September 7, 2021 • 35 mins
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Things Discussed on Episode:
- Biden pledged to ‘follow the science.’ But experts say he’s sometimes fallen short
- Here's what we know about the highly mutated C.1.2 coronavirus variant so far
- Mu COVID Variant, Which Scientists Fear is Resistant to Vaccines, Detected in 39 Countries
- The Masks Were Working All Along
- Past Covid-19 infection ‘gives more protection’
- RNA vaccines seem to produce very different antibody levels
- What Pfizer's scientists consider the 'biggest surprise' about their COVID-19 vaccine
- Most Children With Severe Post-Covid-19 Condition in Fine Health Year Later, U.K. Study Finds
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 POS podcast,
where we equip you to live themost real life possible in the
face of these crises.
My name is Matt Boettger and I'mjoined with one great friend of
mine.
Dr.
Stephen Kissler epidemiologists,the Harvard school of public
health.
How are you?
Stephen Kissler (00:13):
Fine, sir?
Hello, I'm doing all right.
It's happy post labor dayweekend.
Yes.
Matt Boettger (00:19):
Happy post labor day.
Everybody who celebrates laborday in the U S here.
We will make a quickannouncement if you notice where
we're kind of starting to go toevery two weeks.
Maybe we'll go back to everyweek.
It's not because there's not anynews.
Obviously it's just that life isjust crazy for Stephen, myself,
mark, and to get us all to rallyand be every week has been a
little more difficult thanusual.
(00:40):
So we may go back to once aweek.
At some point in time, we maystay every other, every other
week as such, you know, we'rehere.
We want us to continue to behere, but we're trying to
navigate being present andavailable to all of you.
And navigate our own crazylives, right Stephen?
Stephen Kissler (00:56):
Oh yeah.
Matt Boettger (00:56):
Oh yeah.
Well said, well said, so if you,if you can leave us a review,
even if we're going every otherweek give us a little shout out
and let us know how we're doing.
You can do that on applepodcasts and think there's
another other platform you cansupport us that would help us
tremendously.
Maybe even get us to be a littlemore often just to help us get
the support.
We need an offset.
It.
At patrion.com/pandemic podcastsas little as$5 a month can help
(01:20):
a lot as well, as well asone-time gifts at PayPal or
Venmo and both they're all inthe show notes.
So there you go.
Okay.
So I feel like we have a lot totalk about.
There's some things I thinkwe'll try to just breeze right
over.
Just talk about it.
And then Stephen and I talkedbefore we start recording,
there's a couple of things thatseem really fascinating, and I
(01:42):
want to really unpack it withStephen.
I want to learn a lot more.
But before I want to get startedwith this, I saw this article,
Stephen, and I don't know, kindof surprise me.
Not really, but this article isBiden said, he'd follow the
silent side science to experts.
He's sometimes fallen short.
Now, when I kind of dove intothis expert, we're not going to
(02:02):
talk about politics per se, inthat area.
But when I dove in his article,it seemed like the focus of all
things.
And they talked about teachersbeing vaccinated and that
might've been not following CDCguidelines.
But the meat of this wholearticle was really about
boosters and how he didn'tfollow the science.
So I want to pick your brainbecause you're an expert.
(02:24):
So, and we've talked about thisbefore about boosters.
Should we, should we not?
And is it good?
Is it ethical?
And is he falling the science.
With the idea of wanting toadvance boosters for the U S is
he not following science or isthis more than just science?
Is it policy?
And this is just some kind ofswitch bait headline that we
need to just ignore completelyaltogether.
(02:45):
Sure.
Stephen Kissler (02:46):
Yeah.
So, I mean, there's, I thinkthere's two layers of complexity
to this.
So the first.
The thing about it is that, I,I, and many of my colleagues
were w were taken off guards tosome extent when the when the
administration first said that,we'll, we'll be having boosters
(03:06):
for Americans by X date,whatever.
And, and they've actually sent,sort of walked back from that a
little bit.
And there were two reasons whywe were surprised by that.
The first is that there was.
Absolutely emerging evidence atthat point that that the third
dose of the MRN vaccines couldbe beneficial towards giving you
a better immune response, alonger lasting immunity.
(03:27):
And this will make sense off ofwhat we know about immunology
too.
Many of the multidose vaccinesthat we get as kids are also
separated by, on the order ofsix months to a year and that
separation can be reallycritically important for giving
you the long lasting and unity.
So.
Since, and there was someemerging data suggesting that
that might be the case, but westill absolutely, at that point,
(03:48):
hadn't reached what we like tocall a scientific consensus.
There were some studies thatwere supporting this, but one,
one or two studies does not makeproof or does not make, a, a
really compelling story.
The, the whole practice ofscience is sort of steering this
massive ship of human knowledge.
And one, one little study isn'tgoing to do that.
Really.
We need lots of corroboratingevidence from different angles.
(04:09):
So.
What we were waiting for asscientists.
And that's why, when thisannouncement first came out,
right.
Maybe a little premature, eventhough it's probably pointed in
the right direction.
So, now that said, in themeantime there, a lot of that
corroborating evidence has comethrough and it does suggest that
a additional dose of the MRAvaccines can be very effective
at giving you higher levels ofimmunity, longer lasting
(04:31):
immunity, unity.
So, so now the, in some ways thescience has kind of caught up.
And so now it makes a lot ofsense, but, but the timing of it
was was surprising.
The second thing is thatGenerally political
administrations are not thepeople who make these
announcements.
Right.
Like this is, this is somethingthat should be coming from the
FDA.
It requires, at this pointagain, a careful evaluation of
(04:52):
the evidence a carefuldeliberation amongst experts who
know about many different typesof vaccines and about these
vaccines in particular, which iswhat the FDA exists for.
And so that was another thing.
So it was like, why, why are wegetting this announcement from a
the, the white house and notfrom the FDA?
And so it, it, it was sort oflike putting the cart before the
horse.
And so, so that was another oneof the more sort of policy side
(05:14):
with scientific overtones that,that caused some surprises.
And now the last thing ofcourse, is that in the midst of
this now, even though thescience does seem to be
suggesting that a third dose ofMRN vaccines does seem like it
will probably be a very goodidea at some point there's still
a lot of really thorny policyquestions as to how to organize
the rollout.
(05:34):
How do we, yeah.
Giving third doses in the UnitedStates versus first doses in
much of the rest of the world.
How, how does this work?
How do we keep track of things?
Frankly, probably many peoplehave already gone out and gotten
their booster shots because inmany places you can just walk up
and say, I want a vaccine andshe can get it right.
Which is not at all, somethingthat I would recommend at this
(05:55):
point, but as possible.
Sure that people have done it.
And so, one of the big issuesnow is that we, we don't have
very good record keeping aroundwho's gotten which vaccines and
how that plays together, whichmakes doing research a lot more
difficult.
It makes setting policies a lotmore difficult.
So there are a lot of reallythorny questions in here that,
that aren't just science to thatI think we really urgently need
(06:16):
to get sorted out.
And I think that, that seems tobe what this article was
pointing.
Matt Boettger (06:20):
Okay, that makes sense.
So now is the booster shot?
Nothing more than the same?
Shot given at the beginning.
It's not like this new revisedone that's tweaked for the
Delta.
The heap hearing about has beenunder undergoing this is just
the same one that's originated.
There's a third
Stephen Kissler (06:35):
version third.
Yeah.
Currently it seems like that.
Which, which again is aninteresting choice too.
I know my, my colleague, MichaelMina has been very outspoken
about the fact that like, w w wehave the capability of updating
these vaccines, we might as wellgive something that's more
closely related to the Delta.
And one of the reasons why notis because that might be subject
(06:55):
to a more stringent safety andefficacy review, which might
delay, how long it would takefor that to actually get rolled
out.
So again, there are verypractical reasons why we might
use the original dose, but rightnow that that is the case that
it's the original Formulationthat is currently being used for
for these third doses.
Now I imagine some of ourlisteners will probably notice
(07:17):
that I've been sort of steeringaway from calling it a booster
and been calling it a third doseof the series as well.
And part of that is because It'ssplitting hairs a little bit,
but and, and definitely, boosteryour shot is, is the thing that
has really been prevalent in themedia.
But I think really what we'retrying to do here is to
understand, what should theactual series of COVID
(07:38):
vaccination be?
And when you think of, when youthink of something like tetanus,
we get booster shots every 10years or so.
Right.
And you need that for life.
And so what a booster shotimplies is that it's sort of
something that's ongoing inperpetuity, but we're not sure
that that's going to be the casefor COVID right now.
Really what we're trying to dois work out, how long should the
series be and how far apartshould they be?
(07:59):
Sequenced it's it's possible.
We might need it.
COVID shots, as booster shots,sort of like we do the flu, it's
sort of like we do for tetanus.
But I'm actually hopeful thatmaybe actually what we need is
like a two or three dose seriesand then we're done.
And so that's part of what we'retrying to work out too.
And we're just not sure what youmean.
Settings we're going to be in,so it, okay.
