
Covid-19: The T Cell Story - xearl
https://berthub.eu/articles/posts/covid-19-t-cells/
======
nodamage
> And wherever we look, infections level off before 10%-20% of the population
> is infected. This is somewhat mysterious.

This is not really true.

Bergamo had a 58% infection rate as of last month:
[https://bergamo.corriere.it/notizie/cronaca/20_maggio_22/ber...](https://bergamo.corriere.it/notizie/cronaca/20_maggio_22/bergamo-
test-sierologici-cittadini-583percento-positivo-un-giorno-51-contagi-
piu-8f6ac032-9c44-11ea-aab2-c1d41bfb67c5.shtml)

Several prisons have seen infection rates in the 70-80% range:
[https://www.npr.org/sections/coronavirus-live-
updates/2020/0...](https://www.npr.org/sections/coronavirus-live-
updates/2020/04/20/838943211/73-of-inmates-at-an-ohio-prison-test-positive-
for-coronavirus)

The USS Theodore Roosevelt had an infection rate of 60%:
[https://www.cdc.gov/mmwr/volumes/69/wr/mm6923e4.htm?s_cid=mm...](https://www.cdc.gov/mmwr/volumes/69/wr/mm6923e4.htm?s_cid=mm6923e4_e&amp;deliveryName=USCDC_921-DM30202)

A better explanation for the leveling off is simply that social distancing and
lockdowns have reduced the spread of the virus.

~~~
lsllc
In Massachusetts (where we have been hit pretty hard by C19) we're trending
downwards in a significant way and have been for a few weeks now. But I see
more human activity out and about than ever (at least compared to March/April
and mask wearing / social distancing is has been pretty obviously in decline
for a number weeks now). The state is now well into it's re-opening phase 2
and even with the recent protests, there were only a handful of new
infections.

Could this not be some version of "herd immunity"? So in cramped conditions
such as a warship, cruise liner or prison the virus just spreads so damn
quickly (given the 5-14 day incubation) that we see most people getting
infected really barely before the incubation is over for the index patient).

However in "normal" societal conditions (i.e. where people go to their jobs
and are back to their homes at night and are only exposed "occasionally", e.g.
on the commuter rail or maybe in a store) that the virus spreads much more
slowly and coupled with asymptomatic carriers who (controversially may not
"shed" the virus as much, or at all) that reduces the overall input to R0 such
that it spreads more slowly and "fizzles out" with R0 < 1.

Presumably "herd immunity" isn't a binary thing ... we don't just go from 59%
with raging infections at R0 = ~5-6, then suddenly at 60% infected R0 drops to
<1? (or whatever numbers you believe "herd immunity" happens at). Maybe the R0
curve just flattens more quickly than we thought?

~~~
remote_phone
I think what you’re seeing is exponential growth. Meaning, after crushing the
curve, things start all over again with slow growth and then pick up again in
2 months. We are beginning to see the exponential growth explode in Arizona,
Texas and Florida now I think.

~~~
lsllc
I'm not sure how it's exponential, if you look at the graph for the current #
of cases [0], then you can see it's more or less flat (and the new case %-age
has been around 2-3%), between deaths and (most) people recovering, the number
of active cases must at least flat and most likely getting smaller?

[0]
[https://en.wikipedia.org/wiki/COVID-19_pandemic_in_Massachus...](https://en.wikipedia.org/wiki/COVID-19_pandemic_in_Massachusetts#Statistics)

------
lymeeducator
T cell responses are interesting. Infectolab ([https://www.infectolab-
americas.com/](https://www.infectolab-americas.com/)) and its originator Armin
(Germany) are using T cell responses for tick borne diseases like: Borellia
(Lyme), Bartonella and Babesia because antibody testing is difficult for these
(broken via CDC specs as most labs won't test key proteins 31, 34 and never
indicate which antibodies are present). Bartonella is very hard to test for
with antibody and PCR. It really depends on lab specialty. The sars-cov-2
antibody tests are unpredictable in quality, so nearly useless (my dr is 0-50
via Quest and many people had + PCR).

In short, our immune context (genetic phenotype) is unique! We need a lot more
data from everyone to start making accurate correlations. We do not measure
T-cells, cytokines, mast cells, b-cells, HLA (partly how we potentially make
antibodies) at any meaningful level to provide much confidence. Many
natural/industrial substances suppress our T-cell responses and generally
innate immune system (metals, mold toxins, etc), so we also need to start
accounting for those.

It's a long road we have in front of us. Hopefully the medical system supports
patient data ownership and research to improve on our obvious ignorance.

