November 29, 2021 • 43 mins
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Things Discussed on Episode:
- Scientists rapidly identified the Omicron variant. But firm answers about its impact could take weeks
- Covid: South Africa 'punished' for detecting new Omicron variant
- South African doctor who raised alarm about omicron variant says symptoms are ‘unusual but mild’
- Moderna Announces Strategy to Address Omicron (B.1.1.529) SARS-CoV-2 Variant
- Pfizer said an updated version of its COVID-19 vaccine will be 'ready in 100 days' if the new Omicron variant is resistant to its current vaccine
- COVID-19 booster shots might offer better protection than the first two shots, study says
- Children and teens are less likely to need Covid-19 boosters, Fauci says. Here's why
Mark as Played
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 face
today's crisis.
My name is Matt Boettger, andI'm joined with my one good
friend once again, Dr.
Stephen Kissler andepidemiologist at the Harvard
school of public.
From one us citizen to anotherhappy Thanksgiving.
Stephen Kissler (00:15):
Hello?
How are you?
Hello?
Matt Boettger (00:17):
Good, good, good.
How was your Thanksgiving?
Was it splendid full of Turkey,stuffing, gravy, everything to
make you go into a coma?
Stephen Kissler (00:23):
It was splendid and we did go into a food coma.
A little bit unconventionalthough.
There's so we stayed in Bostonthis year.
We just had two friends over, soit was a pretty small
Thanksgiving.
So the bird was fittinglysmaller too.
We ended up doing chickeninstead of Turkey.
And yeah, but otherwise it wasa.
Matt Boettger (00:40):
Awesome.
Yeah, we're here.
We had a wonderful Thanksgivingand got to see Nana.
The boys were just incrediblyexcited.
It's been all day.
We had planned not to cook thatmuch on Thanksgiving and to try
to be with Nana and the boys.
But in fact, we cooked all day.
So a big that's one of ourregrets where next year we're
doing.
So
Stephen Kissler (00:59):
that's the way to do
Matt Boettger (01:02):
it is so those of you who have family and have
little ones, you know what,probably the feeling I'm
guessing if you have to cook thewhole meal yourself with like
kids under eight or seven.
But it was a wonderful time.
It's still been a wonderfullywarm weather here in Colorado,
which is a great, but also.
Fearsome with the mountains.
It's pretty dry.
We went to go cut our tree down.
We go down to the Mount, we goup to the mountains and cut her
(01:23):
own Christmas tree and we don'thave there.
And there was no snow anywhereto be found, which was our first
year going up with nothing.
So, hopefully we get someprecipitation soon.
Now we're giving a gearing upfor Christmas.
So during this time, Stephen,something really just percolated
quickly.
I couldn't believe this.
And so well, you know what,before I do that, let's just
quickly say.
(01:43):
If you can support us, pay apatrion.com/pandemic podcast,
this is a$5 a month can help ora one-time gift, a PayPal Venmo
in the show notes.
And then also before I get intothe craziness with OMA Cron and
the variant, there were tworeviews that came in that were
wonderful.
Let's see here.
I'm trying to look at the firstone here.
My notes are going, oh yeah.
So we're going to go and skipthat for now because it just
(02:04):
skipped all over, but we had twogreat reviews.
Thank you so much.
Keep them coming.
Let's see if I can get this onegoing.
Here we go.
I'm very happy to discover thispodcast.
I've been listening mainly inthe last couple of months.
I really appreciate the scope ofthe information.
What is discussed is backed upby the most recent data in a
rapidly changing environment.
It is really helpful to havedata, to make informed decisions
about behaviors this week, whichwas probably a couple weeks ago.
(02:26):
For example, they providedconcrete ways to help make
family gatherings more safe.
Thank you for your work.
You're doing that.
It's awesome.
That is from counts 11.
So love those usernames.
So thank you so much north woodsor wherever your name is.
I'm assuming that's not yourreal name.
But thank you so much for that.
And there was another one.
I won't read it now, but we'llget into this, but I just want
to pick your brain for that.
(02:47):
Another five-star review fromdragon wings, one to 1 21, but
this person, he or she works inthe jail.
So apparently he or she haswritten a public service and
talking about how this idea oflike, wait a minute.
It seems as though in the jails,it's oftentimes the first to hit
away.
And so why not use this as anindicator of what's to come?
And has this been somethingthat's been looked at among your
(03:10):
colleagues or at least maybe notjails, but in general, like
different little pockets,information, pockets by which
seemed to get Kindle fasterbefore other places.
Stephen Kissler (03:19):
Yeah.
So this is a great question andabsolutely something that we've
been thinking about and workingon over the course of the
pandemic.
So, Earlier on in I guess thiswas probably like mid 20, 20.
I had a, a series ofconversations with a reporter
named Deborah Becker at WBURhere in Boston.
And among the things that shereports on his his, his
presence.
(03:40):
And she had been doing that prepandemic as well, but really,
especially once the pandemichit, there were a lot of
questions about the role of thepandemic in prisons the extent
to which prisons were equippedto handle outbreaks and sort of
what we can.
Well, we can infer from what'shappening in prisons for, you
know, for the wider populationand vice versa, what, you know,
how we can manage the spread ofCOVID in prisons based off of
(04:03):
what's happening in the widercommunity.
So it's true that in a lot ofcases That in I'll say more
generally that these sort ofcongregate care settings or, or
places where lots of people areliving together in close
proximity.
So prisons of course, but alsonursing homes long-term care
facilities and places like thateven schools to some extent
(04:24):
although many of those wereclosed early on in the pandemic.
Are definitely places where thevirus can often gain an early
foothold.
I think one of the clearestexamples of that with some of
the the first major wave, whichhappened in the summer in
Arizona one of the initialindicators of that was a major
prison outbreak.
And so, it's absolutely truethat that in many cases These
(04:47):
places where lots of people arein close proximity.
And prisons is of course, one ofthe, one of the key examples of
that that we see early spread,but it's not always the case
because a lot of times theseplaces are also places where
there's less interaction withthe surrounding community.
And so oftentimes what we see isthat COVID will.
Spread rapidly through one ofthese communities.
(05:08):
And on average, they're probablyon the early end, but sometimes
they're not you know, sometimesthey get spared to some extent
until later on in the wave.
And then they see their majorsurge.
And one of the difficulties withprisons both was protecting the
prison population itself.
And with sort of inferring, youknow, what might be in store for
the rest of the population isthat.
(05:29):
You know, oftentimes theirtesting is really frankly, not
up to snuff.
That's been one of the realdifficulties is getting solid
information about the number ofCOVID cases in prisons, because
as you can imagine, there tendto be pretty underserved.
And there's not a lot ofinterest in, you know, testing
doing surveillance withinprisons, even though frankly,
there really should be.
And so, In a lot of cases,prisons are places where
(05:51):
absolutely there's a lot ofCOVID transmission happening.
But a lot of it, we just don'tknow an awful lot about.
And so there's been a lot ofeffort there for prison rights
advocacy which, you know, and Ithink that this you know, gets
towards a much larger sort ofprinciple of the overall
pandemic, which is the, youknow, we, we are all in this
together, you know, rich, poorIn prison out of prison, you
(06:12):
know?
And and it's easy to adopt thesort of protectionist mindset
and to sort of only payattention to what's happening in
our population and the peoplethat we normally see.
Even speaking from just anepidemiological perspective,
that's a foolish thing to do.
Because the virus is going tospread everywhere and, you know,
none of us is healthy or safeuntil all of us is healthy and
(06:33):
safe.
And the, and so I think thatthat really, really strongly
advocated.
Better surveillance, better carein all of these vulnerable
populations including the prisonpopulation.
So very great point, definitelysomething that we're looking at,
but also something that we needto do a lot more work on to both
protect the prison population assuch and to then, you know, have
a better sense of what'shappening in those communities
(06:55):
so that we can have a bettersense of the broader community,
both what's to come and what'salready happened.
Matt Boettger (07:00):
Great.
That's perfect.
And thanks for making thatnuance between like, like the
descriptive and theprescriptive, like it's one
thing to describe what's goingon in prisons and how that might
be able to tell us what's comingin the future.
But at the same time, that's notthe point because they're not
meant to be a series of lab ratsto let us know what's coming.
And in fact, there's aprescriptive element by which
the it's like, it's going backto way back in March of 2000, we
(07:22):
talked about that great CS Lewisquote.
The rats and the seller.
And when you quickly turn on thelight too, you see the rat and
he's slowly being around.
They go away, but the lightdidn't cause a lot, the rats
it's the suddenness.
And so the suddenness of thispandemic has really revealed
some of the areas by which wehave.
We are weak in participating inhelping those who need that
assistance.
And so we need to use that as aprescription to make things
(07:45):
better.
So we don't have to use this asa scarily as a way to protect
ourselves, but let's continueon.
Before we get to Alma Cron.
Let's talk about the flu becauseyou know, it's been, I've been
out of a week.
I've been trying to take sometime off family.
I haven't really beenparticipating in looking at the
news on the flu that much andselling to get your analysis of
like what you've heard or seenit right now with the flu
(08:06):
compared to last year.
Is it re raising its ugly headis it's it's it's you know,
where are we at when it comes toflu?
Yeah.
Compared to last year, but lastyear, but in general.
Stephen Kissler (08:18):
Yeah.
So, flu is spreading here in theUnited States and around the
world.
And currently in most placesacross the U S it's still at
pretty low levels which is notterribly surprising.
Usually our flu season starts tocome in, you know, maybe around
now, but oftentimes it's skeweda little bit later towards
January, even February when westart to see a lot of high
(08:39):
levels of flu transmission.
So it's a little early to say itdoes look like some places in
the mid and mountain west.
Actually New Mexico has quite afew cases right now.
It seems.
But a lot of the rest of thecountry is.
So bad at the moment.
The main flu strain that we'reseeing in the U S right now is H
three and two.
So with flu, we have a couple ofdifferent strings right now is
sort of the two major ones are Hone N one and H three and two,
(09:02):
and every three or four years,they sort of trade off.
So you'll have three or fouryears of age, three and two, and
then three or four years of ageone-on-one they differ a little
bit in terms of how infectiousthey are, how severe they are.
But for the most part, they'repretty interchangeable.
And so, the, the fact that it'sthat particular strain
circulating is more of sort of aepidemiological curiosity and
something that I'm payingattention to, but it's not
(09:22):
necessarily something that willaffect our day-to-day lives.
So right now transmission mostlyseems low across most of the.
And is roughly in line with whatwe expect to see around this
time of year on average.
But we're watching it closelybecause there's definitely flew
around and cases are starting totick upwards in line with how
they would normally tickupwards.
So I do expect there to be a fluseason this year.
And it's impossible to say atthis point how bad it will be.
(09:45):
One of the things, of coursewe've been thinking about a lot
now, too, is that, you know,especially with the news about
the Omicron variant you know,the question is now to what
extent will these things besuperimposed on top of each
other?
And that of course could causesome issues as we move forward.
But right now there's not a lotwe can say about what exactly is
in store.