That's not to say that weshouldn't be using the term
booster, but that's, that's sortof why I've been steering away
(08:20):
from it.
It's cause we're not really sureabout that yet.
Matt Boettger (08:22):
That makes sense.
And for those of you listeningno, Stephen is not next to a
dentist office for the drillingsomebodies teeth.
It's actually construction workoutside and we have no choice,
but he's got the
Stephen Kissler (08:33):
window closed.
Yeah.
Sorry about that.
No, it's okay.
It's like right outside.
So
Matt Boettger (08:38):
living in the city life, man city life.
Okay.
So let's get straight into it.
The reason why would be onebooster is why we're talking
about boosters because there'sso many variants.
And so I want to get caught upto speed with you, Stephen.
So we know about the Delta.
This has been the headlinesforever.
I like to get the status from onyour end.
Now there's a C1 to have no cluewhy he doesn't have a Greek
(08:59):
letter, but maybe you canexplain why maybe it's too early
or whatever.
That seems like something to beaware of.
Can you talk about that?
And there's the mu these twoseem to be really kind of
percolating to the surface andthe media outlets I heard about
Mo maybe evading the vaccineimmunity.
Where are we at in this?
Where do you expect it to go?
(09:21):
I, I heard about with Moo at onepoint in time, the U S was the
only place in the world by whichit was rising.
Sounds like that's differentnow.
So that's maybe good news, butguest cuts to speed.
Where are we at and where shouldwe be concerned?
Stephen Kissler (09:33):
Yeah.
So, first a point on the naming.
So, these different viruslineages all have the Sort of
long mouthful letter plus awhole bunch of numbers, plus a
whole bunch of dots.
And, and that, when we weretalking about and B 1 6, 1 7
0.2, all of these things that's,that's still going on under the
(09:54):
surface and, and, and thosethose names are very useful and
informative for those of us whoare, frankly nerds and are
interested in, like figuring outhow all of these things are
related to one another.
So the first thing that one ofthe virus gets is, is one of
those associations, but thenonce it becomes classified by
the CDC or the world healthorganization as a variant of
interest or a variant ofconcern, meaning that we've seen
(10:17):
a major outbreak of thisparticular variant in a location
and.
No genetic markers that suggestthat it's something that we
ought to be paying attention to.
And then we give it a Greekletter.
So C1 two, hasn't gotten a Greekletter yet because it hasn't
quite crossed that threshold ofconcern yet.
Whereas new and alpha betagamma, Delta, et cetera have all
sort of crossed that level ofconcern at some point.
(10:39):
And so that sort of gives us ashorthand for referring to these
different.
Got it.
Nope.
You're right.
We've been hearing a lot moreabout both the variant, the new
variant and yeah, and I think,rightly the question is like,
how concerned should we be?
So, as with most of thesevariants, in some ways it's the
same old story playing itselfout again in that So we have a
(11:00):
variant they've each beenincreasing in particular
geographic locations.
And so that's 0.1 of concern,because if, if a variant is able
to increase in prevalence, thenthat suggests that it is for
some reason more transmissiblethan whatever is spreading at
the current moment in thatparticular location.
So, That's sort of 0.1 0.2 thenis, okay.
(11:20):
So does the variant contain thegenetic markers that we know to
be associated with things thatwe might be concerned about?
So there are different ways oftesting for this, for example,
in laboratories you can sort oftweak the structure of different
parts of the virus.
Remaking the virus itself.
And then you can expose that todifferent antibodies and see if
that has the ability to getaround some of our immune
(11:41):
response.
And so we know what some ofthose mutations are, even if
they haven't yet emerged innature.
And so when we start to seethose things emerge, we can say,
okay, well this, this at leasthas one of those markers that
could make it get around ourimmune system or could make it
more transmissible.
We don't know for sure if itdoes, but it's, it's definitely
something worth being concernedabout.
And, and for the, for the mew inparticular, that's something
(12:01):
that we've seen where it's, ithas some of these mutations, but
we haven't yet seen how thatplays out in the real world.
Totally.
So, the key thing about both ofthese variants and really about
everything that we've seen sincethe Delta has come out and you
were alluding to this during theintroduction to this bit So far,
it doesn't seem like anythinghas really been able to
out-compete Delta.
Even the mew, get emerged.
You can see the sort of ebb andflow of different variants
(12:24):
sometimes because sometimes aviral strain will get lucky.
It will reach a community andthere will be a couple of super
spreading events and it willrise and prevalence.
And all of a sudden we'll say,oh, here's something that we may
be out to be concerned about,but the real concern.
As happened with alpha and ashappened with Delta is when you
see that outbreak, like we sawin the UK, like we saw in India,
(12:45):
and then it startsrecapitulating itself in many
different places, because thatsuggests that there's this
robust ability to out-competewhatever is there in the first
place.
Whereas it seems like thesevariants so far, wherever they
have emerged, they've kind ofbeen driven out again by Delta.
And so no matter what mutations,no matter what.
Functions.
We call them phenotypes.
(13:05):
These, these viruses have ifthey're not able to spread in
the context of another spreadingvirus, then they're never going
to really take off.
They might cause smalloutbreaks, but they'll
eventually be driven away by thething that is more
transmissible, which iscurrently the Delta.
And so right now it really seemslike.
Delta's the thing, that, that isthe thing where consistently
(13:27):
wherever Delta is spreading,nothing else has really been
able to hang on for long.
And so that's the upshot.
And so there's, there's,definitely a lot of chatter and,
and these are things that weneed to be paying attention to
you.
But right now, the thing that'son my mind is Delta.
Yeah.
Matt Boettger (13:41):
And then it kinda reminds me of Lambda where I
remember early on talking aboutLambda was in south America.
There was a lot of worry aboutthis and then it just never
really could get an edge,because of the Delta.
And so it's clearly it seems tobe possible.
The variant could evolve.
The dad's actually is maybe moredangerous.
Can bring people quicker tohospital could be so, so changed
(14:04):
that it evades even vaccines,but then just dies off.
But that doesn't, it doesn'thave the capacity to compete
with Delta, which might not beas dangerous, but it's just so
vibrant and so contagious thatit just dominates everything
else.
Is that true?
That you could have worsevariants in the sense of
hospitalization?
But because they don't, they'renot quite as V that viral ENT,
(14:24):
so to speak, they just can'tcompete with Delta.
So Delta keeps it at bay,
Stephen Kissler (14:28):
right?
Yeah.
And just to note on terms, andthis is super confusing, you
would, you would think that,viral, it means contagious, but
actually viral int is usuallywhat we use to describe the
clinical severity.
And so, yeah, just just a pointto our listeners.
So, so actually, right.
So, so.
Amend that statement for what Ithink you were saying.
(14:49):
Was it just that there might bemore violent or more clinically
severe strains that sound veryconcerning, but if they aren't
as contagious or transmissibleas the Delta, then they're not
really going to be able to takeoff.
And so that's, that's the realconcern is that generally an
increase in contagiousness ortransmissibility is usually a
much bigger.
Okay.
Matt Boettger (15:08):
Great.
Thank you for thatclarification.
I'm the lay man that I'm anexpert on the show.
Okay.
Yeah.
So let's, that sounds good.
Like hopeful news, at least whenit comes to the one too.
Now I'm guessing because it's Cgoing from B to C, that means
there is a stronger change.
Is that how it goes?
Like a, B, C it's it's it'smore, it's changed more
dramatically.
So
Stephen Kissler (15:27):
now it's a new letter.
Yeah.
Thankfully, somehow there'sactually something that makes
sense about this whole thingthat intuitive.
Exactly.
Matt Boettger (15:37):
Great.
Good to know.
Okay.
So I want to make a quick justbookmark this.
We're not going to talk muchabout this.
I read this from the Atlantic,the masks were working all
along.
I know every once in a while wecome back, we talk about this,
but this seems to be anincredible study done in
Bangladesh.
Probably the best study done yeton the ethicacy of masks.
We're not going to talk aboutthis, but I'm going to put in
(15:58):
the show notes.
It's a great read.
Just proves the point of howpowerful and really good mass
are to help keep COVID at bay.
Again, not the only tool in ourtoolbox, but another one that's
just really great along with allthe other ones as well.
So please check that out in theshow notes.
So we have two big subjects wewant to talk about that I think
(16:23):
are really interesting.
I saw this Stephen and a handfulof article.
Banging over and over this drum,this idea, this came from
Israel, the study in Israelthat's that, that, that
apparently showed that naturalimmunity is more effective than
the vaccine when it comes to theDelta variant.
(16:47):
Now, is this true?
Or how, how do we navigate this
Stephen Kissler (16:50):
terrain?
Yeah.
So, th first of all, it seemslike.
This study, it was pretty wellconducted.
So I'm, I'm inclined to thinkthat this is probably the case.
And and part of that too isbecause it also aligns with what
We might think from from justthe theory of immunology.
So one of the things thathappens in our immune systems is
(17:12):
that we our immune system isgreat at identifying things that
we've been infected with.
And one of the ways that we getbetter and longer lasting
protection is to be exposed tolots of very slightly different
things.
