Novelty and immunity: Why were we so blind to the obvious?

Seeing the light on serology.

In “Why do people still believe in Covid?” Jonathan,

Martin Neil

, and

Norman Fenton

pulled together threads about PCR testing to remind readers that claims about a spreading novel virus causative of a unique disease are baseless and the WHO’s pandemic declaration was unwarranted, if not fraudulent.

There are persistent counterclaims to “nothing novel was going around” which warrant attention. Both stem from the concept of building herd immunity against a new SARS-like virus.

The first regards serological data and retrospective testing of stored samples purporting to detect the presence of SARS-CoV-2 antibodies at low levels of positivity. This, it is alleged, is evidence that a novel virus was ‘out there’ but was ‘spreading silently’ and hadn’t yet made its way through the population.

The second affirms serology as evidence of the virus’s novelty but highlights other ways the immune system fights coronavirus infection. Essentially, a novel virus is presumed and the ability for most people to fight it off with no or few complications is emphasized.

A confession

Before addressing these points, we have a confession:

Each of us can point to tweets and articles that show our own interest in using tests to find out how long “the virus” had been in a country or how many people in an area had been infected, and accentuating pre-existing immunity to argue against mandates.

We weren’t considering things like what serology can measure, whether stored samples were fit to be tested for such an agent, or what it means to be “immune” to a coronavirus. Nor were we fully appreciating how testing of various kinds affirmed the official story about a viral threat that needed to be taken seriously via lockdown or ‘protecting’ some people in a focused way until herd immunity was reached and/or a shot available.

We are now.

What is a serology test, and how is one developed?

A serology test is a measurement of the presence of antibodies which react to an antigen - said to be one of the proteins on the virus, to gauge whether there has been previous contact with said-antigen.

We will ignore the fact that, certainly as regard assaults on the respiratory system, the “heavy lifting” of the immune system is performed within the mucosal lining of the respiratory tract, making an assumption that things measured in the blood are actually indicative of prior “contact” with - and immunity to - ”the virus” somewhat moot.

This point - and other doubts about whether there was anything truly novel and dangerous actually “spreading” - are part of the inevitable conclusion of this study of L.A. nursing home residents , as discussed here:

If It's So Deadly, Then Why Wasn't it Deadly?

When considering the relevance of serological tests, it is critical to appreciate the basics of their development - see here for a primer (pun intended)¹:

The essential steps are:

• Antigen selection

• Assay development

• Calibration and validation using antibody-positive and antibody-negative sera

People mistakenly think that the output of antibody testing is a binary positive or negative, without considering what’s “inside the box.” Antibody-antigen binding is not an all-or-nothing proposition whereby an antibody definitely either binds to an antigen or doesn’t; binding can be non-existent, strong, or anything in between.

The amount of binding will depend on a number of factors, including how much antibody is present and, crucially, how similar the antigen is to those previously encountered, which will determine how well antibodies to the earlier exposure “fit” (to a greater or lesser extent) the new one.

So, what you end up with during development is a graph depicting the amount of binding with increasing amounts of antibody. To this the test developers have to apply cut-offs, deciding that above a certain level is “positive” and below a certain lower level is “negative”. Similar to what happens with PCR tests, the results aren’t binary – i.e., YES/NO – a continuum and cut-offs are established.

Positive and negative controls are needed:

1. Serum from people who did mount an immune response to the antigen (positive)

2. Serum from people who did not mount an immune response to the antigen (negative)

The recipe = antigen + positive-testing sera + negative-testing sera

Whence these “ingredients” for SARS-CoV-2 antibody tests?

The antigen used in the SARS-CoV-2 antibody test was created using recombinant technology - i.e., made according to the “formula” resulting from sequencing “the virus” in January 2020. It was NOT derived from anyone who was actually sick with a novel illness.

We are open to correction if anyone can prove Perplexity.ai wrong:

(Perplexity gives 13th Jan as the date the sequence was deposited in GenBank whereas Eddie Holmes’ public post about it was dated the 10th; this is not material to the points being made here.)

The positive and negative controls (ie antibody positive and antibody negative samples) are defined, respectively, as sera from people who did and did not test positive for SARS-CoV-2 using the “gold-standard” PCR test for “the virus”.

Again, we’re interested to hear from anyone who says this is wrong:

So “gold standard” PCR tests for SARS-CoV-2 were developed from a constructed sequence” – not from someone with a distinct clinical illness – which was the same sequence used to make the antigen.

It feels like we need one of these:

Perplexity concurs:

“Necessary given the urgency of the situation” sounds like an excuse. No evidence of an urgent situation was ever supplied. As descussed here, simultaneously high positivity rates on PCR and antibody tests in New York City very early in ‘the emergency’ strongly suggest that neither a unique nor a single agent was being detected.

Without reviewing all of the uncertainties around testing for SARS-CoV-2 antibodies, we note that the CDC seemed to understand the limitations early on. Answering a question during a media telebriefing on 12 February 2020, Nancy Messoinier said,

We have the beginnings of the serological tests, because we now have patients in the United States, we’re able to collect additional specimens but we have to collect them over time so that we can have the appropriate timing of specimens to make sure that we understand what the immune response looks like.

Once we complete the gathering of those specimens from the patients we’ll be able to pretty rapidly, I would say within a couple of weeks, three weeks, four weeks, be able to have a test available but right now, we’re still in the range of testing of gathering the appropriate specimens from the patients in the U.S.

