I expect our experts in molecular diagnostics will have some thoughts about driving a "pseudo-epidemic" caused by testing inaccuracies and extreme unprofessionalism. It’s a very direct accusation.
But that aside, I'm interested in looking at the rapidly evolving research looking at pre-existing immunity in the population, what we know, don't know, hypothesise and simply can have a best guess at. I'm not claiming to be right or wrong, just listing some thoughts.
I will focus on the first part claiming high levels of population-wide immunity, namely 50% of the population was “immune” to SARS-CoV-2 back in 2019. The first sentence.
This originates from multiple observations this year that T cells from about 50% of the unexposed population react to SARS-CoV-2-derived peptide pools in vitro.
https://www.nature.com/articles/s41577-020-0389-z
The hypothesis following from this: these cells were generated during prior infection by common cold-causing coronaviruses (CCC), and are present in many of us, poised to respond to SARS-CoV-2. A fine hypothesis, currently under investigation.
It is clear to the authors (of this review at least) that this doesn’t directly correlate to ‘immunity’ in vivo. They ask for restraint in making “overgeneralizations or conclusions in the absence of data”.

Used to be so normal, but sounds like a distant dream in 2020.
What they mean (my interpretation) is that we need clinical studies correlating previous CCC exposure to clinical outcomes in SARS-CoV-2 infection. They recognize in vitro is not in vivo. This is perhaps not "confirmed", even in the BMJ review linked.
https://www.bmj.com/content/370/bmj.m3563
I am cautious for the following reason: if it doesn’t immediately compute to multiple experts in this field who MADE these findings, publishing their high quality primary data in Science, Cell etc… WHY is anybody else so convinced?!
Is this what sparked ‘we only need 10% to reach herd immunity’ supported by many signatories of the now useless #GreatBarringtonDeclaration? To get to 60%? I really hope not.

Vaccines will anyway bury this idea. Not needed anymore.
We have seen studies where previous exposure to CCC was correlated with SARS-CoV-2-driven ICU admission. They say there is ZERO influence on the attack rate. I believe this was the first study of its kind.
https://www.jci.org/articles/view/143380
In other words: no significant effect of previous exposure to CCC on catching SARS-CoV-2. Hear it from the last author himself (and comments from Shane Crotty). Don’t take MY word for it. https://twitter.com/JosephMizgerd/status/1333410089949073411?s=20
So the first study along these lines shows that previous CCC exposure does NOT render you immune to SARS-CoV-2 after exposure to CCC, but that it MAY modulate severity after hospitalization in high risk groups. That's an important distinction to make.
For the last part: if this is the PHE study referred to in the article describing 'prior immunity', I have a couple of questions to the interpretation. It's a big study let's look at some aspects...
https://www.medrxiv.org/content/10.1101/2020.11.02.20222778v1.full.pdf
I don’t agree that this study shows "prior immunity" to SARS-CoV-2.

It correlates abundance of T cells recognizing SARS-CoV-2 peptides to subsequent symptomatic SARS-CoV-2 infection.

That certainly SOUNDS similar, right? But there are some complexities.
Correct me if I'm wrong, but more T cells detected using T-SPOT may simply reflect more robust immune responses to previous CCC, thus leaving behind an abundance of memory T cells recognising multiple CCC-derived antigens, which can crossreact with SARS-CoV-2-derived peptides.
Thus, we may simply be identifying those who have, for whatever reasons, stronger immune responses to CCC in general. If that were true, these participants may be associated with more mild outcomes. This can be simple heterogeneity.

Any experts out there disagree with this?
To nail this point, you would need to show that the SAME participants do not have the same pattern of stronger T cell responses to peptides from other pathogens. If your significance disappears after normalizing for this, we have a stronger claim.
It’s a puzzle why you would select a study to make a point about pre-existing immunity that uses a study endpoint that is a +ve PCR test – something the article later calls into serious question. We should notice this apparent contradiction.
Finishing up: It occurs to me that this confusion is the consequence of simple terminology. What does it mean to be ‘immune’?
/ɪˈmjuːn/ - adj – «Having a high degree of resistance to a disease»

... among other definitions
In vitro T cell reactivity to SARS-CoV-2 peptides is NOT the same as being “immune” to SARS-CoV-2. These terms appear to be used interchangeably in this debate so keep an eye out for this subtle difference.
Whatever side of the argument you’re on, the data simply isn’t yet there to say with confidence that you’re significantly protected from SARS-CoV-2 by previous CCC exposure, however intuitive it may be. My advice would be to act as if you’re not.
And if you truly hate this lockdown, the very best thing you can do is get vaccinated as soon as possible. ;)
You can follow @andrew_croxford.
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