And that sort of helps us, learnin, in the case.
SARS cov two, it helps us sortof learn the shape of the virus
(17:32):
in our immune system.
And so when we've been exposedto just the vaccine we learn
about what that vaccine, spikeprotein looks like, but of
course, the vaccines justcontain sort of the, the.
Elements of and the structure ofjust one part of the virus.
It's a very critical part.
And it's the one that our bodyprobably recognizes most easily,
but it's just one part.
(17:54):
Whereas the virus contains,these little spikes, which the
vaccines capture, but alsothere's a surface and there's
all sorts of little nooks andcrannies that that our immune
system is going to respond to.
So when we have a naturalinfection, the immune system is
probably going to identify partsof the spike in parts of the
other bits of the virus.
And we'll give you a an immuneresponse that is different than
the one that we get from thevaccine.
(18:15):
So.
When you have natural infectionand vaccination, you've been
exposed to a couple of differentthings.
And so that sort of gives yourimmune system sort of this wider
breadth of things that it canidentify.
And so it makes sense thatnatural infection plus
vaccination might be better thanjust two doses of the vaccine
for providing broaderprotection, especially against
the variants that have emergedsince the vaccines were
(18:38):
originally formulated.
That's not to say that, thevaccines are useless and we
should all just, we should haveall just gotten natural
infection, the great Barringtondeclaration people were.
Right.
Because to get that naturalinfection, it's a very costly
thing, you had to have about, ofCOVID in the first place.
And.
That's not good.
So the vaccines prevent you fromgetting COVID in the first
place, which is the pointaltogether.
(18:58):
And even if there is a bit of anedge in the amount and the
really, I think the, the bigthing is like the duration and
the breadth of protection thatyou get from natural infection
plus vaccination versus justvaccination alone.
You know that that difference isstill very small compared to the
difference in somebody who'stotally immune naive and
(19:21):
somebody who's been vaccinated.
So, absolutely.
You get the vaccine, it's, it'sstill makes an awful lot of
sense.
But I think, what, what this isdoing is it's helping us to
learn about how the immunesystem works.
And I think it's making a casefor adjusting our vaccine
formulation because that wouldhelp do.
What this natural infection plusvaccine is doing for us in the
first place.
(19:41):
Yeah.
So all of that is to say thatit's, it's sort of a complex
landscape, but I, but I do thinkthat that's probably the case.
Yeah.
Now what does this mean forpolicy to, you could also
envision a world in which thetraditional course of vaccines
consists of two vaccines, but ifyou have a previous confirmed
PCR infection, then maybe, maybeall you need is one dose of the
vaccine.
After that, we don't know forsure.
(20:02):
But I, definitely I know thatEric Topo has been sort of
arguing for that saying thatthat probably makes a lot of
sense.
And so, this is part of theconversation that's happening
right now.
So this, this study and thesekinds of findings do have really
practical Outcomes in, in, howwe, how we deal with the
vaccine.
Great.
Matt Boettger (20:20):
Now to rewind this, just so I could, there's a
couple of pieces that aremissing for me in light of what
we spoke about maybe eightmonths ago.
And I think I can reverseengineer this.
I'm going to do this as alayman, and then you can correct
or modify whatever I'm saying iswrong.
Because right now we're sayingnow, particularly in the Delta
variant, that it could be true,that natural immunity is better
(20:40):
than the vaccine, but you kindof give all the cab caveats of,
that doesn't mean the vaccines.
Now we right, eight months ago,we said the vaccine was better
than natural immunity by largeamount.
So what seems to be acontradiction?
I think I'm going to reconcileand say, because the vaccine, I
think you just said it already,the vaccine originally was made
for particular strain ofcoronavirus, which actually made
(21:03):
it more effective than naturalimmunity, but because of the
Delta on the scene now, which isobviously we couldn't prophecy
in the future, we had no ideaabout variants.
We had this crazy Delta.
Natural immunity may now have anedge because it had a particular
complexity about it.
That's not in the vaccine thatmay give it a slight edge to
handle the particular variant.
(21:24):
So both can be true because whatI said.
Stephen Kissler (21:27):
Exactly.
And there's, there's oneadditional point to that too,
which is the time that haselapsed.
So when you get vaccinated,you're that, you're, you're
getting dosed with this thingthat like your body is, it goes,
it's PR it's perfectlyformulated so that your body
mounts, this massive immuneresponse.
Right.
And so oftentimes your body willnow.
This year, I produce tons andtons and tons of antibodies
(21:50):
after a vaccine that is ordersof magnitude much, much higher
than what you get from a naturalinfection, but those antibodies
also decline over time.
And so at some point, do theysort of converge at similar
levels?
And so then what you weretalking about kicks in as well.
So maybe for the first couple ofweeks after vaccination, the
vaccine is actually much betterthan natural infection at
protecting you, but then athome, The antibody levels
(22:13):
converge.
And then you have thisadditional protection from
natural infection by having thisbroader response as well, that
causes the natural infection togive you the slight edge, some
number of weeks out.
So all of those things are kindof in play.
Thanks for bringing that up.
Yeah.
Matt Boettger (22:27):
Great, man.
If it's complicated, speaking ofcomplication, let's talk with
you.
You did the best segue ever,Stephen, because you talked
about antibodies.
So this is the other big stuffyou want to talk about.
There's two articles.
Unreal.
And I'm going to bring themtogether and I want Stephen to
help understand.
So this first one says that RNAvaccines seem to produce very
(22:48):
different antibody levels.
Now I'll put this in the shownotes.
The one thing I want tohighlight is this idea that it
talks about how Madonna kind ofMadrona has been this kind of in
the spotlight recently as beingthis kind of this winner right
now of, of, of, of running therace on the, on the various.
That it mentioned that like theModerna antibody response was
significantly more than thePfizer when you compare them at
(23:11):
the same time, like two ordersof two to three times more.
Right.
So you would think, oh my gosh,Madeira might be two or three
times more effective than five.
Of course, this article thenmade the caveat, wait a minute,
wait a minute.
We still haven't done this yet,but we need to look at another
level of not just antibodies,but neutralizing antibodies, and
that could bring the dirt andPfizer on the same playing
(23:33):
field.
We don't know, but it could.
So that's one article that Iwant to highlight.
I want you to talk about theother article, which I think is
related is this article is whatPfizer scientists consider the
biggest surprise about theirCOVID-19 vaccine.
And I'll read this because thisis important.
This came from I'll put in theshow notes, the aspect of
Pfizer's coronavirus vaccinethat really stunned the company.
(23:55):
Scientists was the fact thatvaccinated participants in the,
in the phase three efficacytrial had protections against
the pathogen by day 12, a timeat which there was barely any
antibody response, stat newsreports.
That that was the biggestsurprise.
Now then the next next paragraphsays it's possible.
(24:17):
He suggested that's moreimportant to measure cellular
immunity than look for robustantibody response.
So I want to repackage all ofthis, but during the huge
antibody response, it's better.
Maybe we need to look at neutralantibodies and then that'll
bring it down.
Wait a minute.
Maybe antibodies are somewhatirrelevant.
So maybe it's something else weadd in this mix.
(24:39):
What's going on?
How can we parse and put thisall together?
Stephen Kissler (24:43):
Oh man.
Th these are, these are great,great, great questions.
And I, I really want toempathize with the, with the
complexity of this.
So I'm, I I, I spend my timethinking about these kinds of
things all the time, and itstill makes my head spin.
I've got a textbook onimmunology.
That's like sitting out hereright now that I'm trying to
read it so that I can learnabout these kinds of things,
(25:03):
because they still confuse meall the time.
So, so we'll try to walk throughthis and and see see where we
get.
Right.
So Pfizer and Medina as you say,they're good, a couple of
studies that suggest thatMadrona has sort of been holding
up a little bit better thanPfizer has in, in the face of
the new variants.
And as time has elapsed sincevaccination.
So, a first of all, to theextent that that's true, like
(25:27):
you said, there's potentially ahigher antibody response and,
and it does seem like it mayprovide elevated protection
against Symptoms, further outfrom the vaccine as well.
So there, there are some studiesthat, that are actually looking,
not just at antibody levels, butat actual physical correlates of
protection.
And, and it seems like Medinamight have the edge there too.
So Y we had sort of thoughtabout these vaccines as
(25:48):
virtually equivalent.
Well, The two key differencesbetween the majority and the
Pfizer vaccine, or is thatfirst, the Medina has a longer
span of time between first andsecond dose.
And that's one of the bigquestions about the third doses
that we've been talking abouttoo, is that, not only do the
doses matter, but the amount oftime between them does too.
And generally the longer youhave between the doses, the more
(26:08):
durable your immune response isgoing to be.
So it's possible that even justthat one week makes a bit of a
difference.
The other thing is, and that.
I'm inclined to think that thismight actually be a bigger
thing, is that there's theMadrona dose is actually just
bigger.
You just get more?
Yeah.
I think it's like two to threetimes you get on like almost
twice or three times as muchstuff injected into you with the
(26:30):
maternal vaccine is what thePfizer my hunters that, that
might make a difference too.
