?
Because not only were wecomparing Delta against Omicron,
but also more people werevaccinated and.
Between the Delta and theunderground waves.
And so there's a little bit ofconfounding there too, where
we're vaccinated.
People may be less likely toshow peak viral loads, but, but
the conclusion is still thesame, right?
Like, even so Omicron is able tospread explosively.
(35:25):
Why?
So I think there are a couple oflikely reasons for this.
And the most obvious thing is,is, is that there's an increased
infectiousness on a per viralper, per viral particle basis.
And that can happen for a numberof reasons.
One of them is that maybethere's a differences in Omicron
that allow it to be more stableand aerosols.
And that's something that hasbeen studied by a lot of Aerosol
(35:46):
engineers and experts, you know,people who study fluid dynamics
and such.
And, and that, that's a reallyinteresting thing because it
actually does seem like,Sometimes the more transmissible
variants on their viral surfacesactually have different sort of
electrical charges in a way.
Like they have differentproteins that have different
electrical charges that attractdifferent kinds of molecules to
them when they're suspended andaerosols.
(36:08):
Could potentially protect themas they move around from being
sort of denatured and dehydratedin the air.
So that's one possibility.
The other that I think is alsovery likely is that it's better
at binding to ourselves.
It's just better able to A thirdpossibility is that it actually
binds slightly different typesof cells or cells in different
parts of the body.
And that may actually be part ofthe difference in severity as
(36:30):
well.
That it seems like Omicron ismaybe less detectable in the
nose, but more detectable in thethroat.
At different stages ofinfection.
And so maybe that's just the waythat it's getting into our
bodies is a little bit differentand that sort of gives it an
edge for transmission too, butwe don't observe any of that in
the raw amount of virus that'sbeing produced.
So, so I think that's, you know,that that's one of the key
takeaways from the study.
(36:51):
The second thing you know, isthat we, we found that people
remain positive at potentiallyinfectious levels of virus for.
Generally well over five days.
And so w w when we posted thispre-print and we're working on
sort of the full submission nowfor a peer reviewed article, but
this pre-print, we were, we weresort of reviewing that in light
of the CDC has updated guidancethat after five days you could
essentially end isolation.
(37:12):
I, yes, but you should also beaware that like, if you end up
isolation after five days, thereis a good chance that you're
still infectious.
So you still, you know, try todistance and mask and all of
those things.
And I think the best strategy isto use a rapid test to detect.
That you're negative before youleave.
So that would be myrecommendation, but that's sort
of the other thing that we weretrying to evaluate with this
study is just how long are youpositive with Omicron?
(37:36):
And it seems like you can bepositive with Alma crown for
just as long as you werepositive with the other viruses,
the other variants as well.
Matt Boettger (37:41):
Okay, great.
Super helpful.
It seems like Kate measuringviral loads because you, one of
the easiest things to do as ascientist.
Right?
So these other things I'mguessing are these kind of like
more like just Intuit, likeintuitive theories, because I
would imagine.
How would you study a viralproduct called a virus, a virus
(38:02):
particle to see whether it'squalitatively more infectious
than a non I'm?
Sure.
That's a whole other level oflike, I don't even know if it's
even, you can even do that.
If this is just like theoriesof, well, it's not this, and
it's probably this, this, this,or this.
How do we actually define.
We have no clue or maybe you dohave glues.
I have no idea.
Stephen Kissler (38:17):
Yeah.
So, so there are, there arestudies you can run to, to sort
of get closer and closer to thatinformation.
I think probably the next stepand something that we're
thinking about doing is what arecalled viral culture studies.
So then what you can do is for agiven viral load, you can
isolate that virus and spirit ona plate and see if it grows.
And so, so one way.
(38:38):
Of of measuring infectiousnessis to just to see if the virus
is viable on a plate that isseated with the types of human
cells that we have in our noseand whatever.
And so, so that's one way youcan also measure with much
larger epidemiological studies.
You can actually see, you know,you can try to compare very into
variant how many new infectionsare caused.
If you're tracking people veryclosely, then you can maybe
(38:59):
reconstruct.
How infectious, they were atdifferent points in their viral
load trajectory, but that that'sreally difficult and haven't
seen many studies of that typeat all.
But those are really, probablythe two best ways to go about
it.
The other way potentially isusing animal models.
But that's also not very goodbecause.
Our animals, one animal toanother differs, a ton in immune
response and the cells that weuse and such, so that that's a
(39:22):
very rough proxy, but it'ssomething people have tried.
Okay,
Matt Boettger (39:25):
great.
Thanks buddy.
I appreciate the answering allmy questions.
I hope this was helpful to allthe listeners here to get a
little information about.
Totally keep you on your game.
Little newbie mat, trying to gettheir simple questions answered.
All right, well that wraps upthis episode.
Thank you all for listening.
Again, you want to support us.
You can do that atpatrion.com/pandemic podcast or
(39:46):
one-time gift to PayPal Venmo inthe show notes, please leave a
review and leave some comments.
I'd love to get over 200 by.
I think the first week of Marchwould be our two year
anniversary.
It'd be an awesome little giftto us.
And I think that wraps it up.
Of course follow Stephen S T E PH E N K I S S L E R on Twitter.
I did that more and more everyweek now, as my main focus of
(40:10):
updates.
If you want to get ahold of us,matt@livingthereal.com, just an
email, and I will forward itdirectly to Stephen and mark.
Those of you who are newlisteners in the past few
months, you probably thinkingwho in the heck is mark.
I've never heard of this dude.
He used to be a part of ourshow.
He still is, but he's been verybusy at home with a lot of
stuff, but I would imagine he'llreport back sometime soon.
I have a wonderful two weeks.
(40:30):
We'll see you in two weeks.
Take care.
And bye-bye.
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