Pandemic En Croûte – another slice
Something a little special for independence day: using generalised linear modelling to reveal just how flaky the pastry is (rev 1.0)
I hope subscribers are enjoying this dish on this most auspicious of days. The eagle-eyed will have noticed I started my modelling run at 16 Sep 2020 rather than at the onset of the pandemic back in Mar 2020. This is because I wanted to highlight the impact of lateral flow devices that became available during Sep 2020. The best way to generate the illusion of a pandemic is to ensure members of the public poke their nose as often as possible and to get them to tune in to sober news bulletins at breakfast: there’s something about a smart suit, blue tie and posh accent.
What I’ve done while the kettle boils is to run my model for the period 12 Mar 2020 – 15 Sep 2020 but omit the independent variable for rolling 7-day LFD tests. Here’s what popped out a few moments ago:
The Pearson bivariate correlation for this fetches up at a rather sexy r = 0.984 (p<0.001, n=188), which means variation in the amount of testing and number of people tested using PCR accounts for 96.8% of the variation in daily cases that we observe. This leaves just 3.2% of the variance for anything the virus decided to do; an improvement on the 1.4% declared in the previous newsletter.
The plainest English I can speak at this point is to say our illustrious leaders have made a mountain out of a mole hill. They know it, you know it, they know that you know it, you know that they know that you know it and I can believe that it is not butter.
Cogitation & Coffee
Yesterday I sat thinking about the astonishing results I had baked whilst scoffing flapjack still warm from the oven. I asked myself several times how it was possible that a simple linear model based on tests and people tested alone could predict the daily variation in new cases so accurately that you couldn’t insert a credit card between observed and predicted time series.
I pondered on the inter-dependence between testing regime and disease prevalence in that we’d expect the authorities to ramp up testing when outbreaks were getting vicious and cool the regime down when things were calmer. This would generate a relationship for sure but because of the intrinsic inertia in such a colossal enterprise we wouldn’t ever see a perfect relationship. I got to thinking how well the authorities could predict matters in advance but that boils down to guessing what a (novel) virus is going to do next month. Nope, no joy there either!
I eventually settled on the notion that what we had was a dynamic situation so darn perfect that the tests themselves must somehow be generating the cases. If the tests were random in nature then my model would track daily new cases perfectly but with a great deal of noise (scatter). Non-random results were the only logical conclusion which got me thinking as to what the tests could be testing for. I realised it had to be something that was already endemic in the population that had both seasonal and non-seasonal components. It was then that my cheeky mind settled on the idea of a test that tests for fragments of stuff arising from old and not so novel viruses of all flavours, and the contents of those mysterious exosomes perhaps.
In a nutshell my models suggest that the PCR test appears to be a test that tests for itself, and it might be a jolly good idea to have another good long look at the primers used. Right now I’d put good money on them not being unique or novel.
Coming up... Pandemic Au Naturel whereby I go full geek and tackle serial autocorrelation within multiple regression in order to squeeze out a more robust model from my nozzle. Not for the faint-hearted.
I and others have observed for the entire span of the covid era that it was a test-demic. We openly called it this. But all was from very general observations, not hard math like you have done. Thanks for the excellent work.
As for your theory about the PCR test, I have maintained a similar theory since about Sept 2020. There are 2 major problems with the PCR test, both of which tend to cause your theory to become more likely. The 2 are:
1. PCR tests will find anything if you ramp up cycles past a certain threshold. This was regularly done, with many labs using 40 cycles or more, though it was known to be inaccurate past about 20 to 25 cycles.
2. PCR tests originally looked for a match of only 3 fragments of the published SARS-cov2 genome. When variants came around they dropped down to matching only 2 fragments. As there are only 3 ways to match 2 out of 3 fragments, the 4th variant (omicron) was identified by a match of only 1 fragment, and that one match was not allowed to be the S-gene. This told me that while it was possible that an omicron variant existed it was most likely that the PCR test would now be finding things that were not even a coronavirus.
Finally, of great interest to your theory that the PCR tests were picking up some endemic virus is that 1 of the 3 fragments is a perfect match of a fragment found in pantoea: Your theory exactly.
I offer the following links and quotes as proof:
"There is a perfect match of one of the N primers to a clinical pathogen (Pantoea)...."
https://cormandrostenreview.com/report/
"Pantoea species have been isolated from feculent material, in soil, water, plant (as epiphytes or endophytes), seeds, fruits (e.g., pineapple, mandarin oranges), and the human and animal gastrointestinal tracts, in dairy products, in blood and in urine."
https://www.sciencedirect.com/topics/medicine-and-dentistry/pantoea
UK labs: "There is higher risk of encountering false positives when testing for single genes alone, because of the possibility of cross-reactivity with other HCOVs and prevalent nasopharyngeal bacteria or reagent contamination."
https://probabilityandlaw.blogspot.com/2021/02/uk-lighthouse-laboratories-testing-for.html?m=1
"As things stand, a person who tests positive with any kind of test may or may not have an active infection with live virus, and may or may not be infectious."
https://www.bmj.com/content/371/bmj.m4851
"The S-gene encodes a surface protein, the spike protein, which is a homotrimeric glycoprotein complex essential for infectivity."
https://www.thermofisher.com/blog/behindthebench/why-s-gene-sequencing-is-key-for-sars-cov-2-surveillance/
"A new variant of the coronavirus (COVID-19) was identified in the UK in mid-November 2020. The UK variant of COVID-19 has changes in one of the three genes which coronavirus swab tests detect, known as the S-gene. This means in cases compatible with the UK variant, the S-gene is no longer detected by the current test. When there is a high viral load (for example, when a person is most infectious) absence of the S-gene in combination with the presence of the other two genes (ORF1ab and N genes) is a reliable indicator of the UK variant in COVID-19."
https://www.ons.gov.uk/peoplepopulationandcommunity/healthandsocialcare/conditionsanddiseases/bulletins/coronaviruscovid19infectionsurveypilot/19march2021#percentage-of-those-testing-positive-compatible-with-the-uk-variant
Most tests generally target a large number of genes. Currently, the tests in India test E, N and Rd Rp genes and if one of these genes is identified as positive, the test result would be positive. "
https://m.jagranjosh.com/current-affairs/what-is-sgene-how-will-it-confirm-the-presence-of-omicron-covid19-variant-1638425372-1