Clarifying SARS-CoV-2, pt. 1

Why believe that a VIRUS killed unhealthy adults? (Oh...)

Da Virus Theory

Let’s step back and appraise, as aliens observing from space, the recent flare-up of skepticism regarding the relationship between a certain widely experienced, invisibly transmitted illness reported across the world (a.k.a., a “virus,” exactly as the word has meant since before vaccines existed), and statistically recorded deaths.

Prima facie, this skepticism seems reasonable. The humans of Western nations down on Earth below live in a time when such formerly innocuous conditions as hot weather or the unavailability of electricity prompt outbreaks of death.

Humans used not to even have electricity. Now, when it is taken away, they die.

Clearly, some number of Western humans are at every moment having their lives prolonged by artificial processes, up to and including the manipulation of air temperature, but more generally by medical fussing. Medicine creates dependency.

Is it not then reasonable for humans to propose that the outbreaks of death attributed to infection with SARS-CoV-2 were in fact manifestations of disruptions to these ongoing artificial processes? Of course.

But what is the proposal for why the same old, vulnerable humans dependent on those processes would be invulnerable to SARS-CoV-2?

Certain possibilities are available:

1. SARS-CoV-2 does not exist.

2. SARS-CoV-2 exists, but does not cause excess disease; it is just another exhibit in the viral zoo.

And etc. For now, I am not including theories that discern between “virus” (an invisibly transmitted agent of disease) and “virus” (the RNA life-form known as SARS-CoV-2), as these do not necessarily critique “da Virus Theory.” I.e., if one wants to propose that genetically marked poisons are being sprayed on Amazon packages, this does not necessarily imply any particular interpretation of whether people are dying more because of the agent vs. other things. (It might certainly be the case that proponents of said theories believe one thing or the other on the latter front, but there is no necessary link between that belief and their pet feelings about RNA.)

Critiques of the “default” interpretation of why more Western adults started dying in 2020 and kept doing so afterward must include an argument for discounting the appearance of an agent of invisibly transmitted experiences of illness, either explicitly or implicitly. If no defense of those propositions is offered, then the critique hasn’t actually put forward a case; at best, they have waved off the prosecution’s evidence without an argument.

The Defense Opens

The case for a “non-default” interpretation of heightened adult deaths centered on, I think, 2, has recently become the topic of a debate between Will Jones of the Daily Sceptic and the coalition of minds in PANDA:

Further alternative explanations for excess deaths other than a novel deadly virus spreading from Wuhan

In my commentary on Verduyn’s essay, I will first acknowledge the strength of a (generic) reasonable doubt argument; second, point out how the “default” case — the virus caused deaths — is not outlandish; and finally I will assess whether the “non-default” case — the virus did not cause deaths — is convincing, and discuss evidence that “da Virus” did cause deaths.

i. Reasonable Doubt Is Reasonable

“Other stuff can cause excess deaths,” is not “therefore the virus SARS-CoV-2 did not,” just as “Other people could kill the deceased, jury” is not “therefore my client did not.” Of course, in a murder trial, the latter might be sufficient; but as aliens we can observe that the standards of a murder trial do not apply to what humans actually believe is true in day-to-day life. Again, it is reasonable to doubt the agent; but doubt alone is not sufficient for every-day appraisal of reality.

The defense must convince other humans to discount the notion “people got sick with an invisibly transmitted agent.” They must prove innocence. This discounting, in practice, either takes the form of denying illness occurred or accrediting experienced illness to “the baseline,” i.e. the fact that some amount of people always get sick and die — except when this process is artificially postponed. In the West, it was being postponed, and then due to the social contagion inflicted in response to the announced virus, it stopped being postponed.

Again, as the aliens observing this metaphorical court case from our metaphorical space-ship, we can acknowledge that this argument is prima-facie sound, perhaps even convincing. But it does not accomplish the work of actually appraising the evidence. And, without dismissing this argument, we can note an implication that should guide the same appraisal going forward:

1: It should be expected that some measure of excess death by other causes occurred, but this would not mean that excess deaths from the virus did not.

2: Variations in excess death by region wouldn’t, in fact, argue against a virus at all.

Point 1 should be obvious, yet perhaps often goes unnoticed. There is no definable quantity of evidence of death-by-other-causes, including iatrogenic death, that implicitly lets the virus “off the hook.” But, the quantity certainly isn’t “any.” Showing that just one instance of medical murder occurred doesn’t imply that all deaths were medical murder. With no clear standard available, we must appraise the balance of evidence as best we can.

ii. Western adults dying more from a virus is not inexplicable, nor an emergency

Point 2, above, involves coming to grips with the counter-intuitive semi-paradoxes that arise from prolonging natural death. Western humans are better protected against the deadliest threats that Earth likes to throw at humans, such as infectious bacteria, diabetes, and cancer. But thanks to this exogenous protection (we have plenty of bacteria, diabetes and cancer, but medicine ameliorates it), Western humans are less protected against weaker threats, such as power-outages, heat waves, or a hypothetical novel coronavirus developed in a lab (and updated afterward). Weak threats cannot find victims in competition with strong threats. By protecting themselves against strong threats, the West accumulates hoards of victims for weak threats. And, by having a lower baseline death rate, the West functions as a more sensitive tool for measuring the appearance of a weak threat.