An agency report about “early spread” that included phylogenetic analysis and retrospectively identified cases said,

"Results of serologic testing are not presented here, because serology (i.e., testing for antibody to SARS-CoV-2) is likely to be a relatively insensitive means of detecting a newly emergent virus, particularly when the specimens were collected at random rather than from persons most likely to be infected (in contrast, for example, to viral testing of outpatients or hospitalized patients with acute respiratory disease) and because serologic assays generally do not approach 100% specificity unless some form of confirmatory testing is available.

For example, a hypothetical serologic survey in the Seattle metropolitan area (population of 3.5 million) conducted after the first 3,500 infections would find a true seroprevalence of 0.1%, whereas the use of an assay with 99% specificity would be expected to produce false positives in 10 times as many samples. Serologic surveys, nonetheless, are useful in tracking the progress of the pandemic once established and have the potential advantage of detecting all infections, regardless of the symptom profile.

So, even if we play along with the idea that SARS-CoV-2 was a “new” agent from a bat cave, wet market, or laboratory, it sounds like retro-testing samples that were collected for other purposes (as in the case of the Red Cross blood study), cannot be linked to an individual (e.g., wastewater), or which, at most, could only be connected to individuals experiencing mundane flu-like symptoms, is inappropriate and very little can be inferred from the results. We therefore see no reason to believe that testing early samples collected and retained for purposes would yield results that could be used to say SARS-CoV-2 was “new” or started “spreading” at a certain point in time.

Apparently, it’s only when an arbitrary human decision about the existence of a pandemic is made that the “progress” of the identified agent can be “tracked.” The CDC reinforced the idea that a new virus could be followed through a population presumed to be “naive” by launching a serology dashboard with rates derived for each state. Looking back, it’s easy to see how such data-reporting tools validated claims about a new spreading threat.

“Pre-Existing” Natural Immunity: An argument against novelty?

The novelty trope - and the notion of needing to ‘achieve’ herd immunity - is also reinforced (however unintentionally) by an emphasis on ‘pre-existing’ natural immunity. A recent post on X by Kulvinder Kaur about this study is a good example of a line of thinking that surfaced in 2020:

Kulvinder’s summary post reads:

New Peer-reviewed study with international scientific collaboration from Harvard, Cambridge et al further supports (as I've emphasized since 2020) the critical importance of PRE-existing cross-reactive natural Tcell immunity against SARSCoV2.

[Quoting study] "Our study provides unique data on the dynamics of seasonal human coronaviruses and SARSCoV2 immunity in Senegal and underscores the importance of understanding the role of pre-existing immunity in shaping Covid-19 outcomes globally.

In 2019, SARSCoV2 emerged as a new human coronavirus, even though worldwide populations were known to be regularly exposed to seasonal human coronaviruses (hCoVs) responsible for the 'common cold'.

Although associated with mild illness, these hCoVs are classified in the same Coronaviridae family as the SARS coronaviruses, which include SARSCoV1, SARSCoV2, and Middle East Respiratory Syndrome (MERS) and share genetic and structural similarities. hCoVs are globally endemic and estimated to be responsible for up to 15–30% of pre-pandemic annual respiratory infections, which are seasonal (e.g., fall and winter) and most prevalent, though undercounted, in young children.. Pre-existing hCoV immunity could reduce transmission and ameliorate symptoms of the related SARSCoV2.

Multiple US and European studies described CD4+ Tcell reactivity in SARSCoV2 unexposed individuals, attributed to pre-existing memory responses to hCoVs. In a UK household study, exposed contacts that remained PCR-negative showed significantly higher frequency of cross-reactive (p = 0.0139) and nucleocapsid (N)-specific IL-2 secreting memory Tcells (p = 0.0355). Swadling et al. in a study of potentially abortive SARSCoV2 infection in UK healthcare workers (HCWs) described pre-existing Tcell reactivity directed against the early transcribed replication-transcription complex (RTC).

We observed substantial levels of pre-existing cross-reactive immunity to SARSCoV2, stemming from prior exposure to seasonal hCoVs.

Our analysis of cellular responses demonstrated cross-reactivity to SARSCoV2 with 80.0% and 82.2% showing IFN-γ responses against S and N, respectively.

Our study uniquely analyzed both antibody and cellular responses in Senegalese women, demonstrating that pre-existing immunity against human coronaviruses can induce cross-reactive Tcell responses against SARSCoV2.

Cross-reactive T cell responses play a protective role in protection against COVID-19. Cellular responses were shown to map to cross-reactive recognition of SARSCoV2 by Tcells induced by human coronaviruses.”

To which Jonathan responded:

In other words, if people have so much natural immunity against the constructed thing named SARS-CoV-2, is that not an argument against its novelty - with the most that could be said is “it” is novel to human discovery, invention, or imagination but not to the human body?

Concluding remarks

Earlier in the Covid scam, we more or less accepted the WHO's story about a "novel" virus against which humanity possessed some naturally-acquired resistance, and whose approximate "arrival" or emergence could be deduced through serological testing.

Our objections to the dystopian measures imposed on humanity by governments worldwide were based on the premise that although “it” was “novel” (an assertion which we now reject), “it” wasn’t as dangerous as claimed because of “natural immunity”.

We fell into that trap because we failed to grasp both the circularity of test development, and the fact that it was predicated on a contrived sequence.

In retrospect, we see how the "herd immunity" proposition blinded us to flawed assumptions underlying the official narrative.

Whilst difficult to prove one way or another, the debate about “herd immunity” versus “containment” now appears as if it may have been deliberately propagated - or at the least permitted - as a distraction from a more pertinent question:

Was there anything spreading at all?

1. Some early CDC guidelines on “COVID-19 Antibody Testing” can also be found here.