
New Data on T Cells and the Coronavirus - walterbell
https://blogs.sciencemag.org/pipeline/archives/2020/07/15/new-data-on-t-cells-and-the-coronavirus
======
est31
> [T]his paper shows that these patients still have (17 years later!) a robust
> T-cell response to the original SARS coronavirus’s N protein, which extends
> an earlier report of such responses going out to 11 years. This new work
> finds that these cross-react with the new SARS CoV-2 N protein as well. This
> makes one think, as many have been wondering, that T-cell driven immunity is
> perhaps the way to reconcile the apparent paradox between (1) antibody
> responses that seem to be dropping week by week in convalescent patients but
> (2) few (if any) reliable reports of actual re-infection. That would be good
> news indeed.

~~~
mycall
Could a lab theoretically take your T-cells and "upgrade" them with all kinds
of immunity robustness against say 100 viruses?

~~~
frisco
Totally. This is called "adoptive cell transfer" and it's one of the hottest
areas of biotech at the moment.

[https://en.wikipedia.org/wiki/Adoptive_cell_transfer](https://en.wikipedia.org/wiki/Adoptive_cell_transfer)

~~~
ineedasername
Wow, sure it's not at "super human" immune system levels yet, but this is the
type of research that feels like we're entering SciFi territory.

~~~
_jahh
you type into your glowing device connected nigh-instantaneously to a hefty
proportion of the world.

~~~
vkou
So, like an 1840s telegraph, but a bit better and with more spyware?

~~~
adrianN
This cell transfer thing is just like a vaccination, but better. And a 2020
car is just like an 1820 train, but better. And a computer is just a
programmable loom, but better.

~~~
3pt14159
Haha, I was with you until the computer comparison. A 2020 car can go an order
of magnitude faster than a 1820 train. A 2020 computer can go so much faster I
can't even estimate how many orders of magnitude with certainty.

------
walterbell
In addition to these promising results, note that southern U.S. states have
been dealing with a dust storm from the Saharan desert, which increased air
pollution in late June,
[https://www.yaleclimateconnections.org/2020/06/saharan-
dust-...](https://www.yaleclimateconnections.org/2020/06/saharan-dust-storm-
expected-to-cause-dangerous-air-pollution-in-u-s-this-week/)

 _> The dust cloud is bringing dangerously high levels of fine particulate
pollution (PM2.5, particles less than 2.5 microns or 0.0001 inch in diameter)
and PM10 (particles less than 10 microns in diameter). Air pollution
aggravates COVID-19 symptoms, leading to expected increases in hospital
admissions from the disease in regions where dust concentrations spike._

We don't yet have good data to correct for the health impact of breathing in
these minute particles from Africa, especially for those with pre-existing
conditions.

~~~
nickthemagicman
I'm in the south. Not a sign of dust here. Even my dark colored car is clean.

~~~
walterbell
It was several weeks ago. Some photos here, [https://www.msn.com/en-
us/weather/topstories/the-sahara-dust...](https://www.msn.com/en-
us/weather/topstories/the-sahara-dust-storm-has-reached-the-us-mainland-heres-
what-it-looks-like/ar-BB160EHk)

~~~
nickthemagicman
In New Orleans saw nary hide nor hair of the dust. Maybe it's coastal areas
only?

------
rossdavidh
"The paper speculated that this might be due to cross-reactivity with proteins
from the “common cold” coronaviruses”, and raised the possibility that there
might be a part of the population that has at least some existing protection
against the current pandemic."

...this might explain why different parts of the world (e.g. east Asia,
including Australia and New Zealand, vs. western Europe) have vastly different
outcomes that don't seem to correlate well to genetics, culture, or policy. If
a "common cold" coronavirus hit east Asia in the past, but never made it to
western Europe, it could explain the different impact.

~~~
wolco
There are two different strains. An older one based in Asia that appears
weaker. A newer one found in Italy.

This research came out months ago but no one is mentioning this.

~~~
crowbahr
Was the research peer reviewed? Published in any journals? Rigorous?
Documented?

~~~
noodlenotes
They're referring to a paper published in Cell.

"Tracking changes in SARS-CoV-2 Spike: evidence that D614G increases
infectivity of the COVID-19 virus"
[https://www.cell.com/cell/pdf/S0092-8674(20)30820-5.pdf](https://www.cell.com/cell/pdf/S0092-8674\(20\)30820-5.pdf)

There's a more infectious mutation that overtakes the original form wherever
it spreads, including Asia, although it's not more severe. I guess Asian
countries would have an advantage because they faced the original form first
and got their act together, while Europe and the East Coast of the US faced
the more infectious variant early on. (The West Coast, on the other hand,
started out with the original form, probably because the virus came directly
from Asia. The variant didn't even show up in the Bay Area until May, for
example.)

~~~
twic
It's true that the G614 form overtook the D614 form, but that is not
necessarily because it's more infectious - it could be drift and fixation.