Matt Boettger (10:02):
Then you made a segue perfectly to Omicron.
So this was crazy Stephen,because like, you know, it was
funny.
On Thanksgiving.
I was talking to mysister-in-law, you know, and
she's like, you sound like anepidemiologist to make it
because I hang out with one.
So I'm just the messenger.
She was wanting informationabout like, you know, the
(10:24):
booster, this kind of stuff.
And then I was just talkingabout, oh yeah, we're.
You were talking about how, youknow, we do think that some
point in time, hopefullyrelatively soon that these
variants are going to like levelyour time.
And, you know, I wouldn't evenlook at the news.
I literally, as I'm probablytelling her, this is probably
now blowing up all over in themedia.
Cause I was not checking.
Then that night I checked inlike, oh my gosh, just so I was
(10:44):
telling her about this story.
This blew up and it's like,literally overnight.
And I want you just to go and goevery direction you want to on
this.
But like, you know, my questionsare, first of all, like how did
this become a sensationovernight?
And where are we at with this?
How bad could it be?
I know we're still in the woods.
It's still early on.
(11:05):
But the who came out with stuff,Pfizer is talking about it with
journeys, talking about it.
Gosh, it's probably gonna be onSesame street next week.
Right.
So
Stephen Kissler (11:14):
where are we?
Does the Greek alphabet.
Matt Boettger (11:18):
So where, where are we in this?
And.
Yeah, let's start with that.
Before we talk about how thismight change our game plans for
the next three weeks or so as wegear up for Christmas.
Stephen Kissler (11:30):
Oh boy.
Yeah.
So, I can maybe start by talkingabout my own experience,
learning about the variance.
So similarly, you know, we'd hadThanksgiving.
I was none the wiser and it waslargely away from my phone.
And it wasn't until that eveningthat I sort of checked in and
noticed that a lot of mycolleagues were already starting
to talk about this new variantwhich at that point didn't even
(11:50):
have a name.
It only took about a day for theworld health organization to
give it the name of Omicron andclassify it as a variant of
concern which is unbelievablyrapid.
And so one of the things that Iwant to talk about as we move
forward to sort of like why.
So quick.
And so, yeah, so I, I tried tolearn as much as I could about
it in the next hours and days,basically.
(12:11):
So basically everything I'mgoing to spread back to you all
are the things that I've beenstudying up on over the last few
days and the sorts of thingsthat my colleagues have been
talking.
And we've, we sort of findourselves in, again, this
situation that we've sofrequently found ourselves in
where you know, we, as thescientific community, as well as
the broader public are trying tomake sense of something where
the pieces just aren't quiteadding up yet.
(12:33):
And eventually we'll have theright mental model to understand
what's happening and why all ofthe things that we've observed
have happened.
But it's really interestingbecause I don't think that it's
often that we get to see.
As sort of, you know, as thehuman population sort of putting
together knowledge on the fly.
And we've gotten thatopportunity a lot of times
during this pandemic and here'shere's yet another one.
So after we talk a little bitabout sort of the, the speed
(12:56):
with which this gainedattention, I also want to talk
about some of the unknowns whatwe know, what we, don't, why we
don't, when we will.
And those sorts of those sortsof questions as well.
So, You'll notice them.
I'm also clearing my throat alittle bit.
I I I got boosted this pastSaturday, and so I'm still
feeling slightly under theweather.
I think that my lymph nodes arestill draining, so that's way
(13:17):
too much information for all ofyou on the podcast, but I just
want to be, I just want be sure.
With with what's going on overhere.
I can talk about that experiencetoo, because I think that
actually one of the bigquestions with over is, is the
question about vaccines andboosters and will they hold up.
So, as I forget all of thesedifferent points that I've just
made please remind me because Iinevitably will.
Right.
So, so I think that one of thethings that has been especially
(13:40):
Remarkable about this variant.
And this is true for me as wellas for many of the people who
aren't specialists.
So I've spoken with just howquickly this variant has gained
attention.
So like what happened here?
I think there are a couple ofthings behind this, so first and
I think probably mostimportantly it was a lot of very
swift and responsible efforts onthe part of the south African
(14:02):
public health administration.
They detected that somethingstrange was going on, they were
seeing, you know, South Africahas just made it through a major
Delta wave of infection.
And then they started to see anincrease in cases in particular,
one of the things that raised.
Is that they're PCR tests, whichwe talked about a long time ago,
usually have three differenttargets.
(14:23):
So basically your, your tests,your PCR tests will try to
detect three distinct parts ofthe virus.
And they noticed that in a lotof cases, they were getting
positives on two of those partsthat a negative.
If you cast your minds way backto the beginning of this year,
that's the same thing thathappened with the alpha variant,
where there was this targetfailure this SG and target
failure or ESSA dropout that washappening with the alpha variant
(14:46):
because the, the spike proteinof the virus was mutated in this
one part that the PCR testsdetected.
So the tests were still turningpositive.
It's not that they weren't.
But they noticed that we're sortof, Groundhog day style
repeating this, where, where allof a sudden there are these
dropouts again.
And so they're like, well,what's happening.
So they very quickly got on it.
They started sequencing some ofthese samples and noticed that
(15:08):
what they were sequencing wasreally pretty different than a
lot of what they had seencirculating before.
So more on that in a moment, butthey they detected the variant
and very quickly held a pressconference.
We're very clear about what theyknew, but they didn't know and
shared this information with theworld which is exceptional.
That's exactly what we want.
(15:28):
And so.
As opposed to a lot of othersituations in which it's taken a
lot longer for these things tobe detected.
There were a couple of strokesof luck and a couple of strokes
of genius.
And that got us into thissituation where we detected this
thing very quickly, very earlyon.
And so it was really able tospread the information was able
to spread very quickly aroundthe world to the great, great
credit of the south Africanscientific community and
(15:50):
political community as well now.
Yeah.
So I think, I think I'll leavethat there for now.
We can sort of circle back to abroader discussion
Matt Boettger (15:57):
on that in a moment.
Quick question on that.
So then just so you know, yousaid the alpha, did the Delta
not have that because, so then,so then it didn't have that kind
of, so it was gone for a whileand then it raises its ugly head
again.
Okay.
Exactly.
Continue to get that narrative.
Stephen Kissler (16:13):
Yep.
Yup.
And so, you know, that's, that'san interesting point because I
think the next thing that Youknow the question of like, why
is there so much attentionaround this?
You know, we've had, we've hadmultiple other variants.
We've had, you know, the mewvariant and the Lambda variant.
And in a lot of previouspodcasts, we sort of talked
about these and it's sort oflike, yeah, these are like
issues for certain parts of theworld.
But like ultimately, you know,none of them have shown this
(16:33):
really at the ability toout-compete Delta.
And so, you know, something topay attention to you, but, you
know, Delta's the thing.
So why, why this one now?
And so there are a couple ofreasons.
So first while South Africaactually has a relatively low
vaccination rate compared to TheU S in many European countries,
although a high vaccination raterelative to many of its
(16:54):
neighbors in the Africancontinent it has also had a lot
of spread.
And so despite relatively lowvaccination rates there out to
be a pretty high level ofprevious of immunity from
previous infection.
So already starting to see anuptick in cases with a new
variant is a bit of an alarm andactually begins to point towards
something that looks like maybeimmune evasion.
So that's, you know, sort of thefirst alarm bell that started.
(17:18):
So as they sequence to the viruswe were able to sort of get some
more insight into what mightmake this variant special.
And so the second thing that wassuper alarming was the, just how
mutated to this virus is.
It really is carrying a lot ofmutations relative to anything
that we've seen previously.
(17:38):
And so.
It's really hard to pinpointwhere exactly it came from.
I mentioned that it has this SGand dropout, and so in some
sense, that kind of makes itsound similar to the alpha
variant.
And maybe it's more closelyrelated to that, but it really
seems like this is somethingthat evolutionarily has kind of
diverge pretty profoundly fromprevious things that have been
(17:59):
circulating and has picked up alot more mutations and things
that we've seen previously.
A lot of these mutations.
Spike domain of the V of thevirus.
And so what that points to isthat it's been sort of actively
selected for and that thesearen't just a bunch of random
variants or a bunch of randommutations, but actually that
they probably, you know, andI'll talk more about the
(18:20):
implications of that in amoment.
And then, yeah, and then a lotof the mutations that we've seen
There've been laboratory studiespreviously that have looked at
the effects of different singlepoint mutations.
So you can take you, you cansort of deconstruct the virus
and pull off its differentsegments, including the spike
protein so that the virus is nolonger sort of infectious.
It can't spread, but then youcan do these laboratory
(18:41):
experiments.
That look at how how well thatspike protein binds to different
human cells and how well theantigens that are produced by
that protein are, are, areneutralized by human antibodies,
for example.
And so you can do a lot ofexperiments that can then
implicate different mutations ofsaying like these particular
(19:01):
mutations.
If they show up in nature wouldbe.
It turns out that the OMAvariant contains a lot of those
mutations, both mutations thathave been implicated in better
binding to the human receptors.
So probably a greatertransmissibility and places that
tend to be immunogenic.
So places where we expect there,if there are mutations that it
(19:21):
might get around some amount ofof our immune response.
So that's another reason why itgained so much attention so
quickly is because it was like,wow, this is really sort of, you
know, coming out of it's unlikethings that we've seen before,
and it's really carrying a lotof these mutations that at least
in theory could give it a lot ofthese concerning
characteristics.
So I think that those, thosethings combined are part of why
(19:43):
it's risen so quickly to thegeneral attention.
And so now we're sort of.
Frustrating situation where wehave this variance, we know that
it's grown in one part of theworld.
We know that it's been detectedin other countries.
We know that it carries thesemutations that could make it
concerning, but we don't yetknow how those actually play out
in the real world.
And that's, you know, one of thebig issues because one of the
(20:06):
big challenges with genetic andmicrobiological studies.
You know, as, as such, you know,with viruses and with
everything, is that we'rebeginning to get a good sense of
what happens when you mutatesort of one small part of the
genome, but things get much,much more complicated when you
mutate multiple parts togetherbecause the, the protein
(20:26):
structures interact with eachother in ways that aren't really
very well predictable.
And how those then interact withhuman physiology is also very
unpredictable.
And so it's really unclear sortof how this constellation of
mutations is going to play outin the real world.
And the only thing that we canuse to know for sure is actually
observing what happens.
And so we're in this sort offrustrating waiting period where
(20:48):
we we don't know exactly howit's going to behave.
So what do we do?
Well, I think one of the usefulthings is to think about is we
do have a rough timeline forwhen we expect to have more
information about thesedifferent characteristics.
And so the three characteristicsthat we're usually interested in
most with new variants areimmune escape as the first
(21:09):
transmissibility as the second.
So how infectious is it andseverity is it more or less
severe than, than previousvariants?
And so, I think that that's sortof the order in which we can
expect to understand newinformation about this.
So in terms of immune escape oneof the nice things.