And so, okay.
Yeah, so there's, there's thattoo.
So, so that might help us startto understand some of these
differences between the two, butyou bring up an important point
that, we've been looking a lotat antibody levels.
And is that what matters?
So, here again, the answer isyes and no.
(26:51):
So absolutely.
The antibodies that you canmeasure in a person's blood
stream.
Generally correlate with theamount of protection that you
get from infection, but it'snot, it's not equivalent to
protection.
One of the key differences isthat the relationship between
levels of antibodies in theblood and protection from
infection is not linear.
(27:13):
Just what we like.
So basically what that means isthat if you have, If the
difference between, say yourantibody levels in some random
units is 10 versus 20, thatmight be different than the
difference between 20 and 30 and30 and 40.
Because really maybe what weneed is some baseline level of
antibodies in our system.
And that if you're below that,then you have a chance of
(27:33):
getting infected.
If you're above that, you're notgoing to get infected.
And so if both vaccines aregiving you these astronomical
antibody levels, Then thedifferences between those
antibody levels.
It might not matter as long asyou're past that threshold.
And that, that actually seems tobe a pretty good mental model
for how immunity works.
So that's one reason why wehaven't been too concerned
about, these differences inantibody levels, because they
(27:54):
can be really hard to interpret,especially when both numbers are
very high.
Furthermore, the immune systemis very complex and what these
antibody levels are measuring isreally just one arm of the
immune system.
And in fact, it's the arm of theimmune system that for much of
the pandemic we've thought to beis maybe not the most critical
one.
Oftentimes we think aboutantibodies as these B cell
antibodies, but we've also beenthinking about, T cells, which
(28:17):
seemed to be the really criticalelement of the response which is
just a different, a differentpart of the immune system.
And so that also offers adifferent type of protection as
well.
So definitely, higher levels ofantibodies.
Probably on average lead tobetter protection, but that
difference might be very, veryslight.
Last thing.
So you had mentioned to thisstudy that if Pfizer was looking
(28:38):
at their clinical trials and wewere 12 days in and they were,
people were already starting toshow an immune response, that's
crazy.
They, they hadn't had that manyantibodies in their blood, so,
so where is this protectioncoming from?
And I think that what this isgetting at is something that
I'm, again, still learning lotsabout, which is that, our, our
bodies are not just bags ofcells.
(28:59):
We are these incredibly diverse.
And complicated biologicallandscapes and immunity sort of
plays out on each of thesedifferent levels in different
ways, in really important,different ways.
So for example, you think aboutthe way that you get infected
with a respiratory virus andgenerally it enters through your
mouth or nose and it fuses toyour epithelial cells.
(29:20):
And And once it's able to dothat, then it gets into your
cells and starts to proliferate,and then it can sort of migrate
down in your throat and intoyour lungs.
And then it can maybe cause asystemic infection.
And so there are all of thesedifferent stages, but one of the
critical things that can preventyou from getting infected in the
first place is if you, if youget a good immune response in
those.
Cells and those epithelialcells, which are already really
(29:42):
chockfull of immune stuff.
And so, and so getting a vaccineprobably does give you some
amount of immune protection fromthat first layer of defense that
you might not be able to measurein your bloodstream yet, because
it takes just a longer period oftime for those antibodies to
Mount up in your, in your bloodsystem.
Right.
You know your body in all of itsbrilliant wisdom, sort of
(30:04):
preferentially allocate some ofthat protection towards the
places where you're, whereyou're going to need it first.
And so that might be part of whywe've been seeing some of the
protection, on day 12, thatdoesn't really seem to make
sense if you're just measuringbloodstream antibodies in the
first place.
Now of course, w w the longlasting protection also seems to
be reversed in a sense whereactually that, that epithelial
protection, that sort of firstlayer of protection might
(30:26):
actually be much more temporaryand your bloodstream protection
might be much longer.
And so that might be part of thereason why we're seeing very
good protection against severedisease, which is when you want
lots of antibodies circulatingin your blood, but why we're
starting to see lots ofbreakthrough infections, because
they're able to get into thenose and cause that initial
infection.
Proceed further.
So not only are there differentplaces in the body where the
(30:49):
immune system acts differently,but the duration of immunity in
those different places isprobably different.
And all of this sort of playsinto this constellation of
things that we're starting tosee here very complex.
So again, I always want to tryto bring this back to like, what
does this imply for us?
Well, first of all, Do you seemto be good again, they're
protecting against severedisease which is great and
that's really what we want.
But we would also like somethingthat prevents us from getting
(31:11):
infected in the first place.
And they do that too.
They, they do lower thatprobability, but not quite to
the same degree.
There's some suggestion thatNasal spray vaccines might do a
better job of that.
And we already have things likethat for flu.
Especially for kids.
Kids will often get a nasalspray flu vaccine rather than an
injection.
And so we might start to thinkabout that.
Get immunity in the parts of thebody that need it most to
(31:33):
protect us from infection atthese different places.
And so I think that's a reallyinteresting area for further
work too.
So I wouldn't be surprised if atsome point we get a nasal spray
COVID vaccine that's suggestedmaybe even in addition to the
injections to give us sort ofthis broader spectrum of
response in the different, ourbody that need it,
Matt Boettger (31:49):
man.
That is fascinating.
Stephen, number one, do you, doyou play music?
Yeah, I do.
Okay.
Because.
I like hearing you talk on thiswhole epidemiology immune.
And like, it sounds like abeautiful orchestration of
music, the way like the firststarts with, with the nose and
the other, and then it goes tothe, then, then it hands over to
this other kind of major playerin the, in the, so I thought,
(32:09):
man, totally not.
I think.
Ironic that you are, you playmusic, but yet you're an
epidemiologist.
I think they're both just likebeautiful orchestration, so
Stephen Kissler (32:19):
fast.
Thanks.
And I think there's somethinginherent to it too.
There's one of the things thathas attracted me to infectious
diseases in the first place.
And actually some of the maththat I've done too, is that
there's, there's a certainpoetry to it.
That's, that's sort of inherentin the thing itself.
And so, yeah, there's, there's areal beauty to it that yeah.
Matt Boettger (32:34):
It was gorgeous.
Yeah.
Thank you for the explanation.
And so then this may be going alittle bit too far.
You talked about the nasal sprayand he talked about, and I know
there's other nasal sprays werelike natural nasal sprays.
Are these things that, I mean,clearly I'm not advocating a
replacement.
I'm not like that, whatever thatindex, whatever that stuff is,
that, that horse stuff, I'm nottrying to say this stuff and
(32:55):
saying like, is, does this showwhilst like nasal sprays are,
can be.
A nice extra bonus of doing,because that is an area of
entrance, that those thingscould help a little bit with the
protection as well, in general,not just COVID, but just like
cold and that kind of stuff.
Is that why we have nasal spraysas a protection?
Or is it more of just like, ah,to keep them keep them wet?
Stephen Kissler (33:17):
Yeah, it's right.
So.
I think that, for, for the nasalspray vaccines, that makes a lot
of sense because it's basicallysending the, sending the
antigenic stuff to the placesthat that's going to get exposed
to the virus first.
Now there are, of course, othernasal sprays that sort of help
keep your nasal passages wet.
And, and that probably helps tosome degree.
Not so much through the immuneresponse, but as one of the
(33:40):
hypothesis, why why respiratoryinfections are more common in
the winter months is partlybecause it's just drier.
And so one of the ways you mightprotect against that is by
making your nasal passages alittle bit more tropical.
And one of the ways to do thatis through a nasal spray.
Right.
And so, so, so that's sort ofmore of like a physical and
physiological thing.
I, I haven't done the researchinto, to, to like compare rates
of infection in different peoplewho have used a nasal spray or
(34:02):
not.
So I can't, I can't speakintelligence, but sure.
It would make sense.
And it would be a differentmechanism.
Similar idea that basicallyyou're, you're sort of paying
attention to the part of thebody that is exposed first.
And if you can prevent aninfection from happening in the
first place, then you save yourbody a lot of trouble down the
Matt Boettger (34:20):
line.
Yeah, absolutely.
No, thanks for sharing.
That was great, Stephen.
Yeah.
One last thing I'll just mentionhere.
Why I didn't talk to Stephenabout this?
I just saw this article.
I'm always interested in abouthow COVID and children.
Cause I have three little boysrun facts, but they didn't, who
knows when that's going to beavailable.
But I saw this article, mostchildren with severe post COVID
19 condition in fine health yearlater.
(34:42):
So just a study following kidsafter a year who've had severe,
it looks right.
Is promising that these likeeither long holler, what are you
going to call it resolve overtime, right?
Naturally or back to their norm.
Healthy reality.
So just a little drop of hopefor that as well.
Thank you again, Stephen.
This was awesome.
I learned a lot and I guessingour listeners learned a ton as
(35:03):
well.
If you wanna support us again,patrion.com/pandemic podcast,$5
a month.
One time gift Venmo, PayPal onthe show notes.
S a S T E P H E N K I S S L E R.
And Twitter.