The news and views bit on that Cell paper puts it in context:

[https://www.cell.com/cell/pdf/S0092-8674(20)30817-5.pdf](https://www.cell.com/cell/pdf/S0092-8674\(20\)30817-5.pdf)

Another study didn't find an effect on transmission:

[https://www.biorxiv.org/content/10.1101/2020.05.21.108506v4](https://www.biorxiv.org/content/10.1101/2020.05.21.108506v4)

> The D614G mutation displays only three independent emergences that qualify
> for inclusion in our analyses. While this limits our power to detect a
> statistically significant association with transmissibility, the low number
> of recurrent mutations leading to the D614G allele suggests that, rather
> than being a driver a of transmission itself, it arose early and went up in
> frequency by hitchhiking with one of the deepest branches in the global
> phylogeny as the SARS-CoV-2 population expanded.

People are still working on this, and it should become clearer in time.

------
andrewseanryan
If there is a nearly harmless coronavirus going around, whether it is a common
cold or previously unidentified virus (as the article suggests), that provides
partial immunity to COVID, what is stopping us from purposefully infecting
people with a less harmful illness to protect from COVID? Isn’t this how the
first idea of vaccines came about with Cowpox and smallpox?

~~~
BurningFrog
> _what is stopping us from purposefully infecting people with a less harmful
> illness to protect from COVID?_

Something like will be illegal in (guessing) 4 separate ways.

It's too far outside too many boxes. Sit down!

~~~
Izkata
Definitely too far if handled by government, but if the possibility exists as
individual choices, some people would definitely go for it. Chickenpox parties
are a thing, after all.

~~~
BurningFrog
True.

You can also make a good argument for variolation. Which is to infect yourself
with a _small_ amount of viruses.

This will (ideally :) create a small infection that your immune system can
beat off in time, and then you'll be immune after a minor time sick.

Apparently, people did this with smallpox in the pre vaccine era.

------
dalore
It's not new, it's more evidence:

At the end of May, however, an immunological study by the University of Zurich
was published, which for the first time showed that the usual antibody tests
that measure antibodies in the blood (IgG and IgM) can detect at most about
one fifth of all coronavirus infections.

[https://www.biorxiv.org/content/10.1101/2020.05.21.108308v1](https://www.biorxiv.org/content/10.1101/2020.05.21.108308v1)

At the same time, the Swiss study may explain why children usually develop no
symptoms (due to frequent contact with previous corona cold viruses), and why
even hotspots such as New York City found an antibody prevalence (IgG/IgM) of
at most 20% – as this already corresponds to herd immunity.

The Swiss study has in the meantime been confirmed by several more studies:

A Swedish study showed that people with mild or asymptomatic disease often
neutralized the virus with T-cells without the need to produce antibodies.
Overall, T-cell immunity was about twice as common as antibody immunity.

[https://news.ki.se/immunity-to-covid-19-is-probably-
higher-t...](https://news.ki.se/immunity-to-covid-19-is-probably-higher-than-
tests-have-shown)

A large Spanish antibody study published in Lancet showed that less than 20%
of symptomatic people and about 2% of asymptomatic people had IgG antibodies.

[https://www.thelancet.com/journals/lancet/article/PIIS0140-6...](https://www.thelancet.com/journals/lancet/article/PIIS0140-6736\(20\)31483-5/fulltext)

A German study (preprint) showed that 81% of the people who had not yet had
contact with the new corona virus already had cross-reactive T-cells and thus
a certain background immunity (due to contact with previous corona cold
viruses).

[https://www.researchsquare.com/article/rs-35331/v1](https://www.researchsquare.com/article/rs-35331/v1)

A Chinese study in the journal Nature showed that in 40% of asymptomatic
persons and in 12.9% of symptomatic persons no IgG antibodies are detectable
after the recovery phase.

[https://www.nature.com/articles/s41591-020-0965-6](https://www.nature.com/articles/s41591-020-0965-6)

Another Chinese study with almost 25,000 clinic employees in Wuhan showed that
at most one fifth of the presumably infected employees had IgG antibodies
(press article).

[https://www.medrxiv.org/content/10.1101/2020.06.13.20130252v...](https://www.medrxiv.org/content/10.1101/2020.06.13.20130252v1)

A small French study (preprint) showed that six of eight infected family
members of Covid patients developed a temporary T-cell immunity without
antibodies.

[https://www.medrxiv.org/content/10.1101/2020.06.21.20132449v...](https://www.medrxiv.org/content/10.1101/2020.06.21.20132449v1)

~~~
jhpriestley
1\. Dozens of localities have controlled the virus via lockdowns, social
distancing and masking, they all show similar curves to NY but with lower
peaks. NY therefore offers no evidence that herd immunity has been reached.

2\. Your Spanish study shows 90% of those with a positive PCR test also had
antibodies. The low symptomatic positive rate could be easily explained by
other seasonal illnesses with identical symptoms.