In some sense about that is thatwe can continue to do these
laboratory studies with theOmicron variant and look at
(21:30):
neutralizing antibody Sera fromso, so parts of the blood that
generally neutralize viralinfections, and we can see sort
of in the laboratory to whatextent are previous immunities,
both from vaccination and orfrom previous infection, stand
up against the Omicron variant.
We can also look atEpidemiological evidence from
people who have been vaccinated,who had been previously infected
(21:50):
and see whether or not theybecome infected again.
So these studies are underwayand I think that that's probably
the first thing that we'll getinformation on probably in the
next one to two.
Okay for transmission, that'sgoing to be a little more on the
order of two to four weeks,because we actually have to see
this thing spread in multiplecontexts to understand sort of,
to what extent did it justhappen to gain a foothold in
(22:11):
South Africa versus to whatextent is it sort of more
broadly transmissible in otherpopulations with different age
distributions, with differentlevels of immunity across the
population with different typesof interventions in place and
masking, et cetera.
So that'll take a little bitlonger And so I think that
probably something realistic fora very clear estimates of the
transmissibility is two to fourweeks.
(22:31):
Severity is much more difficult.
So there've been these reportsfrom one of the doctors in South
Africa who was saying that like,you know, it, it seems like
these infections that I've beenseeing are actually pretty mild
generally, and that, you know,that's very good news if that's
truly the case.
But I really want to cautionagainst using anecdotal evidence
too much.
One of the things we know isthat it takes a while for severe
(22:52):
cases to become severe.
And we haven't really beenpaying attention to this variant
for a very long time.
And because of that you know,because it can take weeks for a
person to really become severelyill with COVID-19, it's going to
take probably on the order ofone to two months to really
understand the degree to whichthe severity of the Omicron
barrier differs from theseverity of previous various.
(23:15):
Now, with all of these things.
I don't know if I can say it's agood thing or a bad thing, but
the more severe Omicron is onany of these axes, the sooner
we'll have information about it.
So if the spread is absolutelyexplosive, if it's really got a
much higher reproduction numberwe'll expect it to take off much
more quickly in differentplaces.
And we'll know that a lotsooner.
Similarly, with the severity, ifit causes symptoms sooner, or if
(23:38):
it causes much more severesymptoms, then we'll probably
know that pretty quickly.
So in some sense, the longerwe're waiting to answer these
questions the better.
And so, that's, you know, that'sone thing to keep in mind as we
move forward, but that's, youknow, that's, that's some of the
complexity that's facing us isthat, you know, there's, there's
so many people, both scientistsand nonscientists out there sort
of trying to make theseprojections and, and assessments
(24:00):
about the data and what is, andwhat isn't.
And right now it's just like, Wejust don't and can't possibly
make some of these conclusionsyet because the data just
doesn't exist and we can sort ofhazard some guesses in some
direction, but, oh boy, it'sgoing to be a little while.
So I think we just have to hangon.
Matt Boettger (24:14):
Yeah, that's helpful now.
Okay.
So there's a number of questionsand we'll talk about the booster
in just a second.
But looking back so far, youknow, we haven't seen anything
in the U S but I think I waslooking at your Twitter feed,
which I think is a great triggerfor you to follow.
He repeats a lot of greatpeople, great scientists.
So like it, see.
Among the scientific community.
That's probably here in the U Ssomewhere.
(24:35):
It's just that we aren't as goodas South Africa and the places
are to actually do the geneticor whatever we, the, the
sequencing and actually see ifit exists.
Is that, should we just kind ofassume it's probably on some
level in the U S by now,already?
Stephen Kissler (24:48):
Yeah.
So I would assume that weprobably have some cases here in
the U S Some of the, you know,some of the fact that we haven't
detected it may have to do withwith sequencing, but you know,
we've actually, in the last fewmonths, we've actually done an
awful lot to ramp up oursequencing capacity.
And so, while we may not besequencing as high of a fraction
of of cases as for example, theUK we've really made up made up
(25:11):
a lot of ground in that area.
And frankly, I'm actually alittle bit surprised that.
Detected any of them yet?
Especially because we know thatwe can detect this variance with
PCR as well, not just throughsequencing.
So we're definitely looking forthis variant, both through
sequencing, but also throughthis S gene target failure.
And we haven't detect.
(25:33):
Either to my knowledge in theUnited States.
So while I do expect that itprobably is circulating here
already given how many otherplaces in the world it is.
I do think that the fact that wehaven't detected it yet suggests
that it's not, you know,rampant.
And that really probably what wehave in the U S has mainly
dealt.
Matt Boettger (25:50):
Okay.
So then now take into like, whatdo we do in this situation?
Because now, okay, so nowthere's this Alma Cron, you
know, we're a little bit afraid.
There's a lot of unknowns.
Granted, there could be someinformation coming soon.
Maybe we don't want it to comesoon.
Like you said, we want to comelater.
Give us a little bit insight.
This, this falls, you know,right before the holidays, we
just got into a holiday.
(26:11):
We just had family.
Now we have a little gap and nowwe're going to get ready for the
holidays again.
So what, what do we do in thissituation?
So let's come back to thebooster as one, one solution and
talk about to what extent can weput some hope that the booster
and the vaccine may, if notcompletely address this Omicron
(26:34):
variant at least offer somelevel of
Stephen Kissler (26:37):
protection.
Yeah.
So, You know, the, thedefinitive evidence about the
vaccine's effectiveness againstOmicron, like everything else is
going to be sometime in coming.
But I think we do have goodreason to believe that our best
protection that we currentlyhave against Macron is still the
vaccine.
And that's because the vaccinehas largely held up pretty well.
(26:58):
Again, in terms of severedisease and hospitalization and
death against all of thevariants that we've seen so far.
So even though it was originallyformulated against the founding
strain, essentially It's interms of those most severe
complications that tell a prettywell against alpha against
Delta.
And so, chances are, it willstill provide a decent degree of
(27:19):
protection against our McCroneas well.
Going back to some of ourearlier discussions in previous
podcasts about the immune systemthere are multiple arms of the
immune system and it seems likewith The SARS, cov two the T
cell immunity, which is harderto measure it seems to be really
key to these responses.
And it seems to be in many wayssort of what the vaccines elicit
(27:39):
that really protects us from thesevere disease.
And so.
While a lot of the antibodystudies that have been
circulating about the Macronvariant have sort of been
alarming in the sense that, youknow, it has all of these
mutations in these immunogenicsites.
A lot of those are stilloriented towards this B cell
type immunity, the things thatyou can measure very easily in
in the plasma and that.
(28:01):
And so I think that we're goingto have to wait even longer to
understand sort of what the Tcell type response is against
Homa crown.
I Relatively optimistic that thevaccines will still hold up.
I do think, you know, frankly, Ido think that Omicron will take
probably a bigger hit on ourprevious immunity and
vaccination immunity than any ofthe previous variants that we've
seen before.
Just because it's so heavilymutated in the spike protein.
(28:22):
So I do think that there'llprobably be more breakthrough
infections even than we've seenwith Delta.
I do think that there willprobably be more symptomatic
infections even in vaccinatedand previously exposed people.
And I think we need to readyourselves for that, but I do
also think that the vaccineswill probably end almost
certainly before.
A good and currently our bestprotection against the worst
outcomes from from the variants.
(28:44):
So I would still highlyrecommend getting boosted.
I, as you mentioned before, Ican't remember if this was while
we were on air or previously,but some of the vaccine
manufacturers are alreadystarting to talk about updates.
And again, this is one of thegreat benefits of using the RNA
vaccines because they can.
Quickly be updated and ramped upto to account for these
antigenic shifts.
These, these changes in the, inthe surface of the virus
(29:06):
protein.
My biggest concern about that isactually not so much the
scientific hurdles, but theregulatory ones.
And so it'll be interesting tosee how long it takes for those
things to be approved to betested in the ways that they
need to be tested before theycan be.
But some of that will alsodepend on how much of a issue
the Democrat variant becomesbecause we may reach a scenario
(29:26):
where you know, if, if it isreally spreading rampantly and
it is, you know, a seriousissue, then it will have to
start considering theseemergency use authorizations
again, for some of these updatedvaccines as well.
And for just a point ofreassurance about that, I think
it's worth remembering that weupdate our flu vaccine every
year too.
And there's an expeditedregulation process for that.
Really there's, there's anexisting paradigm for this, that
(29:47):
we do this already.
And so my hope is that we'll beable to sort of slot this into
the same sort of update vaccineupdate paradigm that we have
already existing.
But that's way beyond my paygrade.
I have no idea what that'sactually gonna look like.
Matt Boettger (29:59):
I'm sure.
You know, I remember hearing,gosh, a year ago, two years ago,
maybe it's urban legend, butthat like, oh, with the MRI and
a vaccine, things can be morequickly adapted and put out
there, like without.
All the regulatory hoops thatyou have to jump through.
Is that, do you remember hearingsomething like that or is that
just like an urban legend that Iread a couple of years ago, that
(30:21):
there was some hope that itcould be tweaked faster and just
put right back out?
Stephen Kissler (30:24):
Yeah.
So, again, you know, from a,from a molecular and a
scientific point of view, that'sabsolutely true.
And that's the big, the bigvalue, but I think the
regulatory steps are just awhole different beast and I have
no idea what goes into those.
So.
Matt Boettger (30:36):
And then you taking a couple of things I want
to go back to.
So you have the Omicron, whichis highly, you know, has all
these different kinds ofmutations, right?
Uh it's it's, it's one of thosethings where I'm thinking my
mind.
Not every mutation, right.
Is, is a benefit.
I would imagine.
Like, I, I guess this is, thisis the complexity, right?
(30:57):
When you have smaller amounts ofmutations, you can, like you
said, you can measure if you'reout to how, how, you know, how
much worse is going to be, butit's not unimaginable,
unimaginable to have a series ofmutations that.
Not great, but in anorchestrated reality, they
actually begin to, to go againsteach other on some particular
(31:19):
kinds of this mutation byitself.
It's really great.
But with this mutation, itactually neutralizes that and
make it not effective.
Is that also just part of thecomplexity of knowing how these
actually work together with ourown own immune
Stephen Kissler (31:30):
cells?
Exactly.
You know, and related to that isyou know, also a lot of our
uncertainty about sort of whatthe virus does to our bodies.
We have a decent sense of, forYou know, what, what leads to
infection.
We know that there's this ACE tobinding and viral replication
within the cells, but whatactually makes the virus
clinically severe is still apretty big mystery, frankly.
(31:52):
And so, we don't have a goodsense of what different
mutations do and how those mightaffect clinical severity.
And that's, that's why that'ssort of one of the big questions
right now because this wholeconstellation of mutations.
We know it might be implicatedin immune escape and they might
be implicated in increasedtransmissibility.
We have no idea what they woulddo to clinical severity and it
could go either way, frankly.
(32:13):
I, I'm glad that you broughtthat point up because you know,
there's been a lot of sort ofspeculation, especially, you
know, amongst sort of the, thegeneral public and even
politicians on Twitter, sort of,suggesting that the natural way
for pathogens to evolve is forthem to become more
transmissible, but less.