Policies portrayed as “grandma-killing” would obviously be innocuous in a region without grandmas; but becomes controversial in areas with artificially inflated numbers of grandmas.

Again, we must assess the evidence as it is. Are there places with divergent outcomes despite similar demographics (yes)? What do we make of them?

But in general, it bears remarking that the prosecution’s case is not outlandish. Supposing someone really did develop a competent, novel virus, why wouldn’t it cause a lot of deaths in the West?

As adults, humans bear memory immunity to the things that made them sick as children. Why bother, unless that same immunity is protective? This protection is apparent in the relationship between humans and influenza A — when H1N1 crossed back over in 1918, older adults were protected while younger adults were not, because (I have argued) they were immune from prior exposure.¹ This is believed to have happened again with H2N2, H3N2, and “pandemic” 2009 swine flu, even if younger adults were not as dramatically affected by any of those.²

Adults experience immune senescence, a process which arguably begins (at least on a population level) in puberty. What keeps them alive as their immune system loses vigor is the suitcase full of “cliff’s notes” accumulated during childhood — their antibodies and T Cells trained to recognize common viruses. If these things did not prolong life even in reproductive age, adults arguably wouldn’t have them (though the argument for an evolutionary benefit to post-reproduction-age protection is just as strong).

These protective cliff’s notes, further-more, are not invisible; they are perhaps the most testable qualities in all of biology. Again, when it comes to influenza A, the blood of adults can be used to measure when particular strains stopped being present in childhood, decades and decades later, simply by seeing whether it stops those strains from making lab animals sick. In 1936, the blood of those born before 1926 stopped mice from being infected with swine flu; the blood of those born afterward didn’t.³

Results from Davenport, et al. (1953, 1956). When flu strains stop being present in childhood (Swine in early 20s, PR8 in early 40s, etc.) humans no longer make antibodies for them: Childhood immunity remains visible in adulthood.

No one’s blood could boast the same claim for SARS-CoV-2 in 2019. In England in early 2020, a survey of school-kids failed to find antibodies in a single donor. The virus and its proteins did not “pre-exist” in humans.⁴

Earth’s entire population of adults lacked the cliff’s notes for this particular threat. Three years later, and nearly the reverse is the case — immunity has been acquired. It is essentially irrelevant, again, whether this change resulted from a competently self-spreading RNA life-form or from something sprayed onto Amazon packages. The change happened.

It is not outlandish, again, to propose that some adults died “extra” along the way. Nor can this proposal be dismissed by reference to the “baseline” — because the baseline consists of viruses that most adults already have immunity for. If Evil Mr. Fauci got up on the news in 2004 and announced that a new coronavirus, NL63, had just been discovered, using the same ACE-2 receptor as SARS-1, he would have been describing a virus that (it had simultaneously been discovered) “virtually all sera from patients 8 years of age or older” could neutralize.⁵

The prosecution’s case, a.k.a. the “default” or “da Virus” theory of why Western nations have recorded excess deaths since 2020, is just as reasonable as doubt of the same.

Nor does this case cede anything to the litany of egregious measures waged in and upon the West in response to the virus. One thing ignored when referring to excess deaths in terms of “sigmas” is that in the West, the baseline (age-adjusted) rate had been dropping for 100 years. This means that smaller and smaller absolute increases can cause larger and larger percentage increases; and so a large percent increase doesn’t imply a lot of people are actually dying.

Many places experienced death rates in 2020 and afterward that were comparable to 20 years prior. Scotland, for example, recorded 64,093 deaths in 2020 with a population of 5.47 million; it recorded 60,291 deaths in 1999 with a population of 5.07 million.⁶ That’s a few hundred saved deaths in a “pandemic” year.

Since Scotland’s population is older now than in 1999, age-adjusted “savings” would be even greater.

The world wasn’t actually on fire in the year 1999; there was no emergency. People made and watched movies, potentially even in Scotland. Likewise, one can claim that SARS-CoV-2 caused excess deaths without claiming that it was an emergency.

Under “da Virus” theory, which says the recent extra deaths in the West that still result in fewer deaths than used to be commonplace at the turn of the millennium were caused (to some extent) by the virus, it still remains true that all reactions were disproportionate to the threat.

In Part 2: The specifics of the “other causes” case, and the evidence for “da Virus.”

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1. See “1918, I Love You.”

2. Citations pending.

3. See “OAS Lit. Review / Timeline Pt. 1.”

4. See “The Quiet Corona-Can.”

5. Hofmann, H. et al. “Human coronavirus NL63 employs the severe acute respiratory syndrome coronavirus receptor for cellular entry.” Proc Natl Acad Sci USA. 2005 May 31;102(22):7988-93.

6. https://www.nrscotland.gov.uk/statistics-and-data/statistics/statistics-by-theme/vital-events/general-publications/vital-events-reference-tables/2021/list-of-data-tables