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Independent research & views related to the COVID Event | Jessica Hockett, PhD

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The Fallacy of Trust: Revisiting the Reliability of SARS-CoV-2 Antigen Testing Methods [Republication]

With disturbing revelations about antibody testing

Prof Martin Neil, Dr Jonathan Engler, Prof Norman Fenton, & Jessica Hockett PhD

Originally published to Where Are the Numbers? on 9 April 2025. Republished to Wood House 76 on 17 August 2026. 

In October 2023, we* explored the role of antigen testing during the pandemic in our article on Operation Moonshot in the UK.

At the time, we reached some bold conclusions, including:

  • The reliability of mass testing for SARS-CoV-2 hinges on the accuracy of the tests used—whether PCR or lateral flow tests (LFTs).
  • PCR tests and LFTs were seemingly adopted to amplify SARS-CoV-2 positivity rates, shaping public perception of a pandemic.
  • Few acknowledged the glaring disparity between PCR and LFT positivity rates, with many still trusting PCR tests despite their flaws.

We argued that LFTs inadvertently exposed how flawed PCR testing was, revealing much lower positivity rates. Ultimately, we concluded that LFTs were more specific and sensitive than PCR tests.

But here’s the kicker: we were completely wrong!

Had we dug deeper back then, we would’ve uncovered shocking truths that flipped our conclusion on its head — in fact, both LFTs and PCR tests were both fundamentally flawed and unreliable for detecting SARS-CoV-2, whatever one’s view of what that actually is.

How antigen testing works

Antigen (LFT) testing works by incorporating human antibodies within the test kit that are designed to specifically bind to antigens, such as proteins associated with SARS-CoV-2. When a sample containing the virus is introduced, the antibodies in the test kit react with these viral antigens, producing a positive result if the target antigens are present in the sample.

So the antibodies need to be specific to the antigen for the tests to work. If the pairing of one to the other is not one-to-one then the tests will flash positive for other antigens (and potentially other viruses).

So how bad are LFTs?

To understand the background, let’s revisit PCR testing. These tests were designed to detect at least two of three gene (RNA) targets (E-gene, N-gene (nucleocapsid), and S-gene) to identify SARS-CoV-2. However, as we’ve previously reported, PCR tests often cross-reacted with other viruses like common colds and influenza due to their lack of specificity. Worse still, many PCR tests declared positives based on detecting just one gene (usually the N-gene or E-gene) rather than two out of three.

PCR tests detect the genes (RNA), whereas antigen tests detect the proteins produced by the genes and play a critical role in packaging the viral RNA for replication and assembly.

From the reported research if you target a single gene, such as the N-gene (nucleocapsid) the test is inevitably going to be highly cross reactive with other viruses. But what about LFTs? Surely they didn’t make the same ‘mistake’…right? 

Wrong!

Research shows that most antigen tests targeted the protein associated with only one protein — the N (nucleocapsid)-protein — which is notorious for cross-reacting with other viruses.

Dobano et al (2021) say:

“COVID-19 patients elicit strong responses to the nucleocapsid (N) protein of SARS-CoV-2 but binding antibodies are also detected in pre-pandemic individuals, indicating potential cross reactivity with common cold human coronaviruses (HCoV) and questioning its utility in seroprevalence studies.”

While antigen tests targeting the N-protein are claimed to be generally specific, cross-reactivity with common cold coronaviruses is possible if test antibodies are not optimized for unique SARS-CoV-2 epitopes of the N-protein (sometimes called sub-regions of the full protein).

On this Dobano et al say:

“We investigated the immunogenicity of the full-length and shorter fragments of the SARS-CoV-2 N protein, and the cross reactivity of antibodies with HCoV. We identified a C-terminus region in SARS-CoV2 N of minimal sequence homology with HCoV that was more specific for SARS-CoV-2 and highly immunogenic. IgGs to the full-length SARS-CoV-2 N also recognized N229E N, and IgGs to HKU1 N recognized SARS-CoV-2 N.”