And it's not entirely true.
So absolutely pathogens evolveto become more transmissible,
(32:34):
you know, that's, that's whatthey do that is, that is, you
know, a natural selection at itsvice.
Severity is often just sort of aunintended and unfortunate side
effect of just pathogens doingwhat they do now, if there is a
pathogen that where severitylimits its ability to spread.
So for example, if you showsevere symptoms before you ever
(32:56):
become contagious, then yes.
All of a sudden that severity isunder evolutionary pressures.
Decrease so that the pathogen isable to spread before.
You know, before you know thatit's there pathogens want to be
sneaky.
Right.
But with the case of SARS, cov,two, most of the spread happens
before any of us know that we'reinfected in the first place.
And so its severity is notreally under selective.
(33:17):
At all.
And because of that it's kind ofanybody's guess which direction
severity might go.
And so, yeah, so I think thatwith this particular virus, we
don't necessarily expect theseverity to decrease just based
off of evolutionary principles.
It could happen, but if it doeshappen, it's, it's by having.
Matt Boettger (33:36):
Yeah, great.
That's really helpful.
Now I want to go back to anotherthing was one of the tweets that
you shared with the what's thatlady's name again, if you want
Stephen Kissler (33:43):
to follow up.
Yeah, so there's Dr.
Emma HOD Croft is the one Ithink she has been doing some
really excellent work on Theviral genomics understanding
sort of like what's going onwith, with this variant and how
it stacks up against the othersthat we've seen so far.
And
Matt Boettger (33:58):
so one of the things she mentioned was this
kind of goes a little step abovejust virology and that kind of
stuff, but policy, right, assoon as the Alma Cron happened,
there was all of these kinds oflike travel bands and, you know,
see, she said, look, basicallyI'm paraphrasing.
Travel bands have never workedto actually stop the
transmission and plus it justpunishes those people and you
(34:20):
know, which I could kind of seeit now.
Cause now you even have articleswith South Africa.
It's like, now you're punishingus because we were so good.
And then of course, now I'mthinking, oh my gosh, now, now
our other countries, when wewant to hide their variants,
because they don't want to havea travel ban because now there's
this pressure.
Like, no, I don't want to be thefirst one to say it because then
guess who's going to put me onthe bad, the naughty list for
Christmas or whatever, you know?
So.
(34:40):
You want to talk, you know,maybe speak in a little bit,
because in my mind I'm thinking,oh, travel bands are like a, an
aggregate mask, right.
It's like, you know, we're gonnaput up, it's like six feet of
distance.
This is now, you know, 6,600miles of distance.
Right, right.
We put a mask on and so justwait, just like it should.
It should help, but maybe that'sit, or maybe it might help, but
it doesn't actually, he doesn'tactually complete prevent.
(35:03):
Can you tell a little bit abouthow the, the history of traveled
band and if it doesn't work, whywe got to this point of just
like immediately, like you're,you're no longer, you're no
longer able to come here or wecan.
Stephen Kissler (35:13):
Yeah.
Yeah.
So, you know, broadly, I reallyagree with what Dr.
Hopcroft was saying about thesetravel bans and the they can be
helpful in some circumstances.
So what travel bands tends to dois they buy you some time.
We haven't really ever been in asetting with a respiratory
pandemic infectious diseasewhere travel bands have totally
(35:33):
prevented the introduction of apathogen.
Especially, you know, especiallywith SARS, cov two, like it
always comes at one point oranother travel bands can slow
that down.
So with the travel ban, youalways need a very clear plan
for what you're going to do withthe time that you're buying
yourself.
The travel ban can never be apolicy unto itself.
And further to that, oncethere's clear documentation of.
(35:57):
Within country transmission,that's a widespread, then the
vast majority of your cases arelikely going to come from that.
And then it doesn't really makesense to maintain the travel ban
because travel bands areextremely disruptive and they
interrupt both the economiclinks between countries, but
also the scientific links.
It becomes a lot harder to sharesamples and to share knowledge
about about the very thing thatwe're trying to.
(36:19):
Prevent the spread of here.
And like you said, it alsoimposes these very strong
incentives for countries to notreport things that are of
international importance.
And so I think that, you know,travel bands do make sense in
some contexts but they need tobe imposed swiftly with a plan
for what to do with the timethat you've gained and they need
to be.
(36:40):
Loosened immediately, as soon asit's clear that there's the
uptake of spread within acountry simply because they're
so, so disruptive.
You know, so I think thatthere's, you know, there's room
for argument around thesethings.
A lot of people have really beencoming out sort of very strongly
against or strongly for travelbands.
And, you know, as is the subjectof this entire podcast, right.
(37:01):
There's like a lot of complexityand nuance here.
But that's precisely because,you know, travel bans like masks
are only effective when done in.
Tandem with a number of otherinterventions.
And so, with these travel bands,we really need to be thinking
about, okay, what do we want todo with the maybe week or two
that we're going to buy withthis extra time?
(37:22):
Because realistically that's,that's all that's going to be.
Matt Boettger (37:25):
Yeah.
That's helpful.
Great.
Thanks for sharing for that.
Let's go back to quickly theboosters, before we wrap this
up.
Just, you know, Stephen, youwere talking about this, Madonna
announced a strategy to addressOmicron, which is really
hopeful.
So just for those who arelistening, I'll put the show in,
I'll put the link in the.
They have three steps by whichthey're going to address
Omicron, which is really great.
First Madrona has already testeda higher dose booster of Emma
(37:47):
MRI.
Now, if you guys think back,back in the original, the first
vaccine one of the things thatmade Medina more effective and
granted I'm just a messenger,that's all stuff that Stephen
and Marcus told me.
So I'm just spitting it back outto save Stephenson words.
And that is basically it was, Ithink almost like twice a dose
of Pfizer.
And so.
That's what made it so powerfuland Pfizer had less dose and
from what I have read, partly sothey could slip in and get FDA
(38:09):
approval faster because with,with a lower dose, you'd
probably have less side effectsand those kinds of things.
So that helps to get approvedfaster.
So it sounds like the boosterfrom a dhurna, it's kind of like
right.
The Pfizer one where it's halfit's, half the dose of what
Madonna was going through.
Is that correct?
Stephen?
Yep.
The current booster.
And so now they're looking at ahigher, that's a booster that's
twice.
(38:30):
I guess that's twice as much init.
So that's their first one.
Second modern is alreadystudying to multi-view Vaillant
booster candidates in the clinicthat were designed to anticipate
mutations such as those.
So that's, that's hopeful.
It's already been in third,maternal will rapidly advanced
an Omicron specific boostercandidate.
So that's our three steps thatare going on.
Pfizer also had a promisebasically of if it is warm, Th
(38:52):
th within a hundred days to havean Omicron booster shot with an
advisor.
And of course, as you juststated, that's the actual
clinical side of things.
The other side, the policy, thesafety, that's a whole other
beast of its own.
It does not mean right.
That in a hundred days wouldhave a vaccine in our arm.
Stephen Kissler (39:11):
Yeah, that's my understanding.
So
Matt Boettger (39:13):
great.
Last couple of things on here,when it comes to boosters there
was an article that came out.
I saw, I read about coverboosters with children and how
we don't know yet.
Of course, cause everything isreally new, but there is a
possibility that you may not,our little kiddos may not need a
booster because their immunesystem is so.
Good.
If you guys would go back maybesix months ago when they were
doing clinical stuff on theoriginal vaccine, just how much
(39:35):
more effective it was, likealmost pretty much a hundred
percent with, with kiddosbecause of their, their, the
response was so great.
And oh yeah.
I think I said anything.
Any last words
Stephen Kissler (39:46):
for you, Stephen?
I think that's it.
Thanks for the whistle stoptour.
Matt Boettger (39:53):
That was awesome.
Oh yeah.
One last question we had at thehome as we prepare for
Christmas.
Any, any, any tips on what weshould do?
For example, my mother-in-lawagain, I'll I can use the, my
own personal story.
Sorry guys.
But hopefully some of thisresonates with you.
She's 87 years old.
She has the maternal vaccine.
She does not have a booster.
Don't know if she's going to getone.
When she's going to get one,Christmas is revving up.
We have some people wanting toinvite us to their home next
(40:16):
week to have dinner in theirhouse.
They're all vaccinated.
Right.
But they're all, but they alsohave high school children that
go to public school.
Right.
And so is this something that weshould, oh, it's okay.
They're all, we're allvaccinated.
Our kids are not our littlekiddos.
Aren't.
So is that a safety thing thatit's okay.
Go head, go have dinner nextweek.
(40:37):
And then that's plenty of timebefore Christmas to have your
mother-in-law in, even thoughshe is flu vaccine, but then the
booster you see othercomplications, or should we
begin to like, you know what,let's play it safe.
You know, Colorado we're in aparticular place where we have a
high amount of transmissionright now.
Do we begin to just kind ofoffer the level of safety, just
kind of quarantine two weeksbefore or still entertain these
(40:57):
events?
Any, any, any ideas of dealingwith
Stephen Kissler (41:00):
complexity?
Oh boy.
Yeah.
It's really difficult.
I think that you know, there's,there's a lot of different
levels on which you can makethese decisions, but I think
that, you know, again, Gettingvaccinated, getting boosted as
the, the best thing that we cando making plans to do that now,
especially if you would like tohave it by the Christmas new
year period of time.
Because by the time we get itscheduled and by the time you
(41:21):
give it the two weeks to sort ofcome into full contact, full
effect, it's you know, it's,it's Christmas kind of do kind
of, kind of got to do it now.
So, yeah, so I think that, youknow, thinking about that and
then Otherwise, it's just youknow, in the interim just doing
everything that we already knowprevents the spread of COVID.
So, if you're gathering inside,keep your windows cracked.
If people are willing to wearmasks, absolutely do it.
(41:41):
And I know her don'tThanksgiving.
I was especially saying thatlike, With vaccination and
testing and ventilation that youcan really sort of not have to
distance and mask.
But again, it's sort of like,you know, this, this risk budget
that we've talked about a coupleof times before to where you
know, for a holiday likeThanksgiving, that you can often
really derive a lot of valuefrom having an unmasked and
(42:03):
distanced sort of gathering Butif there are sort of, you know,
less important, but stillvaluable gatherings you might be
having.
In the meantime, it might beworth sort of saving a little
bit on that risk budget beforethe holiday season by wearing
masks, by meeting outside, ifyou're able to.
So, really just thinking aboutthese next few weeks, you know,
six to eight weeks as acollective unit, and sort of
(42:25):
thinking about where you want tospend your COVID risk and where
you want to save on it.
It's probably the best.
Great.
Matt Boettger (42:30):
Thanks, Stephen.
Good to see a buddy.
Likewise, for those of you whowant to get in contact with
Stephen, you can do that onTwitter.
S T E P H E N K I S S L E R.
I'd really recommend followinghim.
He's got great tweets, retweets,all these guys.