You can follow him, Stephen.
You can reach out to me,matt@livingthereal.com drop a
line.
If you have any questions, we'dlove to answer them.
(35:25):
And I think that is it.
I hope you guys have a wonderfulweek and we'll see you probably
and two weeks, maybe one whoknows no more than two take care
and have a wonderful week.
Okay.
Bye bye.
You're listening to the pandemic POS podcast,
where we equip you to live themost real life possible in the
face of these crises.
My name is Matt Boettger and I'mjoined with one great friend of
mine.
Dr.
Stephen Kissler epidemiologists,the Harvard school of public
health.
How are you?
Stephen Kissler (00:13):
Fine, sir?
Hello, I'm doing all right.
It's happy post labor dayweekend.
Yes.
Matt Boettger (00:19):
Happy post labor day.
Everybody who celebrates laborday in the U S here.
We will make a quickannouncement if you notice where
we're kind of starting to go toevery two weeks.
Maybe we'll go back to everyweek.
It's not because there's not anynews.
Obviously it's just that life isjust crazy for Stephen, myself,
mark, and to get us all to rallyand be every week has been a
little more difficult thanusual.
(00:40):
So we may go back to once aweek.
At some point in time, we maystay every other, every other
week as such, you know, we'rehere.
We want us to continue to behere, but we're trying to
navigate being present andavailable to all of you.
And navigate our own crazylives, right Stephen?
Stephen Kissler (00:56):
Oh yeah.
Matt Boettger (00:56):
Oh yeah.
Well said, well said, so if you,if you can leave us a review,
even if we're going every otherweek give us a little shout out
and let us know how we're doing.
You can do that on applepodcasts and think there's
another other platform you cansupport us that would help us
tremendously.
Maybe even get us to be a littlemore often just to help us get
the support.
We need an offset.
It.
At patrion.com/pandemic podcastsas little as$5 a month can help
(01:20):
a lot as well, as well asone-time gifts at PayPal or
Venmo and both they're all inthe show notes.
So there you go.
Okay.
So I feel like we have a lot totalk about.
There's some things I thinkwe'll try to just breeze right
over.
Just talk about it.
And then Stephen and I talkedbefore we start recording,
there's a couple of things thatseem really fascinating, and I
(01:42):
want to really unpack it withStephen.
I want to learn a lot more.
But before I want to get startedwith this, I saw this article,
Stephen, and I don't know, kindof surprise me.
Not really, but this article isBiden said, he'd follow the
silent side science to experts.
He's sometimes fallen short.
Now, when I kind of dove intothis expert, we're not going to
(02:02):
talk about politics per se, inthat area.
But when I dove in his article,it seemed like the focus of all
things.
And they talked about teachersbeing vaccinated and that
might've been not following CDCguidelines.
But the meat of this wholearticle was really about
boosters and how he didn'tfollow the science.
So I want to pick your brainbecause you're an expert.
(02:24):
So, and we've talked about thisbefore about boosters.
Should we, should we not?
And is it good?
Is it ethical?
And is he falling the science.
With the idea of wanting toadvance boosters for the U S is
he not following science or isthis more than just science?
Is it policy?
And this is just some kind ofswitch bait headline that we
need to just ignore completelyaltogether.
(02:45):
Sure.
Stephen Kissler (02:46):
Yeah.
So, I mean, there's, I thinkthere's two layers of complexity
to this.
So the first.
The thing about it is that, I,I, and many of my colleagues
were w were taken off guards tosome extent when the when the
administration first said that,we'll, we'll be having boosters
(03:06):
for Americans by X date,whatever.
And, and they've actually sent,sort of walked back from that a
little bit.
And there were two reasons whywe were surprised by that.
The first is that there was.
Absolutely emerging evidence atthat point that that the third
dose of the MRN vaccines couldbe beneficial towards giving you
a better immune response, alonger lasting immunity.
(03:27):
And this will make sense off ofwhat we know about immunology
too.
Many of the multidose vaccinesthat we get as kids are also
separated by, on the order ofsix months to a year and that
separation can be reallycritically important for giving
you the long lasting and unity.
So.
Since, and there was someemerging data suggesting that
that might be the case, but westill absolutely, at that point,
(03:48):
hadn't reached what we like tocall a scientific consensus.
There were some studies thatwere supporting this, but one,
one or two studies does not makeproof or does not make, a, a
really compelling story.
The, the whole practice ofscience is sort of steering this
massive ship of human knowledge.
And one, one little study isn'tgoing to do that.
Really.
We need lots of corroboratingevidence from different angles.
(04:09):
So.
What we were waiting for asscientists.
And that's why, when thisannouncement first came out,
right.
Maybe a little premature, eventhough it's probably pointed in
the right direction.
So, now that said, in themeantime there, a lot of that
corroborating evidence has comethrough and it does suggest that
a additional dose of the MRAvaccines can be very effective
at giving you higher levels ofimmunity, longer lasting
(04:31):
immunity, unity.
So, so now the, in some ways thescience has kind of caught up.
And so now it makes a lot ofsense, but, but the timing of it
was was surprising.
The second thing is thatGenerally political
administrations are not thepeople who make these
announcements.
Right.
Like this is, this is somethingthat should be coming from the
FDA.
It requires, at this pointagain, a careful evaluation of
(04:52):
the evidence a carefuldeliberation amongst experts who
know about many different typesof vaccines and about these
vaccines in particular, which iswhat the FDA exists for.
And so that was another thing.
So it was like, why, why are wegetting this announcement from a
the, the white house and notfrom the FDA?
And so it, it, it was sort oflike putting the cart before the
horse.
And so, so that was another oneof the more sort of policy side
(05:14):
with scientific overtones that,that caused some surprises.
And now the last thing ofcourse, is that in the midst of
this now, even though thescience does seem to be
suggesting that a third dose ofMRN vaccines does seem like it
will probably be a very goodidea at some point there's still
a lot of really thorny policyquestions as to how to organize
the rollout.
(05:34):
How do we, yeah.
Giving third doses in the UnitedStates versus first doses in
much of the rest of the world.
How, how does this work?
How do we keep track of things?
Frankly, probably many peoplehave already gone out and gotten
their booster shots because inmany places you can just walk up
and say, I want a vaccine andshe can get it right.
Which is not at all, somethingthat I would recommend at this
(05:55):
point, but as possible.
Sure that people have done it.
And so, one of the big issuesnow is that we, we don't have
very good record keeping aroundwho's gotten which vaccines and
how that plays together, whichmakes doing research a lot more
difficult.
It makes setting policies a lotmore difficult.
So there are a lot of reallythorny questions in here that,
that aren't just science to thatI think we really urgently need
(06:16):
to get sorted out.
And I think that, that seems tobe what this article was
pointing.
Matt Boettger (06:20):
Okay, that makes sense.
So now is the booster shot?
Nothing more than the same?
Shot given at the beginning.
It's not like this new revisedone that's tweaked for the
Delta.
The heap hearing about has beenunder undergoing this is just
the same one that's originated.
There's a third
Stephen Kissler (06:35):
version third.
Yeah.
Currently it seems like that.
Which, which again is aninteresting choice too.
I know my, my colleague, MichaelMina has been very outspoken
about the fact that like, w w wehave the capability of updating
these vaccines, we might as wellgive something that's more
closely related to the Delta.
And one of the reasons why notis because that might be subject
(06:55):
to a more stringent safety andefficacy review, which might
delay, how long it would takefor that to actually get rolled
out.
So again, there are verypractical reasons why we might
use the original dose, but rightnow that that is the case that
it's the original Formulationthat is currently being used for
for these third doses.
Now I imagine some of ourlisteners will probably notice
(07:17):
that I've been sort of steeringaway from calling it a booster
and been calling it a third doseof the series as well.
And part of that is because It'ssplitting hairs a little bit,
but and, and definitely, boosteryour shot is, is the thing that
has really been prevalent in themedia.
But I think really what we'retrying to do here is to
understand, what should theactual series of COVID
(07:38):
vaccination be?
And when you think of, when youthink of something like tetanus,
we get booster shots every 10years or so.
Right.
And you need that for life.
And so what a booster shotimplies is that it's sort of
something that's ongoing inperpetuity, but we're not sure
that that's going to be the casefor COVID right now.
Really what we're trying to dois work out, how long should the
series be and how far apartshould they be?
(07:59):
Sequenced it's it's possible.
We might need it.
COVID shots, as booster shots,sort of like we do the flu, it's
sort of like we do for tetanus.
But I'm actually hopeful thatmaybe actually what we need is
like a two or three dose seriesand then we're done.
And so that's part of what we'retrying to work out too.
And we're just not sure what youmean.
Settings we're going to be in,so it, okay.
That's not to say that weshouldn't be using the term
booster, but that's, that's sortof why I've been steering away
(08:20):
from it.
It's cause we're not really sureabout that yet.
Matt Boettger (08:22):
That makes sense.
And for those of you listeningno, Stephen is not next to a
dentist office for the drillingsomebodies teeth.
It's actually construction workoutside and we have no choice,
but he's got the
Stephen Kissler (08:33):
window closed.