For an antigen test to be specific to SARS-CoV-2 specific epitopes of the N-protein must be tested (Wen et al, 2023), such as the C-terminus or the N-terminus sub-regions. If these epitopes are not tested, and the whole N-protein is used instead, the test will cross react with human coronaviruses.1

However, evidence suggests that during the early phase of the pandemic the antigen tests were testing the whole (full length) N-protein and not epitopes of the N-protein!

Here’s a rundown of some popular antigen tests and their targets:

  • BDVeritor system – targets the N-protein only
  • Abbott Panbio COVID-19 Ag Rapid Test – targets the N-protein only
  • Healgen Coronavirus Ag Rapid Test Cassette – targets the N-protein only2
  • Coris BioConcept COVID-19 Ag Respi-Strip – targets the N-protein only
  • nal von minden NADAL COVID-19 Ag Test – targets the N-protein only
  • Roche-SD Biosensor SARS-CoV Rapid Antigen Test – targets the N-protein only
  • Innova SARS-CoV-2 Antigen Rapid Qualitative Test – targets the N-protein only (this was the test rolled out in the UK)

All of the antigen tests in the above list suffered from the same flaw as PCR tests: cross-reactivity with common viruses like human coronaviruses (229E, OC43, HKU1, NL63), influenza A/B, rhinovirus, and others.3 Notably, the test rolled out across the UK — Innova — is included in the above list.

Here is the 2023 EUA list maintained by the FDA. The majority of the antigen tests listed say they target the N-protein for testing or make no mention of any target protein at all. Given that no information about epitope targeting specificity is given either explicitly or by implication, and it seems reasonable to assume that it is likely that the tests targets the full N-protein rather than specific epitopes.

In granting EUA the FDA note:

“The SARS-CoV-2 nucleocapsid protein antigen is generally detectable in anterior nasal (nares) swabs during the acute phase of infection. Positive results indicate the presence of viral antigens, but clinical correlation with past medical history and other diagnostic information is necessary to determine infection status. Positive results do not rule out bacterial infection or co-infection with other viruses. The agent detected may not be the definite cause of disease.”

This suggests that the FDA are aware of the conclusions of the EPIC studies performed on adults and on children (as we discussed here) – that there is no reliable one-to-one relationship between the findings of tests performed on naso-pharyngeal swabs and the pathogens responsible for respiratory illnesses. They may or may not have also been referring to the additional point that these antigen tests are non-specific and nowhere do any of the granted EUAs say any of the tests use specific epitopes of the N-protein.

The infamous duo, Cormern and Drosten, co-authored a paper reporting a survey carried out to evaluate the quality of antigen produced by commercial laboratories — a topic we previously covered in our Operation Moonshot article. One might expect such a study to be rigorous, but it fell far short of that standard. Instead, each laboratory was tested against only two samples of the common cold, with just one sample each of NL63 and OC43 viruses.4 Unsurprisingly, all but one laboratory (Healgen) passed this minimal challenge with flying colours.

This so-called ‘quality assurance exercise’ was clearly designed to make the tests appear more accurate than they truly were. By setting such a low bar for evaluation, the process effectively rigged the results, ensuring that the antigen tests seemed reliable despite their significant flaws.

So if the antigen testing was suspect, what about the antibody testing?

To believe antigen testing we must believe we have identified the right antibodies that react to the antigen being tested. If the antibodies are not specific to that antigen then the antigen test is not specific.

The Scottish chief scientist office released a report (March 2021) from a research group at the University of Aberdeen. They say:

“When testing the common cold N-protein, we detected antibodies in all the pre-COVID samples and in 170 out of the 171 COVID-19 samples, suggesting a common prevalence of common cold coronaviruses….

…there was a low specificity of the currently available antibody tests, because 38% of the pre-COVID samples were positive for the N-protein (commonly used in current tests), and around 20% to the S protein (also a constituent of the current tests).”

Ng et al, (submitted June 2020, published 2021) and say:

“Serological assays for SARS-CoV-2 may cross-react with antibodies against other human coronaviruses (HCoVs), leading to potential false-positive results.”

“Cross-reactivity has been observed in assays targeting both the N gene and the S gene, indicating that antibodies against other HCoVs can interfere with the detection of SARS-CoV-2.”