He follows the best people, agreat place to be informed and
get the right news.
If you want to support uspatrion.com/pandemic podcast,
(42:51):
please do so$5 a month as littleas that can help us one time
gifts, PayPal, Venmo, all in theshow notes.
And please leave a review if youcan, and inspires us, keeps us
going, and we will see you allin a couple of weeks.
Take care and.
You're listening to the pandemic podcast.
We equip you to live the mostreal life possible and the face
today's crisis.
My name is Matt Boettger, andI'm joined with my one good
friend once again, Dr.
Stephen Kissler andepidemiologist at the Harvard
school of public.
From one us citizen to anotherhappy Thanksgiving.
Stephen Kissler (00:15):
Hello?
How are you?
Hello?
Matt Boettger (00:17):
Good, good, good.
How was your Thanksgiving?
Was it splendid full of Turkey,stuffing, gravy, everything to
make you go into a coma?
Stephen Kissler (00:23):
It was splendid and we did go into a food coma.
A little bit unconventionalthough.
There's so we stayed in Bostonthis year.
We just had two friends over, soit was a pretty small
Thanksgiving.
So the bird was fittinglysmaller too.
We ended up doing chickeninstead of Turkey.
And yeah, but otherwise it wasa.
Matt Boettger (00:40):
Awesome.
Yeah, we're here.
We had a wonderful Thanksgivingand got to see Nana.
The boys were just incrediblyexcited.
It's been all day.
We had planned not to cook thatmuch on Thanksgiving and to try
to be with Nana and the boys.
But in fact, we cooked all day.
So a big that's one of ourregrets where next year we're
doing.
So
Stephen Kissler (00:59):
that's the way to do
Matt Boettger (01:02):
it is so those of you who have family and have
little ones, you know what,probably the feeling I'm
guessing if you have to cook thewhole meal yourself with like
kids under eight or seven.
But it was a wonderful time.
It's still been a wonderfullywarm weather here in Colorado,
which is a great, but also.
Fearsome with the mountains.
It's pretty dry.
We went to go cut our tree down.
We go down to the Mount, we goup to the mountains and cut her
(01:23):
own Christmas tree and we don'thave there.
And there was no snow anywhereto be found, which was our first
year going up with nothing.
So, hopefully we get someprecipitation soon.
Now we're giving a gearing upfor Christmas.
So during this time, Stephen,something really just percolated
quickly.
I couldn't believe this.
And so well, you know what,before I do that, let's just
quickly say.
(01:43):
If you can support us, pay apatrion.com/pandemic podcast,
this is a$5 a month can help ora one-time gift, a PayPal Venmo
in the show notes.
And then also before I get intothe craziness with OMA Cron and
the variant, there were tworeviews that came in that were
wonderful.
Let's see here.
I'm trying to look at the firstone here.
My notes are going, oh yeah.
So we're going to go and skipthat for now because it just
(02:04):
skipped all over, but we had twogreat reviews.
Thank you so much.
Keep them coming.
Let's see if I can get this onegoing.
Here we go.
I'm very happy to discover thispodcast.
I've been listening mainly inthe last couple of months.
I really appreciate the scope ofthe information.
What is discussed is backed upby the most recent data in a
rapidly changing environment.
It is really helpful to havedata, to make informed decisions
about behaviors this week, whichwas probably a couple weeks ago.
(02:26):
For example, they providedconcrete ways to help make
family gatherings more safe.
Thank you for your work.
You're doing that.
It's awesome.
That is from counts 11.
So love those usernames.
So thank you so much north woodsor wherever your name is.
I'm assuming that's not yourreal name.
But thank you so much for that.
And there was another one.
I won't read it now, but we'llget into this, but I just want
to pick your brain for that.
(02:47):
Another five-star review fromdragon wings, one to 1 21, but
this person, he or she works inthe jail.
So apparently he or she haswritten a public service and
talking about how this idea oflike, wait a minute.
It seems as though in the jails,it's oftentimes the first to hit
away.
And so why not use this as anindicator of what's to come?
And has this been somethingthat's been looked at among your
(03:10):
colleagues or at least maybe notjails, but in general, like
different little pockets,information, pockets by which
seemed to get Kindle fasterbefore other places.
Stephen Kissler (03:19):
Yeah.
So this is a great question andabsolutely something that we've
been thinking about and workingon over the course of the
pandemic.
So, Earlier on in I guess thiswas probably like mid 20, 20.
I had a, a series ofconversations with a reporter
named Deborah Becker at WBURhere in Boston.
And among the things that shereports on his his, his
presence.
(03:40):
And she had been doing that prepandemic as well, but really,
especially once the pandemichit, there were a lot of
questions about the role of thepandemic in prisons the extent
to which prisons were equippedto handle outbreaks and sort of
what we can.
Well, we can infer from what'shappening in prisons for, you
know, for the wider populationand vice versa, what, you know,
how we can manage the spread ofCOVID in prisons based off of
(04:03):
what's happening in the widercommunity.
So it's true that in a lot ofcases That in I'll say more
generally that these sort ofcongregate care settings or, or
places where lots of people areliving together in close
proximity.
So prisons of course, but alsonursing homes long-term care
facilities and places like thateven schools to some extent
(04:24):
although many of those wereclosed early on in the pandemic.
Are definitely places where thevirus can often gain an early
foothold.
I think one of the clearestexamples of that with some of
the the first major wave, whichhappened in the summer in
Arizona one of the initialindicators of that was a major
prison outbreak.
And so, it's absolutely truethat that in many cases These
(04:47):
places where lots of people arein close proximity.
And prisons is of course, one ofthe, one of the key examples of
that that we see early spread,but it's not always the case
because a lot of times theseplaces are also places where
there's less interaction withthe surrounding community.
And so oftentimes what we see isthat COVID will.
Spread rapidly through one ofthese communities.
(05:08):
And on average, they're probablyon the early end, but sometimes
they're not you know, sometimesthey get spared to some extent
until later on in the wave.
And then they see their majorsurge.
And one of the difficulties withprisons both was protecting the
prison population itself.
And with sort of inferring, youknow, what might be in store for
the rest of the population isthat.
(05:29):
You know, oftentimes theirtesting is really frankly, not
up to snuff.
That's been one of the realdifficulties is getting solid
information about the number ofCOVID cases in prisons, because
as you can imagine, there tendto be pretty underserved.
And there's not a lot ofinterest in, you know, testing
doing surveillance withinprisons, even though frankly,
there really should be.
And so, In a lot of cases,prisons are places where
(05:51):
absolutely there's a lot ofCOVID transmission happening.
But a lot of it, we just don'tknow an awful lot about.
And so there's been a lot ofeffort there for prison rights
advocacy which, you know, and Ithink that this you know, gets
towards a much larger sort ofprinciple of the overall
pandemic, which is the, youknow, we, we are all in this
together, you know, rich, poorIn prison out of prison, you
(06:12):
know?
And and it's easy to adopt thesort of protectionist mindset
and to sort of only payattention to what's happening in
our population and the peoplethat we normally see.
Even speaking from just anepidemiological perspective,
that's a foolish thing to do.
Because the virus is going tospread everywhere and, you know,
none of us is healthy or safeuntil all of us is healthy and
(06:33):
safe.
And the, and so I think thatthat really, really strongly
advocated.
Better surveillance, better carein all of these vulnerable
populations including the prisonpopulation.
So very great point, definitelysomething that we're looking at,
but also something that we needto do a lot more work on to both
protect the prison population assuch and to then, you know, have
a better sense of what'shappening in those communities
(06:55):
so that we can have a bettersense of the broader community,
both what's to come and what'salready happened.
Matt Boettger (07:00):
Great.
That's perfect.
And thanks for making thatnuance between like, like the
descriptive and theprescriptive, like it's one
thing to describe what's goingon in prisons and how that might
be able to tell us what's comingin the future.
But at the same time, that's notthe point because they're not
meant to be a series of lab ratsto let us know what's coming.
And in fact, there's aprescriptive element by which
the it's like, it's going backto way back in March of 2000, we
(07:22):
talked about that great CS Lewisquote.
The rats and the seller.
And when you quickly turn on thelight too, you see the rat and
he's slowly being around.
They go away, but the lightdidn't cause a lot, the rats
it's the suddenness.
And so the suddenness of thispandemic has really revealed
some of the areas by which wehave.
We are weak in participating inhelping those who need that
assistance.
And so we need to use that as aprescription to make things
(07:45):
better.
So we don't have to use this asa scarily as a way to protect
ourselves, but let's continueon.
Before we get to Alma Cron.
Let's talk about the flu becauseyou know, it's been, I've been
out of a week.
I've been trying to take sometime off family.
I haven't really beenparticipating in looking at the
news on the flu that much andselling to get your analysis of
like what you've heard or seenit right now with the flu
(08:06):
compared to last year.
Is it re raising its ugly headis it's it's it's you know,
where are we at when it comes toflu?
Yeah.
Compared to last year, but lastyear, but in general.
Stephen Kissler (08:18):
Yeah.
So, flu is spreading here in theUnited States and around the
world.
And currently in most placesacross the U S it's still at
pretty low levels which is notterribly surprising.
Usually our flu season starts tocome in, you know, maybe around
now, but oftentimes it's skeweda little bit later towards
January, even February when westart to see a lot of high
(08:39):
levels of flu transmission.
So it's a little early to say itdoes look like some places in
the mid and mountain west.
Actually New Mexico has quite afew cases right now.
It seems.
But a lot of the rest of thecountry is.
So bad at the moment.
The main flu strain that we'reseeing in the U S right now is H
three and two.
So with flu, we have a couple ofdifferent strings right now is
sort of the two major ones are Hone N one and H three and two,
(09:02):
and every three or four years,they sort of trade off.
So you'll have three or fouryears of age, three and two, and
then three or four years of ageone-on-one they differ a little
bit in terms of how infectiousthey are, how severe they are.
But for the most part, they'repretty interchangeable.
And so, the, the fact that it'sthat particular strain
circulating is more of sort of aepidemiological curiosity and
something that I'm payingattention to, but it's not
(09:22):
necessarily something that willaffect our day-to-day lives.
So right now transmission mostlyseems low across most of the.
And is roughly in line with whatwe expect to see around this
time of year on average.
But we're watching it closelybecause there's definitely flew
around and cases are starting totick upwards in line with how
they would normally tickupwards.
So I do expect there to be a fluseason this year.
And it's impossible to say atthis point how bad it will be.
(09:45):
One of the things, of coursewe've been thinking about a lot
now, too, is that, you know,especially with the news about
the Omicron variant you know,the question is now to what
extent will these things besuperimposed on top of each
other?
And that of course could causesome issues as we move forward.
But right now there's not a lotwe can say about what exactly is
in store.
Matt Boettger (10:02):
Then you made a segue perfectly to Omicron.
So this was crazy Stephen,because like, you know, it was
funny.
On Thanksgiving.
I was talking to mysister-in-law, you know, and
she's like, you sound like anepidemiologist to make it
because I hang out with one.
So I'm just the messenger.