Yeah.
Sorry about that.
No, it's okay.
It's like right outside.
So
Matt Boettger (08:38):
living in the city life, man city life.
Okay.
So let's get straight into it.
The reason why would be onebooster is why we're talking
about boosters because there'sso many variants.
And so I want to get caught upto speed with you, Stephen.
So we know about the Delta.
This has been the headlinesforever.
I like to get the status from onyour end.
Now there's a C1 to have no cluewhy he doesn't have a Greek
(08:59):
letter, but maybe you canexplain why maybe it's too early
or whatever.
That seems like something to beaware of.
Can you talk about that?
And there's the mu these twoseem to be really kind of
percolating to the surface andthe media outlets I heard about
Mo maybe evading the vaccineimmunity.
Where are we at in this?
Where do you expect it to go?
(09:21):
I, I heard about with Moo at onepoint in time, the U S was the
only place in the world by whichit was rising.
Sounds like that's differentnow.
So that's maybe good news, butguest cuts to speed.
Where are we at and where shouldwe be concerned?
Stephen Kissler (09:33):
Yeah.
So, first a point on the naming.
So, these different viruslineages all have the Sort of
long mouthful letter plus awhole bunch of numbers, plus a
whole bunch of dots.
And, and that, when we weretalking about and B 1 6, 1 7
0.2, all of these things that's,that's still going on under the
(09:54):
surface and, and, and thosethose names are very useful and
informative for those of us whoare, frankly nerds and are
interested in, like figuring outhow all of these things are
related to one another.
So the first thing that one ofthe virus gets is, is one of
those associations, but thenonce it becomes classified by
the CDC or the world healthorganization as a variant of
interest or a variant ofconcern, meaning that we've seen
(10:17):
a major outbreak of thisparticular variant in a location
and.
No genetic markers that suggestthat it's something that we
ought to be paying attention to.
And then we give it a Greekletter.
So C1 two, hasn't gotten a Greekletter yet because it hasn't
quite crossed that threshold ofconcern yet.
Whereas new and alpha betagamma, Delta, et cetera have all
sort of crossed that level ofconcern at some point.
(10:39):
And so that sort of gives us ashorthand for referring to these
different.
Got it.
Nope.
You're right.
We've been hearing a lot moreabout both the variant, the new
variant and yeah, and I think,rightly the question is like,
how concerned should we be?
So, as with most of thesevariants, in some ways it's the
same old story playing itselfout again in that So we have a
(11:00):
variant they've each beenincreasing in particular
geographic locations.
And so that's 0.1 of concern,because if, if a variant is able
to increase in prevalence, thenthat suggests that it is for
some reason more transmissiblethan whatever is spreading at
the current moment in thatparticular location.
So, That's sort of 0.1 0.2 thenis, okay.
(11:20):
So does the variant contain thegenetic markers that we know to
be associated with things thatwe might be concerned about?
So there are different ways oftesting for this, for example,
in laboratories you can sort oftweak the structure of different
parts of the virus.
Remaking the virus itself.
And then you can expose that todifferent antibodies and see if
that has the ability to getaround some of our immune
(11:41):
response.
And so we know what some ofthose mutations are, even if
they haven't yet emerged innature.
And so when we start to seethose things emerge, we can say,
okay, well this, this at leasthas one of those markers that
could make it get around ourimmune system or could make it
more transmissible.
We don't know for sure if itdoes, but it's, it's definitely
something worth being concernedabout.
And, and for the, for the mew inparticular, that's something
(12:01):
that we've seen where it's, ithas some of these mutations, but
we haven't yet seen how thatplays out in the real world.
Totally.
So, the key thing about both ofthese variants and really about
everything that we've seen sincethe Delta has come out and you
were alluding to this during theintroduction to this bit So far,
it doesn't seem like anythinghas really been able to
out-compete Delta.
Even the mew, get emerged.
You can see the sort of ebb andflow of different variants
(12:24):
sometimes because sometimes aviral strain will get lucky.
It will reach a community andthere will be a couple of super
spreading events and it willrise and prevalence.
And all of a sudden we'll say,oh, here's something that we may
be out to be concerned about,but the real concern.
As happened with alpha and ashappened with Delta is when you
see that outbreak, like we sawin the UK, like we saw in India,
(12:45):
and then it startsrecapitulating itself in many
different places, because thatsuggests that there's this
robust ability to out-competewhatever is there in the first
place.
Whereas it seems like thesevariants so far, wherever they
have emerged, they've kind ofbeen driven out again by Delta.
And so no matter what mutations,no matter what.
Functions.
We call them phenotypes.
(13:05):
These, these viruses have ifthey're not able to spread in
the context of another spreadingvirus, then they're never going
to really take off.
They might cause smalloutbreaks, but they'll
eventually be driven away by thething that is more
transmissible, which iscurrently the Delta.
And so right now it really seemslike.
Delta's the thing, that, that isthe thing where consistently
(13:27):
wherever Delta is spreading,nothing else has really been
able to hang on for long.
And so that's the upshot.
And so there's, there's,definitely a lot of chatter and,
and these are things that weneed to be paying attention to
you.
But right now, the thing that'son my mind is Delta.
Yeah.
Matt Boettger (13:41):
And then it kinda reminds me of Lambda where I
remember early on talking aboutLambda was in south America.
There was a lot of worry aboutthis and then it just never
really could get an edge,because of the Delta.
And so it's clearly it seems tobe possible.
The variant could evolve.
The dad's actually is maybe moredangerous.
Can bring people quicker tohospital could be so, so changed
(14:04):
that it evades even vaccines,but then just dies off.
But that doesn't, it doesn'thave the capacity to compete
with Delta, which might not beas dangerous, but it's just so
vibrant and so contagious thatit just dominates everything
else.
Is that true?
That you could have worsevariants in the sense of
hospitalization?
But because they don't, they'renot quite as V that viral ENT,
(14:24):
so to speak, they just can'tcompete with Delta.
So Delta keeps it at bay,
Stephen Kissler (14:28):
right?
Yeah.
And just to note on terms, andthis is super confusing, you
would, you would think that,viral, it means contagious, but
actually viral int is usuallywhat we use to describe the
clinical severity.
And so, yeah, just just a pointto our listeners.
So, so actually, right.
So, so.
Amend that statement for what Ithink you were saying.
(14:49):
Was it just that there might bemore violent or more clinically
severe strains that sound veryconcerning, but if they aren't
as contagious or transmissibleas the Delta, then they're not
really going to be able to takeoff.
And so that's, that's the realconcern is that generally an
increase in contagiousness ortransmissibility is usually a
much bigger.
Okay.
Matt Boettger (15:08):
Great.
Thank you for thatclarification.
I'm the lay man that I'm anexpert on the show.
Okay.
Yeah.
So let's, that sounds good.
Like hopeful news, at least whenit comes to the one too.
Now I'm guessing because it's Cgoing from B to C, that means
there is a stronger change.
Is that how it goes?
Like a, B, C it's it's it'smore, it's changed more
dramatically.
So
Stephen Kissler (15:27):
now it's a new letter.
Yeah.
Thankfully, somehow there'sactually something that makes
sense about this whole thingthat intuitive.
Exactly.
Matt Boettger (15:37):
Great.
Good to know.
Okay.
So I want to make a quick justbookmark this.
We're not going to talk muchabout this.
I read this from the Atlantic,the masks were working all
along.
I know every once in a while wecome back, we talk about this,
but this seems to be anincredible study done in
Bangladesh.
Probably the best study done yeton the ethicacy of masks.
We're not going to talk aboutthis, but I'm going to put in
(15:58):
the show notes.
It's a great read.
Just proves the point of howpowerful and really good mass
are to help keep COVID at bay.
Again, not the only tool in ourtoolbox, but another one that's
just really great along with allthe other ones as well.
So please check that out in theshow notes.
So we have two big subjects wewant to talk about that I think
(16:23):
are really interesting.
I saw this Stephen and a handfulof article.
Banging over and over this drum,this idea, this came from
Israel, the study in Israelthat's that, that, that
apparently showed that naturalimmunity is more effective than
the vaccine when it comes to theDelta variant.
(16:47):
Now, is this true?
Or how, how do we navigate this
Stephen Kissler (16:50):
terrain?
Yeah.
So, th first of all, it seemslike.
This study, it was pretty wellconducted.
So I'm, I'm inclined to thinkthat this is probably the case.
And and part of that too isbecause it also aligns with what
We might think from from justthe theory of immunology.
So one of the things thathappens in our immune systems is
(17:12):
that we our immune system isgreat at identifying things that
we've been infected with.
And one of the ways that we getbetter and longer lasting
protection is to be exposed tolots of very slightly different
things.
And that sort of helps us, learnin, in the case.
SARS cov two, it helps us sortof learn the shape of the virus
(17:32):
in our immune system.
And so when we've been exposedto just the vaccine we learn
about what that vaccine, spikeprotein looks like, but of
course, the vaccines justcontain sort of the, the.
Elements of and the structure ofjust one part of the virus.