They also say with a sense of some puzzlement that:

“A relatively recent outbreak of HCoV-OC43 in a care facility resulted in infection mortality rates in vulnerable populations comparable with those of SARS-CoV or SARS-CoV-2”.

This particular care-facility outbreak (in 2003) was actually discussed here, where it is suggested that it was the response to the (mistaken) belief that residents had been infected by the pathogen then purportedly causing a “pandemic” (SARS1) which hugely upgraded its mortality rate.

Majdoubi et al (2021) say:

“Pre-existing cross-reactivity to SARS-CoV-2 occurs in the absence of prior viral exposure.

The main finding in this study is that, at a population level, the vast majority of adults show antibody reactivity against SARS-CoV-2 antigens.”

Andersen et al (2021) say:

“….data suggest that pre-pandemic SARS-CoV-2-reactive antibodies were likely elicited by previously circulating beta coronavirus strains, such as OC43.

We found that 2.2% of samples possessed pre-pandemic antibodies reactive to the SARS-CoV-2 full-length S protein, 0.6% of samples possessed pre-pandemic antibodies reactive to the SARS-CoV-2 S-RBD, and 23.9% of samples possessed pre-pandemic antibodies reactive to the SARS-CoV-2 N protein.”

There are startling possibilities to consider here:

  • either whatever caused the tests (which were assumed to be specific for some thing novel) to light up positive was something that was actually widespread pre-pandemic (i.e. it was endemic), and/or
  • these tests are simply detecting the common cold.

It is apposite here to consider what is actually meant by ‘novel’. Before our relatively recently acquired ability to mass-sequence everything around us, novelty would have been defined purely by reference to clinical features and a lack of a protective immune response.

Notably, the results of these studies raise serious questions about whether the early studies that used SARS-CoV-2 seroprevalence data, such as the famous infection fatality rate study carried out by John Ioannidis, contain conclusions that may not have any validity at all.5

The bottom line

In hindsight, neither the PCR or LFT test was trustworthy and the seroprevalence testing was likely picking up cold viruses or an endemic signal novel to detection — and this revelation on its own should be sufficient to force everyone to reconsider everything they thought they knew about Covid-19 diagnostics.

Of course it is possible that the PCR tests and LFT tests all work absolutely perfectly in lab conditions, in the sense they actually do reliably detect a constructed sequence, dubbed SARS-CoV-2, but, as Jonathan and Jessica wrote below, this circularity means that these tests actually have little or no utility as diagnostics in the real-world.

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

*Martin Neil, Jonathan Engler, & Norman Fenton

Footnotes

  1. Note that Wen et al also say “These Abs against NTD and CTD of SARS-CoV-2 N protein do not have neutralizing activity, their contributions to the antiviral response need to be studied further.” This implies that to detect SARS-CoV-2 reliably we must use antibodies that do not appear to fulfill the viral neutralising role normally associated with them. This makes little sense. ↩︎
  2. Healgen claim that their test has NO cross reactivity with other viruses but oddly this is the only test in the list that backs up that claim with data. Even more oddly, the Healgen test is the only test identified by Corman-Drosten (paper) that DOES cross react with other viruses. These contradictory claims cannot both be true. ↩︎
  3. Many of these antigen tests were ‘validated’ against PCR tests which themselves are claimed to detect the N1 and N2 epitopes of the N-protein (both within the N-terminal sub- region). There will have been inevitable circularity given both tests would have been evaluated using lab manufactured proteins, designed to match a computer code, rather than actual samples from humans. ↩︎
  4. We are not, by the way, claiming that a wider panel would have made the test specific enough. Whenever new viruses (whatever they are) are looked for, they are found. In order to rule out cross-reactivity one has to know all the pathogenic signatures which might interfere with the intended result, and as there will always be “known unknowns” this is an impossibility. We are also not here accepting that even if there had been a test which was specific for a particular pathogen, that this would have justified its use at all, let alone as part of a widespread mass rollout which had the effect of creating and propagating an emergency when none was warranted. ↩︎
  5. Note that more modern antibody kits (NativeAntigenCompany and Quanterix) claim to test for specific epitopes of the N protein but these have only been used in research settings and not used in mass testing. We do not know if these kits have been independently evaluated. ↩︎

Works Linked or Referenced

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