She was wanting informationabout like, you know, the
(10:24):
booster, this kind of stuff.
And then I was just talkingabout, oh yeah, we're.
You were talking about how, youknow, we do think that some
point in time, hopefullyrelatively soon that these
variants are going to like levelyour time.
And, you know, I wouldn't evenlook at the news.
I literally, as I'm probablytelling her, this is probably
now blowing up all over in themedia.
Cause I was not checking.
Then that night I checked inlike, oh my gosh, just so I was
(10:44):
telling her about this story.
This blew up and it's like,literally overnight.
And I want you just to go and goevery direction you want to on
this.
But like, you know, my questionsare, first of all, like how did
this become a sensationovernight?
And where are we at with this?
How bad could it be?
I know we're still in the woods.
It's still early on.
(11:05):
But the who came out with stuff,Pfizer is talking about it with
journeys, talking about it.
Gosh, it's probably gonna be onSesame street next week.
Right.
So
Stephen Kissler (11:14):
where are we?
Does the Greek alphabet.
Matt Boettger (11:18):
So where, where are we in this?
And.
Yeah, let's start with that.
Before we talk about how thismight change our game plans for
the next three weeks or so as wegear up for Christmas.
Stephen Kissler (11:30):
Oh boy.
Yeah.
So, I can maybe start by talkingabout my own experience,
learning about the variance.
So similarly, you know, we'd hadThanksgiving.
I was none the wiser and it waslargely away from my phone.
And it wasn't until that eveningthat I sort of checked in and
noticed that a lot of mycolleagues were already starting
to talk about this new variantwhich at that point didn't even
(11:50):
have a name.
It only took about a day for theworld health organization to
give it the name of Omicron andclassify it as a variant of
concern which is unbelievablyrapid.
And so one of the things that Iwant to talk about as we move
forward to sort of like why.
So quick.
And so, yeah, so I, I tried tolearn as much as I could about
it in the next hours and days,basically.
(12:11):
So basically everything I'mgoing to spread back to you all
are the things that I've beenstudying up on over the last few
days and the sorts of thingsthat my colleagues have been
talking.
And we've, we sort of findourselves in, again, this
situation that we've sofrequently found ourselves in
where you know, we, as thescientific community, as well as
the broader public are trying tomake sense of something where
the pieces just aren't quiteadding up yet.
(12:33):
And eventually we'll have theright mental model to understand
what's happening and why all ofthe things that we've observed
have happened.
But it's really interestingbecause I don't think that it's
often that we get to see.
As sort of, you know, as thehuman population sort of putting
together knowledge on the fly.
And we've gotten thatopportunity a lot of times
during this pandemic and here'shere's yet another one.
So after we talk a little bitabout sort of the, the speed
(12:56):
with which this gainedattention, I also want to talk
about some of the unknowns whatwe know, what we, don't, why we
don't, when we will.
And those sorts of those sortsof questions as well.
So, You'll notice them.
I'm also clearing my throat alittle bit.
I I I got boosted this pastSaturday, and so I'm still
feeling slightly under theweather.
I think that my lymph nodes arestill draining, so that's way
(13:17):
too much information for all ofyou on the podcast, but I just
want to be, I just want be sure.
With with what's going on overhere.
I can talk about that experiencetoo, because I think that
actually one of the bigquestions with over is, is the
question about vaccines andboosters and will they hold up.
So, as I forget all of thesedifferent points that I've just
made please remind me because Iinevitably will.
Right.
So, so I think that one of thethings that has been especially
(13:40):
Remarkable about this variant.
And this is true for me as wellas for many of the people who
aren't specialists.
So I've spoken with just howquickly this variant has gained
attention.
So like what happened here?
I think there are a couple ofthings behind this, so first and
I think probably mostimportantly it was a lot of very
swift and responsible efforts onthe part of the south African
(14:02):
public health administration.
They detected that somethingstrange was going on, they were
seeing, you know, South Africahas just made it through a major
Delta wave of infection.
And then they started to see anincrease in cases in particular,
one of the things that raised.
Is that they're PCR tests, whichwe talked about a long time ago,
usually have three differenttargets.
(14:23):
So basically your, your tests,your PCR tests will try to
detect three distinct parts ofthe virus.
And they noticed that in a lotof cases, they were getting
positives on two of those partsthat a negative.
If you cast your minds way backto the beginning of this year,
that's the same thing thathappened with the alpha variant,
where there was this targetfailure this SG and target
failure or ESSA dropout that washappening with the alpha variant
(14:46):
because the, the spike proteinof the virus was mutated in this
one part that the PCR testsdetected.
So the tests were still turningpositive.
It's not that they weren't.
But they noticed that we're sortof, Groundhog day style
repeating this, where, where allof a sudden there are these
dropouts again.
And so they're like, well,what's happening.
So they very quickly got on it.
They started sequencing some ofthese samples and noticed that
(15:08):
what they were sequencing wasreally pretty different than a
lot of what they had seencirculating before.
So more on that in a moment, butthey they detected the variant
and very quickly held a pressconference.
We're very clear about what theyknew, but they didn't know and
shared this information with theworld which is exceptional.
That's exactly what we want.
(15:28):
And so.
As opposed to a lot of othersituations in which it's taken a
lot longer for these things tobe detected.
There were a couple of strokesof luck and a couple of strokes
of genius.
And that got us into thissituation where we detected this
thing very quickly, very earlyon.
And so it was really able tospread the information was able
to spread very quickly aroundthe world to the great, great
credit of the south Africanscientific community and
(15:50):
political community as well now.
Yeah.
So I think, I think I'll leavethat there for now.
We can sort of circle back to abroader discussion
Matt Boettger (15:57):
on that in a moment.
Quick question on that.
So then just so you know, yousaid the alpha, did the Delta
not have that because, so then,so then it didn't have that kind
of, so it was gone for a whileand then it raises its ugly head
again.
Okay.
Exactly.
Continue to get that narrative.
Stephen Kissler (16:13):
Yep.
Yup.
And so, you know, that's, that'san interesting point because I
think the next thing that Youknow the question of like, why
is there so much attentionaround this?
You know, we've had, we've hadmultiple other variants.
We've had, you know, the mewvariant and the Lambda variant.
And in a lot of previouspodcasts, we sort of talked
about these and it's sort oflike, yeah, these are like
issues for certain parts of theworld.
But like ultimately, you know,none of them have shown this
(16:33):
really at the ability toout-compete Delta.
And so, you know, something topay attention to you, but, you
know, Delta's the thing.
So why, why this one now?
And so there are a couple ofreasons.
So first while South Africaactually has a relatively low
vaccination rate compared to TheU S in many European countries,
although a high vaccination raterelative to many of its
(16:54):
neighbors in the Africancontinent it has also had a lot
of spread.
And so despite relatively lowvaccination rates there out to
be a pretty high level ofprevious of immunity from
previous infection.
So already starting to see anuptick in cases with a new
variant is a bit of an alarm andactually begins to point towards
something that looks like maybeimmune evasion.
So that's, you know, sort of thefirst alarm bell that started.
(17:18):
So as they sequence to the viruswe were able to sort of get some
more insight into what mightmake this variant special.
And so the second thing that wassuper alarming was the, just how
mutated to this virus is.
It really is carrying a lot ofmutations relative to anything
that we've seen previously.
(17:38):
And so.
It's really hard to pinpointwhere exactly it came from.
I mentioned that it has this SGand dropout, and so in some
sense, that kind of makes itsound similar to the alpha
variant.
And maybe it's more closelyrelated to that, but it really
seems like this is somethingthat evolutionarily has kind of
diverge pretty profoundly fromprevious things that have been
(17:59):
circulating and has picked up alot more mutations and things
that we've seen previously.
A lot of these mutations.
Spike domain of the V of thevirus.
And so what that points to isthat it's been sort of actively
selected for and that thesearen't just a bunch of random
variants or a bunch of randommutations, but actually that
they probably, you know, andI'll talk more about the
(18:20):
implications of that in amoment.
And then, yeah, and then a lotof the mutations that we've seen
There've been laboratory studiespreviously that have looked at
the effects of different singlepoint mutations.
So you can take you, you cansort of deconstruct the virus
and pull off its differentsegments, including the spike
protein so that the virus is nolonger sort of infectious.
It can't spread, but then youcan do these laboratory
(18:41):
experiments.
That look at how how well thatspike protein binds to different
human cells and how well theantigens that are produced by
that protein are, are, areneutralized by human antibodies,
for example.
And so you can do a lot ofexperiments that can then
implicate different mutations ofsaying like these particular
(19:01):
mutations.
If they show up in nature wouldbe.
It turns out that the OMAvariant contains a lot of those
mutations, both mutations thathave been implicated in better
binding to the human receptors.
So probably a greatertransmissibility and places that
tend to be immunogenic.
So places where we expect there,if there are mutations that it
(19:21):
might get around some amount ofof our immune response.
So that's another reason why itgained so much attention so
quickly is because it was like,wow, this is really sort of, you
know, coming out of it's unlikethings that we've seen before,
and it's really carrying a lotof these mutations that at least
in theory could give it a lot ofthese concerning
characteristics.
So I think that those, thosethings combined are part of why
(19:43):
it's risen so quickly to thegeneral attention.
And so now we're sort of.
Frustrating situation where wehave this variance, we know that
it's grown in one part of theworld.
We know that it's been detectedin other countries.
We know that it carries thesemutations that could make it
concerning, but we don't yetknow how those actually play out
in the real world.
And that's, you know, one of thebig issues because one of the
(20:06):
big challenges with genetic andmicrobiological studies.
You know, as, as such, you know,with viruses and with
everything, is that we'rebeginning to get a good sense of
what happens when you mutatesort of one small part of the
genome, but things get much,much more complicated when you
mutate multiple parts togetherbecause the, the protein
(20:26):
structures interact with eachother in ways that aren't really
very well predictable.
And how those then interact withhuman physiology is also very
unpredictable.
And so it's really unclear sortof how this constellation of
mutations is going to play outin the real world.
And the only thing that we canuse to know for sure is actually
observing what happens.
And so we're in this sort offrustrating waiting period where
(20:48):
we we don't know exactly howit's going to behave.
So what do we do?
Well, I think one of the usefulthings is to think about is we
do have a rough timeline forwhen we expect to have more
information about thesedifferent characteristics.
And so the three characteristicsthat we're usually interested in
most with new variants areimmune escape as the first
(21:09):
transmissibility as the second.
So how infectious is it andseverity is it more or less
severe than, than previousvariants?
And so, I think that that's sortof the order in which we can
expect to understand newinformation about this.
So in terms of immune escape oneof the nice things.
In some sense about that is thatwe can continue to do these
laboratory studies with theOmicron variant and look at
(21:30):
neutralizing antibody Sera fromso, so parts of the blood that
generally neutralize viralinfections, and we can see sort
of in the laboratory to whatextent are previous immunities,
both from vaccination and orfrom previous infection, stand
up against the Omicron variant.