3\. There is no evidence beyond supposition that I can see for the Wuhan
clinical workers having the virus. An alternative explanation is that
protective equipment and protocols were effective.

4\. The idea of 80% of the population being T-cell immune seems inconsistent
with the outcomes on the Diamond Princess.

I think you are cherry-picking data to support a far-fetched theory. The
outcomes in confined places where the virus infects everyone, like the Diamond
Princess or nursing homes, seem especially hard to square with the idea of
widespread t-cell immunity.

Edit: I was misremembering the Diamond Princess, not everyone on the cruise
ship got the virus. However, Marion Correctional Institute in Ohio had 80%
test positive for covid; the Life Care Center in Kirkland, Washington had 2/3
test positive. These don't seem consistent with widespread T-cell immunity.

~~~
dalore
Interesting you mention the Diamond Princess, it actually supports the "far-
fetched" theory. And it's not as far fetched as you think, it's gaining more
ground and does explain places like New York, London, Sweden, India etc.

[https://www.spectator.co.uk/article/immunity-to-
coronavirus-...](https://www.spectator.co.uk/article/immunity-to-coronavirus-
may-be-far-more-widespread-than-thought)

"In the accidental experiment of the Diamond Princess – a close community
where the infection was allowed to spread unchecked for a fortnight in
January, and everyone was eventually tested – only 17 per cent of passengers
and crew became infected."

New York (and similar UK and Sweden) has a higher death rate since they moved
sick patients into care homes and decimated them. As you said everywhere saw
similar curves no matter how strict or lax a lock down they had. Implying
something else is going on and not the lock down.

Studies looking at the impacts of lock down on the curve are showing very
little correlational
[https://www.thelancet.com/journals/eclinm/article/PIIS2589-5...](https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370\(20\)30208-X/fulltext)

“full lockdowns and wide-spread COVID19 testing were not associated with
reductions in the number of critical cases or overall mortality.”

So, to me at least, it does seem far more plausible that t-cells are more a
mitigating factor then lock downs.

If I am cherry picking, seems to be lots of cherry trees to pick from.

I see no reason why t-cell should not offer some protection, like it does with
other coronaviruses. And why we would assume that everyone is just as
susceptible when we know the risk profile varies wildly.

EDIT: for your explaining your edit of "Life Care Center in Kirkland", the
reason they have more antibodies is that we all know the older you get the
less t-cell protection you have. A "life care" center one assumes is full of
old people, hence lower t-cell protection. And it explains why children have
more protection as their t-cell protection is stronger.

~~~
jhpriestley
Everywhere saw a similar _shape_ of curve, i.e. exponential increase until the
lockdown, then slow exponential decrease. The peak of the curve differed
widely, and countries that were slow to lock down like the UK, Sweden and USA
have seen some of the worst outcomes.

Correlating lockdown policy to outcome does not make sense because lockdowns
are instituted in response to case levels in the first place. It is like
correlating fire trucks and fires, and finding that fire trucks cause fires
because there are more of them in dry, fire-prone areas.

Sweden provides something close to a natural experiment, it has similar
culture and climate to its neighbors but a far worse outcome after it did not
lock down.

Prisons are not especially weighted toward older people and they have seen
outbreaks with as many as 80% being infected.

------
xoxoy
curious who wins the vaccine race. my understanding is the RNA vaccines being
researched by Moderna and Inovio don’t stimulate T-cell development, in which
case they seem like poor candidates compared to the adenovirus candidates like
the Oxford one that do.

~~~
dnautics
so mRNA vaccination is an offshoot towards technology which was created about
a decade and a half ago to make more efficient monoclonal antibodies for the
lab. The process is to extract B-cells from a challenged organism (almost
always mouse) and then fuse them as 'hybridomas' with immortal cancer cells,
select single cell clumps that show an immune response out of multi-well
plates, and then use those immortalized cells to make that one antibody
forever.

So indeed the mRNA vaccines come from technology that is highly optimized to
elicit a B-cell response. (Not to say that it doesn't stimulate T-cells, but I
wouldn't be surprised if it didn't).

~~~
rotexo
Wait I’m a little confused. It seems like injecting people with an mRNA, which
their cells then translate into an antigen that provokes an immune response,
is a very different technology from monoclonal antibodies. They are both
related to the immune system, but mRNA vaccines are at least partially about
stimulating polyclonal antibody production, as opposed to monoclonal
antibodies. Can you articulate why you think mRNA vaccines were derived from
monoclonal antibody work?

~~~
dnautics
I just remember talks (I was at a cutting-edge immunology research center, The
Scripps Research Institute in San Diego) about using mRNA vaccination in the
2007-2009 era to make monoclonal antibodies. Oddly, I can't find any
publications from that era on it (but I can find a few papers from 2017-2019
using that exact methodology), so it appears that either i was mistaken, or it
quietly pivoted to human vaccination as a target. It's really not possible for
me to be mistaken about the timeframe, though, since I have been out of
biology since 2015.