~~~
erentz
Note that Armin Labs are considered quacks by many. For one example [1]. I
will leave it to others to do your own research but just wanted to recommend
caution about their use. Especially for diagnosis of Lyme, plenty of tragic
stories of people getting an Armin positive test while negative on the others
and then being encouraged through years of serious antibiotic treatments only
to have always been negative all along.

[1] [https://forums.phoenixrising.me/threads/documentary-
undercov...](https://forums.phoenixrising.me/threads/documentary-undercover-
in-german-lyme-clinics.55493/)

~~~
lymeeducator
I mentioned Armin/Invecto since they are looking at T-cell responses to
pathogens. Much of the prolonged antibiotic treatment is no longer common
practice. It damages the GI, suppresses portions of the immune system and is
in many cases bypassed by 2 resistant forms of Lyme (round body starvation
form & biofilm colonies). Most of my testing has been through Igenex, which
has a lot of experience with antibody testing that places like Quest screw up.
The typical Western Blot for Borellia (Lyme) is not a frequent test for many
of the labs and requires 5 - 7 IgM or IgG that won't form in the patient
because their immune system is too suppressed to manifest all of them. For
example, the outer protein of Lyme does not have to shift and result in
another antibody presentation because the host immune system has not forced it
to. The CDC spec deliberately ignores two specific antibody proteins OSP 31,
34 as do the common tests and instructs most labs not to reveal which
antibodies the patient has. Therefore, that patient might have some, but not
all of the "required" antibodies.

As I mentioned above, metals & mold toxins can generate a lot of inflammation
in some people that manifest as "foggy brain", joint aches, etc. It takes time
and diagnostic testing paired with treatment protocols. Some people cannot
process Aluminum and Mercury forms out of their body without relying on
Glutathione (limited detox pathways, start with HLA genetic SNPs).

It's a good thing most western medicine doctors never prescribe expensive
pharmaceuticals long term ... oh wait ;-)

~~~
erentz
Curious about your thoughts on a patient that tested both the Quest and IgeneX
immunoblots at the same time. The Quest showing 5 positive bands. And the
IgeneX no positive bands. Then repeated the same two tests four months later
at the same time with the same results. So Quest repeatedly CDC positive,
IgeneX repeatedly negative. How would you interpret that?

~~~
lymeeducator
I would ask which Quest lab specifically ran the test as lab quality can vary.
I have not seen mainstream labs return all of the antibody stains present in
some time, they usually indicate (+/-) for IgM (less likely) or IgG (more
likely). The count is also usually indicated (titer level). It also depends
which antibody proteins are present. Many of them overlap with other pathogens
(IE: 41 covers most of the spirochete class: Borellia, Leptospirosis,
Syphilis, etc). It depends on current & historical symptoms and markers like
C3a/TGF-b/MMP-9/CD57,8 and would probably try other tests for markers,
possibly another Lyme specific test at a different, but specialized lab like
Galaxy Diagnostics (well known for Bart), Fry labs or another in NY whose name
escapes me.

------
Animats
The author asks some questions which can be answered by gathering some data.

This suggests going back and re-testing for antibodies some populations from
tightly packed groups - the cruise ship passengers, warship crew, and nursing
home residents. The antibody tests are more accurate than they were two months
ago. The key here is to find out how many people, definitely exposed to the
virus, not only did not show any symptoms, but did not develop antibodies.
That group presumably had some form of pre-existing immunity.

Is anybody doing something like that?

~~~
Animats
It looks like that's already been done, and there are tightly packed groups
where the infection rate was 70-100%, as mentioned above. So, no existing
immunity at all, probably. That was the claim in the original article, but the
data does not bear it out.

~~~
mlyle
Finding densely connected subgroups in special populations (prisons, cruise
ships) with high infection rates doesn't mean that that specifies the
equilibrium herd immunity threshold in other populations.