We can also look atEpidemiological evidence from
people who have been vaccinated,who had been previously infected
(21:50):
and see whether or not theybecome infected again.
So these studies are underwayand I think that that's probably
the first thing that we'll getinformation on probably in the
next one to two.
Okay for transmission, that'sgoing to be a little more on the
order of two to four weeks,because we actually have to see
this thing spread in multiplecontexts to understand sort of,
to what extent did it justhappen to gain a foothold in
(22:11):
South Africa versus to whatextent is it sort of more
broadly transmissible in otherpopulations with different age
distributions, with differentlevels of immunity across the
population with different typesof interventions in place and
masking, et cetera.
So that'll take a little bitlonger And so I think that
probably something realistic fora very clear estimates of the
transmissibility is two to fourweeks.
(22:31):
Severity is much more difficult.
So there've been these reportsfrom one of the doctors in South
Africa who was saying that like,you know, it, it seems like
these infections that I've beenseeing are actually pretty mild
generally, and that, you know,that's very good news if that's
truly the case.
But I really want to cautionagainst using anecdotal evidence
too much.
One of the things we know isthat it takes a while for severe
(22:52):
cases to become severe.
And we haven't really beenpaying attention to this variant
for a very long time.
And because of that you know,because it can take weeks for a
person to really become severelyill with COVID-19, it's going to
take probably on the order ofone to two months to really
understand the degree to whichthe severity of the Omicron
barrier differs from theseverity of previous various.
(23:15):
Now, with all of these things.
I don't know if I can say it's agood thing or a bad thing, but
the more severe Omicron is onany of these axes, the sooner
we'll have information about it.
So if the spread is absolutelyexplosive, if it's really got a
much higher reproduction numberwe'll expect it to take off much
more quickly in differentplaces.
And we'll know that a lotsooner.
Similarly, with the severity, ifit causes symptoms sooner, or if
(23:38):
it causes much more severesymptoms, then we'll probably
know that pretty quickly.
So in some sense, the longerwe're waiting to answer these
questions the better.
And so, that's, you know, that'sone thing to keep in mind as we
move forward, but that's, youknow, that's, that's some of the
complexity that's facing us isthat, you know, there's, there's
so many people, both scientistsand nonscientists out there sort
of trying to make theseprojections and, and assessments
(24:00):
about the data and what is, andwhat isn't.
And right now it's just like, Wejust don't and can't possibly
make some of these conclusionsyet because the data just
doesn't exist and we can sort ofhazard some guesses in some
direction, but, oh boy, it'sgoing to be a little while.
So I think we just have to hangon.
Matt Boettger (24:14):
Yeah, that's helpful now.
Okay.
So there's a number of questionsand we'll talk about the booster
in just a second.
But looking back so far, youknow, we haven't seen anything
in the U S but I think I waslooking at your Twitter feed,
which I think is a great triggerfor you to follow.
He repeats a lot of greatpeople, great scientists.
So like it, see.
Among the scientific community.
That's probably here in the U Ssomewhere.
(24:35):
It's just that we aren't as goodas South Africa and the places
are to actually do the geneticor whatever we, the, the
sequencing and actually see ifit exists.
Is that, should we just kind ofassume it's probably on some
level in the U S by now,already?
Stephen Kissler (24:48):
Yeah.
So I would assume that weprobably have some cases here in
the U S Some of the, you know,some of the fact that we haven't
detected it may have to do withwith sequencing, but you know,
we've actually, in the last fewmonths, we've actually done an
awful lot to ramp up oursequencing capacity.
And so, while we may not besequencing as high of a fraction
of of cases as for example, theUK we've really made up made up
(25:11):
a lot of ground in that area.
And frankly, I'm actually alittle bit surprised that.
Detected any of them yet?
Especially because we know thatwe can detect this variance with
PCR as well, not just throughsequencing.
So we're definitely looking forthis variant, both through
sequencing, but also throughthis S gene target failure.
And we haven't detect.
(25:33):
Either to my knowledge in theUnited States.
So while I do expect that itprobably is circulating here
already given how many otherplaces in the world it is.
I do think that the fact that wehaven't detected it yet suggests
that it's not, you know,rampant.
And that really probably what wehave in the U S has mainly
dealt.
Matt Boettger (25:50):
Okay.
So then now take into like, whatdo we do in this situation?
Because now, okay, so nowthere's this Alma Cron, you
know, we're a little bit afraid.
There's a lot of unknowns.
Granted, there could be someinformation coming soon.
Maybe we don't want it to comesoon.
Like you said, we want to comelater.
Give us a little bit insight.
This, this falls, you know,right before the holidays, we
just got into a holiday.
(26:11):
We just had family.
Now we have a little gap and nowwe're going to get ready for the
holidays again.
So what, what do we do in thissituation?
So let's come back to thebooster as one, one solution and
talk about to what extent can weput some hope that the booster
and the vaccine may, if notcompletely address this Omicron
(26:34):
variant at least offer somelevel of
Stephen Kissler (26:37):
protection.
Yeah.
So, You know, the, thedefinitive evidence about the
vaccine's effectiveness againstOmicron, like everything else is
going to be sometime in coming.
But I think we do have goodreason to believe that our best
protection that we currentlyhave against Macron is still the
vaccine.
And that's because the vaccinehas largely held up pretty well.
(26:58):
Again, in terms of severedisease and hospitalization and
death against all of thevariants that we've seen so far.
So even though it was originallyformulated against the founding
strain, essentially It's interms of those most severe
complications that tell a prettywell against alpha against
Delta.
And so, chances are, it willstill provide a decent degree of
(27:19):
protection against our McCroneas well.
Going back to some of ourearlier discussions in previous
podcasts about the immune systemthere are multiple arms of the
immune system and it seems likewith The SARS, cov two the T
cell immunity, which is harderto measure it seems to be really
key to these responses.
And it seems to be in many wayssort of what the vaccines elicit
(27:39):
that really protects us from thesevere disease.
And so.
While a lot of the antibodystudies that have been
circulating about the Macronvariant have sort of been
alarming in the sense that, youknow, it has all of these
mutations in these immunogenicsites.
A lot of those are stilloriented towards this B cell
type immunity, the things thatyou can measure very easily in
in the plasma and that.
(28:01):
And so I think that we're goingto have to wait even longer to
understand sort of what the Tcell type response is against
Homa crown.
I Relatively optimistic that thevaccines will still hold up.
I do think, you know, frankly, Ido think that Omicron will take
probably a bigger hit on ourprevious immunity and
vaccination immunity than any ofthe previous variants that we've
seen before.
Just because it's so heavilymutated in the spike protein.
(28:22):
So I do think that there'llprobably be more breakthrough
infections even than we've seenwith Delta.
I do think that there willprobably be more symptomatic
infections even in vaccinatedand previously exposed people.
And I think we need to readyourselves for that, but I do
also think that the vaccineswill probably end almost
certainly before.
A good and currently our bestprotection against the worst
outcomes from from the variants.
(28:44):
So I would still highlyrecommend getting boosted.
I, as you mentioned before, Ican't remember if this was while
we were on air or previously,but some of the vaccine
manufacturers are alreadystarting to talk about updates.
And again, this is one of thegreat benefits of using the RNA
vaccines because they can.
Quickly be updated and ramped upto to account for these
antigenic shifts.
These, these changes in the, inthe surface of the virus
(29:06):
protein.
My biggest concern about that isactually not so much the
scientific hurdles, but theregulatory ones.
And so it'll be interesting tosee how long it takes for those
things to be approved to betested in the ways that they
need to be tested before theycan be.
But some of that will alsodepend on how much of a issue
the Democrat variant becomesbecause we may reach a scenario
(29:26):
where you know, if, if it isreally spreading rampantly and
it is, you know, a seriousissue, then it will have to
start considering theseemergency use authorizations
again, for some of these updatedvaccines as well.
And for just a point ofreassurance about that, I think
it's worth remembering that weupdate our flu vaccine every
year too.
And there's an expeditedregulation process for that.
Really there's, there's anexisting paradigm for this, that
(29:47):
we do this already.
And so my hope is that we'll beable to sort of slot this into
the same sort of update vaccineupdate paradigm that we have
already existing.
But that's way beyond my paygrade.
I have no idea what that'sactually gonna look like.
Matt Boettger (29:59):
I'm sure.
You know, I remember hearing,gosh, a year ago, two years ago,
maybe it's urban legend, butthat like, oh, with the MRI and
a vaccine, things can be morequickly adapted and put out
there, like without.
All the regulatory hoops thatyou have to jump through.
Is that, do you remember hearingsomething like that or is that
just like an urban legend that Iread a couple of years ago, that
(30:21):
there was some hope that itcould be tweaked faster and just
put right back out?
Stephen Kissler (30:24):
Yeah.
So, again, you know, from a,from a molecular and a
scientific point of view, that'sabsolutely true.
And that's the big, the bigvalue, but I think the
regulatory steps are just awhole different beast and I have
no idea what goes into those.
So.
Matt Boettger (30:36):
And then you taking a couple of things I want
to go back to.
So you have the Omicron, whichis highly, you know, has all
these different kinds ofmutations, right?
Uh it's it's, it's one of thosethings where I'm thinking my
mind.
Not every mutation, right.
Is, is a benefit.
I would imagine.
Like, I, I guess this is, thisis the complexity, right?
(30:57):
When you have smaller amounts ofmutations, you can, like you
said, you can measure if you'reout to how, how, you know, how
much worse is going to be, butit's not unimaginable,
unimaginable to have a series ofmutations that.
Not great, but in anorchestrated reality, they
actually begin to, to go againsteach other on some particular
(31:19):
kinds of this mutation byitself.
It's really great.
But with this mutation, itactually neutralizes that and
make it not effective.
Is that also just part of thecomplexity of knowing how these
actually work together with ourown own immune
Stephen Kissler (31:30):
cells?
Exactly.
You know, and related to that isyou know, also a lot of our
uncertainty about sort of whatthe virus does to our bodies.
We have a decent sense of, forYou know, what, what leads to
infection.
We know that there's this ACE tobinding and viral replication
within the cells, but whatactually makes the virus
clinically severe is still apretty big mystery, frankly.
(31:52):
And so, we don't have a goodsense of what different
mutations do and how those mightaffect clinical severity.
And that's, that's why that'ssort of one of the big questions
right now because this wholeconstellation of mutations.
We know it might be implicatedin immune escape and they might
be implicated in increasedtransmissibility.
We have no idea what they woulddo to clinical severity and it
could go either way, frankly.
(32:13):
I, I'm glad that you broughtthat point up because you know,
there's been a lot of sort ofspeculation, especially, you
know, amongst sort of the, thegeneral public and even
politicians on Twitter, sort of,suggesting that the natural way
for pathogens to evolve is forthem to become more
transmissible, but less.
And it's not entirely true.
So absolutely pathogens evolveto become more transmissible,
(32:34):
you know, that's, that's whatthey do that is, that is, you
know, a natural selection at itsvice.