It's a very critical part.
And it's the one that our bodyprobably recognizes most easily,
but it's just one part.
(17:54):
Whereas the virus contains,these little spikes, which the
vaccines capture, but alsothere's a surface and there's
all sorts of little nooks andcrannies that that our immune
system is going to respond to.
So when we have a naturalinfection, the immune system is
probably going to identify partsof the spike in parts of the
other bits of the virus.
And we'll give you a an immuneresponse that is different than
the one that we get from thevaccine.
(18:15):
So.
When you have natural infectionand vaccination, you've been
exposed to a couple of differentthings.
And so that sort of gives yourimmune system sort of this wider
breadth of things that it canidentify.
And so it makes sense thatnatural infection plus
vaccination might be better thanjust two doses of the vaccine
for providing broaderprotection, especially against
the variants that have emergedsince the vaccines were
(18:38):
originally formulated.
That's not to say that, thevaccines are useless and we
should all just, we should haveall just gotten natural
infection, the great Barringtondeclaration people were.
Right.
Because to get that naturalinfection, it's a very costly
thing, you had to have about, ofCOVID in the first place.
And.
That's not good.
So the vaccines prevent you fromgetting COVID in the first
place, which is the pointaltogether.
(18:58):
And even if there is a bit of anedge in the amount and the
really, I think the, the bigthing is like the duration and
the breadth of protection thatyou get from natural infection
plus vaccination versus justvaccination alone.
You know that that difference isstill very small compared to the
difference in somebody who'stotally immune naive and
(19:21):
somebody who's been vaccinated.
So, absolutely.
You get the vaccine, it's, it'sstill makes an awful lot of
sense.
But I think, what, what this isdoing is it's helping us to
learn about how the immunesystem works.
And I think it's making a casefor adjusting our vaccine
formulation because that wouldhelp do.
What this natural infection plusvaccine is doing for us in the
first place.
(19:41):
Yeah.
So all of that is to say thatit's, it's sort of a complex
landscape, but I, but I do thinkthat that's probably the case.
Yeah.
Now what does this mean forpolicy to, you could also
envision a world in which thetraditional course of vaccines
consists of two vaccines, but ifyou have a previous confirmed
PCR infection, then maybe, maybeall you need is one dose of the
vaccine.
After that, we don't know forsure.
(20:02):
But I, definitely I know thatEric Topo has been sort of
arguing for that saying thatthat probably makes a lot of
sense.
And so, this is part of theconversation that's happening
right now.
So this, this study and thesekinds of findings do have really
practical Outcomes in, in, howwe, how we deal with the
vaccine.
Great.
Matt Boettger (20:20):
Now to rewind this, just so I could, there's a
couple of pieces that aremissing for me in light of what
we spoke about maybe eightmonths ago.
And I think I can reverseengineer this.
I'm going to do this as alayman, and then you can correct
or modify whatever I'm saying iswrong.
Because right now we're sayingnow, particularly in the Delta
variant, that it could be true,that natural immunity is better
(20:40):
than the vaccine, but you kindof give all the cab caveats of,
that doesn't mean the vaccines.
Now we right, eight months ago,we said the vaccine was better
than natural immunity by largeamount.
So what seems to be acontradiction?
I think I'm going to reconcileand say, because the vaccine, I
think you just said it already,the vaccine originally was made
for particular strain ofcoronavirus, which actually made
(21:03):
it more effective than naturalimmunity, but because of the
Delta on the scene now, which isobviously we couldn't prophecy
in the future, we had no ideaabout variants.
We had this crazy Delta.
Natural immunity may now have anedge because it had a particular
complexity about it.
That's not in the vaccine thatmay give it a slight edge to
handle the particular variant.
(21:24):
So both can be true because whatI said.
Stephen Kissler (21:27):
Exactly.
And there's, there's oneadditional point to that too,
which is the time that haselapsed.
So when you get vaccinated,you're that, you're, you're
getting dosed with this thingthat like your body is, it goes,
it's PR it's perfectlyformulated so that your body
mounts, this massive immuneresponse.
Right.
And so oftentimes your body willnow.
This year, I produce tons andtons and tons of antibodies
(21:50):
after a vaccine that is ordersof magnitude much, much higher
than what you get from a naturalinfection, but those antibodies
also decline over time.
And so at some point, do theysort of converge at similar
levels?
And so then what you weretalking about kicks in as well.
So maybe for the first couple ofweeks after vaccination, the
vaccine is actually much betterthan natural infection at
protecting you, but then athome, The antibody levels
(22:13):
converge.
And then you have thisadditional protection from
natural infection by having thisbroader response as well, that
causes the natural infection togive you the slight edge, some
number of weeks out.
So all of those things are kindof in play.
Thanks for bringing that up.
Yeah.
Matt Boettger (22:27):
Great, man.
If it's complicated, speaking ofcomplication, let's talk with
you.
You did the best segue ever,Stephen, because you talked
about antibodies.
So this is the other big stuffyou want to talk about.
There's two articles.
Unreal.
And I'm going to bring themtogether and I want Stephen to
help understand.
So this first one says that RNAvaccines seem to produce very
(22:48):
different antibody levels.
Now I'll put this in the shownotes.
The one thing I want tohighlight is this idea that it
talks about how Madonna kind ofMadrona has been this kind of in
the spotlight recently as beingthis kind of this winner right
now of, of, of, of running therace on the, on the various.
That it mentioned that like theModerna antibody response was
significantly more than thePfizer when you compare them at
(23:11):
the same time, like two ordersof two to three times more.
Right.
So you would think, oh my gosh,Madeira might be two or three
times more effective than five.
Of course, this article thenmade the caveat, wait a minute,
wait a minute.
We still haven't done this yet,but we need to look at another
level of not just antibodies,but neutralizing antibodies, and
that could bring the dirt andPfizer on the same playing
(23:33):
field.
We don't know, but it could.
So that's one article that Iwant to highlight.
I want you to talk about theother article, which I think is
related is this article is whatPfizer scientists consider the
biggest surprise about theirCOVID-19 vaccine.
And I'll read this because thisis important.
This came from I'll put in theshow notes, the aspect of
Pfizer's coronavirus vaccinethat really stunned the company.
(23:55):
Scientists was the fact thatvaccinated participants in the,
in the phase three efficacytrial had protections against
the pathogen by day 12, a timeat which there was barely any
antibody response, stat newsreports.
That that was the biggestsurprise.
Now then the next next paragraphsays it's possible.
(24:17):
He suggested that's moreimportant to measure cellular
immunity than look for robustantibody response.
So I want to repackage all ofthis, but during the huge
antibody response, it's better.
Maybe we need to look at neutralantibodies and then that'll
bring it down.
Wait a minute.
Maybe antibodies are somewhatirrelevant.
So maybe it's something else weadd in this mix.
(24:39):
What's going on?
How can we parse and put thisall together?
Stephen Kissler (24:43):
Oh man.
Th these are, these are great,great, great questions.
And I, I really want toempathize with the, with the
complexity of this.
So I'm, I I, I spend my timethinking about these kinds of
things all the time, and itstill makes my head spin.
I've got a textbook onimmunology.
That's like sitting out hereright now that I'm trying to
read it so that I can learnabout these kinds of things,
(25:03):
because they still confuse meall the time.
So, so we'll try to walk throughthis and and see see where we
get.
Right.
So Pfizer and Medina as you say,they're good, a couple of
studies that suggest thatMadrona has sort of been holding
up a little bit better thanPfizer has in, in the face of
the new variants.
And as time has elapsed sincevaccination.
So, a first of all, to theextent that that's true, like
(25:27):
you said, there's potentially ahigher antibody response and,
and it does seem like it mayprovide elevated protection
against Symptoms, further outfrom the vaccine as well.
So there, there are some studiesthat, that are actually looking,
not just at antibody levels, butat actual physical correlates of
protection.
And, and it seems like Medinamight have the edge there too.
So Y we had sort of thoughtabout these vaccines as
(25:48):
virtually equivalent.
Well, The two key differencesbetween the majority and the
Pfizer vaccine, or is thatfirst, the Medina has a longer
span of time between first andsecond dose.
And that's one of the bigquestions about the third doses
that we've been talking abouttoo, is that, not only do the
doses matter, but the amount oftime between them does too.
And generally the longer youhave between the doses, the more
(26:08):
durable your immune response isgoing to be.
So it's possible that even justthat one week makes a bit of a
difference.
The other thing is, and that.
I'm inclined to think that thismight actually be a bigger
thing, is that there's theMadrona dose is actually just
bigger.
You just get more?
Yeah.
I think it's like two to threetimes you get on like almost
twice or three times as muchstuff injected into you with the
(26:30):
maternal vaccine is what thePfizer my hunters that, that
might make a difference too.
And so, okay.
Yeah, so there's, there's thattoo.
So, so that might help us startto understand some of these
differences between the two, butyou bring up an important point
that, we've been looking a lotat antibody levels.
And is that what matters?
So, here again, the answer isyes and no.
(26:51):
So absolutely.