~~~
guscost
Similarly, the plural of anecdote is not data. You are completely right, and
nobody has a good rebuttal.

------
christkv
Kind of shows how little we know about the human immune system. Hopefully this
pans out and we won’t see massive new waves. I have an anecdotal example of
that this might be something. A friend and his wife got tested before
delivering their baby and she was positive for antibodies and he was negative.
He might have just beaten the virus before the body even started creating
antibodies.

~~~
neuronic
For my master thesis, I wrote a small tool that would take and analyze raw
genomic high throughput data of various T-cells (chip-seq + rna-seq of th17 to
be precise) and create a regulatory network in Cytoscape. The basis was a
paper relating to The Th17 Project [1].

What I learned is that we are sort of in the very beginnings of understanding
how immune cells work (together), how their plasticity works in terms of gene
expression at any given point in time. For example, environmental
circumstances such as cytokine presence can lead to T-cell types
"transforming" to other types which have other effects etc. but it's not well
understood how this occurs. A very large amount of genes regulate each other,
you get a complicated network of up- and downregulations and it's hard to
reproduce and understand what needs to be done to generate a certain type of
T-cell with certain characteristics and behavior.

And then you haven't even tried doing that in-vivo where you could try to push
the immune system to express genes such that many T-cells of type X are
generated to enhance or fight inflammation. Because then you just disturbed a
complex interacting system with zero idea what the total effect is and whether
"the network" is resilient enough to not crash and burn somewhere somehow.

It's very very complicated with a huge amount of combinatorics involved so
Complex Systems Theory helps to build models helps a bit.

[1]
[http://th17.bio.nyu.edu/pages/index.html](http://th17.bio.nyu.edu/pages/index.html)

------
aberoham
Highly recommend the companion series of podcasts to TWiV if this article
perks your interest:
[https://www.microbe.tv/immune/](https://www.microbe.tv/immune/)

------
ck2
relevant

[https://www.nature.com/articles/s41423-020-0401-3](https://www.nature.com/articles/s41423-020-0401-3)

[https://www.nature.com/articles/s41423-020-0424-9](https://www.nature.com/articles/s41423-020-0424-9)

------
acqq
> Does this mean that if you recently had a Coronavirus that caused a head
> cold that you have a measure of protection?

Apparently, _no_ , as there are no observed differences in the percentages of
infected when the people who have children or work with children are compared
with those who don't. If the stated assumption were true, those that were more
exposed to other coronaviruses (which would be expected among those having or
being close to kids) would be as a group less prone to be infected. That was
apparently not observed.

So the "slowdowns" are just the humans adapting their behavior to reduce their
chances of getting infected. When Rt is 1 the growth is linear, as simple as
that. Less of such changes in the population behavior, more people are getting
infected, faster.

Source: translated transcript of the podcast of Christian Drosten. Hint: also,
don't believe what most of the media says that "he said" \-- I've seen a lot
of "editorialized" reporting of what he says, to the point of the end product
being completely opposite of what he actually said. It's that bad. One really
has to go to the source and read. Unfortunately, it's a lot of work, as the
podcasts are long. So the people who don't read the source tend to have
completely wrong idea what he actually said -- that's also why I'm not giving
the specific link: if one doesn't invest really a lot of energy and find and
carefully the sources, one has more chance to acquire completely wrong
conclusions as "highlights."

~~~
jacobush
These cold viruses circle the globe too, and just because some children had
colds and transferred them to adults, does _not_ mean that they had _exactly_
the strain that could potentially give partial Covid19 immunity.