Severity is often just sort of aunintended and unfortunate side
effect of just pathogens doingwhat they do now, if there is a
pathogen that where severitylimits its ability to spread.
So for example, if you showsevere symptoms before you ever
(32:56):
become contagious, then yes.
All of a sudden that severity isunder evolutionary pressures.
Decrease so that the pathogen isable to spread before.
You know, before you know thatit's there pathogens want to be
sneaky.
Right.
But with the case of SARS, cov,two, most of the spread happens
before any of us know that we'reinfected in the first place.
And so its severity is notreally under selective.
(33:17):
At all.
And because of that it's kind ofanybody's guess which direction
severity might go.
And so, yeah, so I think thatwith this particular virus, we
don't necessarily expect theseverity to decrease just based
off of evolutionary principles.
It could happen, but if it doeshappen, it's, it's by having.
Matt Boettger (33:36):
Yeah, great.
That's really helpful.
Now I want to go back to anotherthing was one of the tweets that
you shared with the what's thatlady's name again, if you want
Stephen Kissler (33:43):
to follow up.
Yeah, so there's Dr.
Emma HOD Croft is the one Ithink she has been doing some
really excellent work on Theviral genomics understanding
sort of like what's going onwith, with this variant and how
it stacks up against the othersthat we've seen so far.
And
Matt Boettger (33:58):
so one of the things she mentioned was this
kind of goes a little step abovejust virology and that kind of
stuff, but policy, right, assoon as the Alma Cron happened,
there was all of these kinds oflike travel bands and, you know,
see, she said, look, basicallyI'm paraphrasing.
Travel bands have never workedto actually stop the
transmission and plus it justpunishes those people and you
(34:20):
know, which I could kind of seeit now.
Cause now you even have articleswith South Africa.
It's like, now you're punishingus because we were so good.
And then of course, now I'mthinking, oh my gosh, now, now
our other countries, when wewant to hide their variants,
because they don't want to havea travel ban because now there's
this pressure.
Like, no, I don't want to be thefirst one to say it because then
guess who's going to put me onthe bad, the naughty list for
Christmas or whatever, you know?
So.
(34:40):
You want to talk, you know,maybe speak in a little bit,
because in my mind I'm thinking,oh, travel bands are like a, an
aggregate mask, right.
It's like, you know, we're gonnaput up, it's like six feet of
distance.
This is now, you know, 6,600miles of distance.
Right, right.
We put a mask on and so justwait, just like it should.
It should help, but maybe that'sit, or maybe it might help, but
it doesn't actually, he doesn'tactually complete prevent.
(35:03):
Can you tell a little bit abouthow the, the history of traveled
band and if it doesn't work, whywe got to this point of just
like immediately, like you're,you're no longer, you're no
longer able to come here or wecan.
Stephen Kissler (35:13):
Yeah.
Yeah.
So, you know, broadly, I reallyagree with what Dr.
Hopcroft was saying about thesetravel bans and the they can be
helpful in some circumstances.
So what travel bands tends to dois they buy you some time.
We haven't really ever been in asetting with a respiratory
pandemic infectious diseasewhere travel bands have totally
(35:33):
prevented the introduction of apathogen.
Especially, you know, especiallywith SARS, cov two, like it
always comes at one point oranother travel bands can slow
that down.
So with the travel ban, youalways need a very clear plan
for what you're going to do withthe time that you're buying
yourself.
The travel ban can never be apolicy unto itself.
And further to that, oncethere's clear documentation of.
(35:57):
Within country transmission,that's a widespread, then the
vast majority of your cases arelikely going to come from that.
And then it doesn't really makesense to maintain the travel ban
because travel bands areextremely disruptive and they
interrupt both the economiclinks between countries, but
also the scientific links.
It becomes a lot harder to sharesamples and to share knowledge
about about the very thing thatwe're trying to.
(36:19):
Prevent the spread of here.
And like you said, it alsoimposes these very strong
incentives for countries to notreport things that are of
international importance.
And so I think that, you know,travel bands do make sense in
some contexts but they need tobe imposed swiftly with a plan
for what to do with the timethat you've gained and they need
to be.
(36:40):
Loosened immediately, as soon asit's clear that there's the
uptake of spread within acountry simply because they're
so, so disruptive.
You know, so I think thatthere's, you know, there's room
for argument around thesethings.
A lot of people have really beencoming out sort of very strongly
against or strongly for travelbands.
And, you know, as is the subjectof this entire podcast, right.
(37:01):
There's like a lot of complexityand nuance here.
But that's precisely because,you know, travel bans like masks
are only effective when done in.
Tandem with a number of otherinterventions.
And so, with these travel bands,we really need to be thinking
about, okay, what do we want todo with the maybe week or two
that we're going to buy withthis extra time?
(37:22):
Because realistically that's,that's all that's going to be.
Matt Boettger (37:25):
Yeah.
That's helpful.
Great.
Thanks for sharing for that.
Let's go back to quickly theboosters, before we wrap this
up.
Just, you know, Stephen, youwere talking about this, Madonna
announced a strategy to addressOmicron, which is really
hopeful.
So just for those who arelistening, I'll put the show in,
I'll put the link in the.
They have three steps by whichthey're going to address
Omicron, which is really great.
First Madrona has already testeda higher dose booster of Emma
(37:47):
MRI.
Now, if you guys think back,back in the original, the first
vaccine one of the things thatmade Medina more effective and
granted I'm just a messenger,that's all stuff that Stephen
and Marcus told me.
So I'm just spitting it back outto save Stephenson words.
And that is basically it was, Ithink almost like twice a dose
of Pfizer.
And so.
That's what made it so powerfuland Pfizer had less dose and
from what I have read, partly sothey could slip in and get FDA
(38:09):
approval faster because with,with a lower dose, you'd
probably have less side effectsand those kinds of things.
So that helps to get approvedfaster.
So it sounds like the boosterfrom a dhurna, it's kind of like
right.
The Pfizer one where it's halfit's, half the dose of what
Madonna was going through.
Is that correct?
Stephen?
Yep.
The current booster.
And so now they're looking at ahigher, that's a booster that's
twice.
(38:30):
I guess that's twice as much init.
So that's their first one.
Second modern is alreadystudying to multi-view Vaillant
booster candidates in the clinicthat were designed to anticipate
mutations such as those.
So that's, that's hopeful.
It's already been in third,maternal will rapidly advanced
an Omicron specific boostercandidate.
So that's our three steps thatare going on.
Pfizer also had a promisebasically of if it is warm, Th
(38:52):
th within a hundred days to havean Omicron booster shot with an
advisor.
And of course, as you juststated, that's the actual
clinical side of things.
The other side, the policy, thesafety, that's a whole other
beast of its own.
It does not mean right.
That in a hundred days wouldhave a vaccine in our arm.
Stephen Kissler (39:11):
Yeah, that's my understanding.
So
Matt Boettger (39:13):
great.
Last couple of things on here,when it comes to boosters there
was an article that came out.
I saw, I read about coverboosters with children and how
we don't know yet.
Of course, cause everything isreally new, but there is a
possibility that you may not,our little kiddos may not need a
booster because their immunesystem is so.
Good.
If you guys would go back maybesix months ago when they were
doing clinical stuff on theoriginal vaccine, just how much
(39:35):
more effective it was, likealmost pretty much a hundred
percent with, with kiddosbecause of their, their, the
response was so great.
And oh yeah.
I think I said anything.
Any last words
Stephen Kissler (39:46):
for you, Stephen?
I think that's it.
Thanks for the whistle stoptour.
Matt Boettger (39:53):
That was awesome.
Oh yeah.
One last question we had at thehome as we prepare for
Christmas.
Any, any, any tips on what weshould do?
For example, my mother-in-lawagain, I'll I can use the, my
own personal story.
Sorry guys.
But hopefully some of thisresonates with you.
She's 87 years old.
She has the maternal vaccine.
She does not have a booster.
Don't know if she's going to getone.
When she's going to get one,Christmas is revving up.
We have some people wanting toinvite us to their home next
(40:16):
week to have dinner in theirhouse.
They're all vaccinated.
Right.
But they're all, but they alsohave high school children that
go to public school.
Right.
And so is this something that weshould, oh, it's okay.
They're all, we're allvaccinated.
Our kids are not our littlekiddos.
Aren't.
So is that a safety thing thatit's okay.
Go head, go have dinner nextweek.
(40:37):
And then that's plenty of timebefore Christmas to have your
mother-in-law in, even thoughshe is flu vaccine, but then the
booster you see othercomplications, or should we
begin to like, you know what,let's play it safe.
You know, Colorado we're in aparticular place where we have a
high amount of transmissionright now.
Do we begin to just kind ofoffer the level of safety, just
kind of quarantine two weeksbefore or still entertain these
(40:57):
events?
Any, any, any ideas of dealingwith
Stephen Kissler (41:00):
complexity?
Oh boy.
Yeah.
It's really difficult.
I think that you know, there's,there's a lot of different
levels on which you can makethese decisions, but I think
that, you know, again, Gettingvaccinated, getting boosted as
the, the best thing that we cando making plans to do that now,
especially if you would like tohave it by the Christmas new
year period of time.
Because by the time we get itscheduled and by the time you
(41:21):
give it the two weeks to sort ofcome into full contact, full
effect, it's you know, it's,it's Christmas kind of do kind
of, kind of got to do it now.
So, yeah, so I think that, youknow, thinking about that and
then Otherwise, it's just youknow, in the interim just doing
everything that we already knowprevents the spread of COVID.
So, if you're gathering inside,keep your windows cracked.
If people are willing to wearmasks, absolutely do it.
(41:41):
And I know her don'tThanksgiving.
I was especially saying thatlike, With vaccination and
testing and ventilation that youcan really sort of not have to
distance and mask.
But again, it's sort of like,you know, this, this risk budget
that we've talked about a coupleof times before to where you
know, for a holiday likeThanksgiving, that you can often
really derive a lot of valuefrom having an unmasked and
(42:03):
distanced sort of gathering Butif there are sort of, you know,
less important, but stillvaluable gatherings you might be
having.
In the meantime, it might beworth sort of saving a little
bit on that risk budget beforethe holiday season by wearing
masks, by meeting outside, ifyou're able to.
So, really just thinking aboutthese next few weeks, you know,
six to eight weeks as acollective unit, and sort of
(42:25):
thinking about where you want tospend your COVID risk and where
you want to save on it.
It's probably the best.
Great.
Matt Boettger (42:30):
Thanks, Stephen.
Good to see a buddy.
Likewise, for those of you whowant to get in contact with
Stephen, you can do that onTwitter.
S T E P H E N K I S S L E R.
I'd really recommend followinghim.
He's got great tweets, retweets,all these guys.
He follows the best people, agreat place to be informed and
get the right news.
If you want to support uspatrion.com/pandemic podcast,
(42:51):
please do so$5 a month as littleas that can help us one time
gifts, PayPal, Venmo, all in theshow notes.
And please leave a review if youcan, and inspires us, keeps us
going, and we will see you allin a couple of weeks.
Take care and.
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