The antibodies that you canmeasure in a person's blood
stream.
Generally correlate with theamount of protection that you
get from infection, but it'snot, it's not equivalent to
protection.
One of the key differences isthat the relationship between
levels of antibodies in theblood and protection from
infection is not linear.
(27:13):
Just what we like.
So basically what that means isthat if you have, If the
difference between, say yourantibody levels in some random
units is 10 versus 20, thatmight be different than the
difference between 20 and 30 and30 and 40.
Because really maybe what weneed is some baseline level of
antibodies in our system.
And that if you're below that,then you have a chance of
(27:33):
getting infected.
If you're above that, you're notgoing to get infected.
And so if both vaccines aregiving you these astronomical
antibody levels, Then thedifferences between those
antibody levels.
It might not matter as long asyou're past that threshold.
And that, that actually seems tobe a pretty good mental model
for how immunity works.
So that's one reason why wehaven't been too concerned
about, these differences inantibody levels, because they
(27:54):
can be really hard to interpret,especially when both numbers are
very high.
Furthermore, the immune systemis very complex and what these
antibody levels are measuring isreally just one arm of the
immune system.
And in fact, it's the arm of theimmune system that for much of
the pandemic we've thought to beis maybe not the most critical
one.
Oftentimes we think aboutantibodies as these B cell
antibodies, but we've also beenthinking about, T cells, which
(28:17):
seemed to be the really criticalelement of the response which is
just a different, a differentpart of the immune system.
And so that also offers adifferent type of protection as
well.
So definitely, higher levels ofantibodies.
Probably on average lead tobetter protection, but that
difference might be very, veryslight.
Last thing.
So you had mentioned to thisstudy that if Pfizer was looking
(28:38):
at their clinical trials and wewere 12 days in and they were,
people were already starting toshow an immune response, that's
crazy.
They, they hadn't had that manyantibodies in their blood, so,
so where is this protectioncoming from?
And I think that what this isgetting at is something that
I'm, again, still learning lotsabout, which is that, our, our
bodies are not just bags ofcells.
(28:59):
We are these incredibly diverse.
And complicated biologicallandscapes and immunity sort of
plays out on each of thesedifferent levels in different
ways, in really important,different ways.
So for example, you think aboutthe way that you get infected
with a respiratory virus andgenerally it enters through your
mouth or nose and it fuses toyour epithelial cells.
(29:20):
And And once it's able to dothat, then it gets into your
cells and starts to proliferate,and then it can sort of migrate
down in your throat and intoyour lungs.
And then it can maybe cause asystemic infection.
And so there are all of thesedifferent stages, but one of the
critical things that can preventyou from getting infected in the
first place is if you, if youget a good immune response in
those.
Cells and those epithelialcells, which are already really
(29:42):
chockfull of immune stuff.
And so, and so getting a vaccineprobably does give you some
amount of immune protection fromthat first layer of defense that
you might not be able to measurein your bloodstream yet, because
it takes just a longer period oftime for those antibodies to
Mount up in your, in your bloodsystem.
Right.
You know your body in all of itsbrilliant wisdom, sort of
(30:04):
preferentially allocate some ofthat protection towards the
places where you're, whereyou're going to need it first.
And so that might be part of whywe've been seeing some of the
protection, on day 12, thatdoesn't really seem to make
sense if you're just measuringbloodstream antibodies in the
first place.
Now of course, w w the longlasting protection also seems to
be reversed in a sense whereactually that, that epithelial
protection, that sort of firstlayer of protection might
(30:26):
actually be much more temporaryand your bloodstream protection
might be much longer.
And so that might be part of thereason why we're seeing very
good protection against severedisease, which is when you want
lots of antibodies circulatingin your blood, but why we're
starting to see lots ofbreakthrough infections, because
they're able to get into thenose and cause that initial
infection.
Proceed further.
So not only are there differentplaces in the body where the
(30:49):
immune system acts differently,but the duration of immunity in
those different places isprobably different.
And all of this sort of playsinto this constellation of
things that we're starting tosee here very complex.
So again, I always want to tryto bring this back to like, what
does this imply for us?
Well, first of all, Do you seemto be good again, they're
protecting against severedisease which is great and
that's really what we want.
But we would also like somethingthat prevents us from getting
(31:11):
infected in the first place.
And they do that too.
They, they do lower thatprobability, but not quite to
the same degree.
There's some suggestion thatNasal spray vaccines might do a
better job of that.
And we already have things likethat for flu.
Especially for kids.
Kids will often get a nasalspray flu vaccine rather than an
injection.
And so we might start to thinkabout that.
Get immunity in the parts of thebody that need it most to
(31:33):
protect us from infection atthese different places.
And so I think that's a reallyinteresting area for further
work too.
So I wouldn't be surprised if atsome point we get a nasal spray
COVID vaccine that's suggestedmaybe even in addition to the
injections to give us sort ofthis broader spectrum of
response in the different, ourbody that need it,
Matt Boettger (31:49):
man.
That is fascinating.
Stephen, number one, do you, doyou play music?
Yeah, I do.
Okay.
Because.
I like hearing you talk on thiswhole epidemiology immune.
And like, it sounds like abeautiful orchestration of
music, the way like the firststarts with, with the nose and
the other, and then it goes tothe, then, then it hands over to
this other kind of major playerin the, in the, so I thought,
(32:09):
man, totally not.
I think.
Ironic that you are, you playmusic, but yet you're an
epidemiologist.
I think they're both just likebeautiful orchestration, so
Stephen Kissler (32:19):
fast.
Thanks.
And I think there's somethinginherent to it too.
There's one of the things thathas attracted me to infectious
diseases in the first place.
And actually some of the maththat I've done too, is that
there's, there's a certainpoetry to it.
That's, that's sort of inherentin the thing itself.
And so, yeah, there's, there's areal beauty to it that yeah.
Matt Boettger (32:34):
It was gorgeous.
Yeah.
Thank you for the explanation.
And so then this may be going alittle bit too far.
You talked about the nasal sprayand he talked about, and I know
there's other nasal sprays werelike natural nasal sprays.
Are these things that, I mean,clearly I'm not advocating a
replacement.
I'm not like that, whatever thatindex, whatever that stuff is,
that, that horse stuff, I'm nottrying to say this stuff and
(32:55):
saying like, is, does this showwhilst like nasal sprays are,
can be.
A nice extra bonus of doing,because that is an area of
entrance, that those thingscould help a little bit with the
protection as well, in general,not just COVID, but just like
cold and that kind of stuff.
Is that why we have nasal spraysas a protection?
Or is it more of just like, ah,to keep them keep them wet?
Stephen Kissler (33:17):
Yeah, it's right.
So.
I think that, for, for the nasalspray vaccines, that makes a lot
of sense because it's basicallysending the, sending the
antigenic stuff to the placesthat that's going to get exposed
to the virus first.
Now there are, of course, othernasal sprays that sort of help
keep your nasal passages wet.
And, and that probably helps tosome degree.
Not so much through the immuneresponse, but as one of the
(33:40):
hypothesis, why why respiratoryinfections are more common in
the winter months is partlybecause it's just drier.
And so one of the ways you mightprotect against that is by
making your nasal passages alittle bit more tropical.
And one of the ways to do thatis through a nasal spray.
Right.
And so, so, so that's sort ofmore of like a physical and
physiological thing.
I, I haven't done the researchinto, to, to like compare rates
of infection in different peoplewho have used a nasal spray or
(34:02):
not.
So I can't, I can't speakintelligence, but sure.
It would make sense.
And it would be a differentmechanism.
Similar idea that basicallyyou're, you're sort of paying
attention to the part of thebody that is exposed first.
And if you can prevent aninfection from happening in the
first place, then you save yourbody a lot of trouble down the
Matt Boettger (34:20):
line.
Yeah, absolutely.
No, thanks for sharing.
That was great, Stephen.
Yeah.
One last thing I'll just mentionhere.
Why I didn't talk to Stephenabout this?
I just saw this article.
I'm always interested in abouthow COVID and children.
Cause I have three little boysrun facts, but they didn't, who
knows when that's going to beavailable.
But I saw this article, mostchildren with severe post COVID
19 condition in fine health yearlater.
(34:42):
So just a study following kidsafter a year who've had severe,
it looks right.
Is promising that these likeeither long holler, what are you
going to call it resolve overtime, right?
Naturally or back to their norm.
Healthy reality.
So just a little drop of hopefor that as well.
Thank you again, Stephen.
This was awesome.
I learned a lot and I guessingour listeners learned a ton as
(35:03):
well.
If you wanna support us again,patrion.com/pandemic podcast,$5
a month.
One time gift Venmo, PayPal onthe show notes.
S a S T E P H E N K I S S L E R.
And Twitter.
You can follow him, Stephen.
You can reach out to me,matt@livingthereal.com drop a
line.
If you have any questions, we'dlove to answer them.
(35:25):
And I think that is it.
I hope you guys have a wonderfulweek and we'll see you probably
and two weeks, maybe one whoknows no more than two take care
and have a wonderful week.
Okay.
Bye bye.
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