So while I agree with your general advice about sources, I don't find your
"apparently" to be apparent at all.

~~~
acqq
> while I agree with your general advice about sources, I don't find your
> "apparently" to be apparent at all.

"Apparently" was used in the sense "I haven't seen and verified the sources
myself" (i.e. the specific scientific material that supports the conclusion of
an expert) but at least I took the effort to get the claim about that
conclusion from a recognized expert directly." That is, I can't give you the
ultimate source that the said expert used for that conclusion, but according
to my understanding from reading a transcript of his podcast he concluded that
and I have chosen to believe him. Experts spend their whole life to achieve
expertise. There are a lot of "preprints" and even fast-approved published
scientific papers floating around, which eventually (even extremely fast) are
recognized to be flawed by the experts, but only after the false claims are
repeated across the media. In such a situation, unless we are the experts
ourselves, and unless we have infinite time available, our best bet is to
trust the experts who are less prone to present or accept false claims. I
consider Christian Drosten one of these.

Being curious, I do check some source scientific works myself, I'm just
admitting that for that particular claim I haven't checked the sources myself
but decided to trust Drosten. I also claim that I at least spent enough energy
to read the exact transcript of his talk and avoided to read "journalistic
interpretations" \-- the expert's statements are very often totally deformed
by retelling. If that's not enough for you and you believe that you can catch
him in an error, I'd really like to know why you even believe to be able to
achieve that. And if you believe that I'm claiming something he hasn't said,
you can check the transcripts of his last two podcasts yourself and write here
if I made an error, I'll be happy to learn more.

At some level every one of us has to trust some experts, the question is just
if we can also recognize these who just claim some expertise but are actually
promoting false claims. I believe that Ioannidis, for example, is an example
of such, and I also see that other experts agree.

For "as close to the experts as possible" sources I also recommend everything
from [https://www.microbe.tv](https://www.microbe.tv) They also admit that
they do make errors sometimes, because they didn't recognize early enough how
serious this virus is going to affect everybody. But getting the coverage from
the experts directly allows one to remain much saner than when reading media
who regularly completely distort what experts actually say. And even when
media accurately quote some single paper, media often falsely reflect what the
whole body of knowledge actually is, as in xkcd "Significant" comics.

~~~
rimliu
You should look for the better source for your claims than some podcasts. It
is already estblished that those who had COVID develop immunity for it, just
not entirely clear how long lasting it is. But given its similarity to the
original SARS it should last quite a long time.

~~~
acqq
> It is already estblished that those who had COVID develop immunity for it

Who claimed something opposite to that and where? I don't understand why you
write that at all.

I'm arguing that getting the coverage directly from the experts who do reflect
the knowledge of the whole fields (and who don't promote some narrow agenda
like Ioannidis) is provably better than getting it from the politicians or the
press. The goal is always to recoginize these who introduce a bias which
distorts the truth.

What are your "better" sources (as in, more expert and less biased) that cover
this pandemics?

------
tacitusarc
This article talks about cell mediated immunity whereby compromised cells are
detected via peptides produced, but there's actually another mechanism that's
still in the early stages of being understood called merocytophagy where an
immune cell can partially "eat" another cell to see if it "tastes" sick.

------
newmana
"It took nine days for the number of infections to grow from 6 million to 7
million, and less than eight days to get to the latest million, so the
pandemic is not slowing down."
[https://www.abc.net.au/radio/programs/coronacast/the-
global-...](https://www.abc.net.au/radio/programs/coronacast/the-global-
hotspots-where-coronavirus-is-still-killing-thousands/12361280)

------
codecamper
What's the qualifications of the author before I go and invest time to read
his/her theories?

~~~
ziga
> Geeky entrepreneur [https://www.linkedin.com/in/bert-
> hubert-b05452/](https://www.linkedin.com/in/bert-hubert-b05452/)

~~~
DangerousPie
So... “none”?

~~~
ahubert
Author here - the article has been read and retweeted by actual world class
experts. Given that the article is now nearly two weeks old, I would have
heard about any gross inaccuracies in there by now. There is some minor
feedback and it needs a few tweaks, but overall it holds up really well.

------
xmichael0
So... Does this mean that we can "self" vaccinate by going maskless and
running around the city and in and out of grocery stores every few days? I am
mostly joking here, but I am also serious, the post implies that we can
develop immunity by getting minor exposures over a period of time. I read the
article twice and probably need it twice more to fully understand it, but
please enlighten me.

~~~
mr_toad
Innate immunity is more like a built-in mask. It’s pretty much the opposite of
building up an immunity.

------
taeric
The amount of frustrations surrounding all of this is mind numbing. I almost
expect we will get vaccinations before we get understanding.

And I share that call-out in this article that not knowing is not a claim that
things aren't working. I just expand it as not a claim that some things have
worked. We need more studies that will frustratingly take time.

