Semantics of the Pandemic, One Year On

Computational Semantics
7 min readMar 1, 2021


Welcome to March and to the first anniversary of CoViD-19 quarantines. It is also 11 months since we presented our semantic analysis of the etiology and progression of the disease. In that time half a million people in the United States have died from fatal outcomes of this disease — essentially all of that preventable — and misguided responses to the pandemic have worked economic destruction and disrupted if not destroyed human lives and livelihood on a scale not seen since the Second World War — again, all of it unnecessary and entirely preventable.Yet Fauci is still at the podium, still spouting the same dangerous nonsense he was spouting about HIV in 1981 when Larry Kramer quite rightly wanted him tried for crimes against humanity and genocide against gay men.

Forty years ago Fauci insisted there would soon be an HIV vaccine. He squandered 25 years with that nonsense. Once he was finally ignored and the fight against HIV turned to blocking the progression of the disease rather than looking to immunize against it, only four years were required to develop effective protease inhibitor therapies. HIV is now an entirely treatable disease, and as viral replication is blocked in infected individuals the viral loads in their titres become undetectable and apparently untransmissable. Without transmissibility and viral replication the HIV virus will presumably die out within this generation.

Last April we noted that CoViD-19, or at least its more dire outcomes, could be both prevented and cured by flavonoids which are natural receptor blockers against viral invasion and replication. Perhaps the best-known of these is elder: at the beginning of the 9th century Charlemagne the Holy Roman Emperor decreed that the landholders of his realms should plant elder and give the elixir to their peasants because of its perceived effect in blocking the spread of the annual influenza. Elder is just as effective as a receptor blocker against CoViD-19. So are quercetin, and white pine and osha (bear root). The use of these medicines is straightforward and simple: a regular maintenance dose will prevent viral invasion. If there are already symptoms the dose should be increased at 12 hour intervals until the symptoms abate. And they will abate. Despite official disapproval of these therapies (which have millennia of evidence supporting their safety and effectiveness) they are being used successfully against CoViD-19. We have been able to compile some hundreds of examples of cures (which of course does not begin to measure the numbers of CoViD-19 infections prevented) and have no examples either of the failure of these therapies nor of bad outcomes in consequence of them.

So are there differences in the several flavonoids and reasons for an individual to select one over another? Absolutely, but understanding those reasons actually requires an entirely different epistemology than the ontological predicate logic which has become the intellectual standard of our society and is taken for granted as the basis of ‘diagnosis’ and medical reasoning as taught for at least the past century and a half in Western medicine. Serendipitously there is an essay by Siddhartha Mukherjee in the current New Yorker Why Does The Pandemic Seem To Be Hitting Some Countries Harder Than Others in which the unexamined assumptions and biases of the incumbent medical establishment are on cringeworthy display. In fact that essay, being so well written and yet so very wrongheaded on the very issues which have brought us the devastation of the pandemic, is an unparalleled starting point from which to approach an utterly different manner of diagnostic thinking and causal reasoning. On that basis you are strongly encouraged to read Mukherjee and then to come back here, where we will be waiting.

So Mukherjee asks a great many questions but has no answers that are entirely convincing even to himself, as he readily admits. The failure to answer those questions is utterly fundamental because 1) it entirely (and obliviously) mischaracterizes the problem; and 2) it employs an ontological (rather than an etiological) methodology which is incapable of analyzing the true problem here even if that problem had been correctly described. At its title the essay is already mired in the epistemological morass from which it cannot escape: the question that needs to be answered is not what are the salient differences between the countries where there are fewer bad outcomes of CoViD-19 infections and those where there are more. The question that we need to answer is what is the etiology and the progression of the disease in those individuals who suffer the worse outcomes, as opposed to the experience of those who do not. This is entirely a question of nature — actually the natures of both the biochemistry of the instance viral invader and the biochemistry of the particular host invaded. It is not at all, or not in any significant way, a question of environment or nurture in which these two natures interact in an instance infection. Yet as early as his subhead Mukherjee has not only assumed that the difference in outcomes is not only primarily a question of nurture or environment but that the salient difference is along the axis of poverty vs. wealth. The bias on display here is exactly the one which Justice Clarence Thomas calls out when he asks why white liberals assume that a school which is majority, or entirely, Black is ipso facto inferior to one which is majority or entirely white, and that the obvious solution (to the problem not quite stated) is to create an integrated, balanced, diverse, equal environment.

One could, of course, treat disease as a social construct (and that is, apparently inadvertently, how Fauci and the incumbent medical establishment are treating CoViD-19). But if we are to practice medicine rather than sociology we will need to examine each instance of the virus as a reified biochemical unit rather than as a typological abstraction, and we must view the infected individual as another reified biochemical unit with which the virus interacts in a manner which is at least potentially unique to that instance encounter of the two. At a more granular level we must examine the particular proteins which that infected individual’s exome encodes because the instance progression of the disease will be a concrete, reified sequence of protein transactions which move toward a fatal outcome, or not.

The scientific investigation which needs to be done (and which has needed doing since HIV) will compile empirical observations of those protein transactions with specific attention to the protein alleles and the sequence mutations which are implicated in inflection point transactions along the paths of most dire progression of the disease. This is a vast undertaking, but it forms the basis for an entirely new era of medicine. In 1799 when George Washington died from over-bleeding to treat a strep throat, Jenner was already achieving the first demonstrable success in modern immunology based on vaccination. For more than 200 years the age of vaccination has supplanted the balancing of humours by purging and bleeding, but it is now necessary to re-assert a more specifically etiological understanding of disease.That etiological understanding is utterly granular to each protein transaction in the path of the disease’s progression, and each of those transactions is utterly specific to the specific protein alleles which apparently determine whether the disease does or does not progress.

Eleven months ago we proposed that the geographic variation in the apparent mortality reported for CoViD-19 might best correlate to the genetic diversity of each infected individual. Note that this is the genetic diversity within the one person (pure individual nature) and does not directly correlate to the apparent genetic diversity within that individual’s community or environment (which is, from the perspective of protein transactions within that individual, essentially an aspect of nurture). The untested hypothesis then was that a ‘melting pot’ society would have a greater number of individuals of more diverse genetic inheritance than a genetic monoculture would. From the beginning of 2020 the reported epidemiological numbers seem to bear this out. When the virus moved from what was essentially a Han Chinese genetic monoculture in Wuhan to Bergamo and Seattle the rate of more dire progressions of the disease jumped by at least an order of magnitude. While the initial hypothesis is still nowhere near rigorously tested, these results are at least consistent with the premise that the exomes of more genetically mixed individuals code for a wider range of unusual alleles of common proteins and that the virus has the ability to trigger a correspondingly unusual progression of protein transactions from that variant material.

The year’s subsequent history of the pandemic offers nothing that we have seen to contradict this hypothesis. Articles like Mukherjee’s raise questions about different outcomes in different geographies that he cannot answer with theories of the disease which he has encountered, but which are elegantly answered by our hypothesis. So for now real progress means abandoning the establishment’s advice to treat the disease as a social construct; use flavonoids as receptor blockers to prevent or to cure the disease; and longer term to re-orient medical understanding around the etiology of demonstrable biochemical transactions. Mukherjee ends his essay by saying that we will effectively reach the end of pandemic without really understanding what happened and, at a scientifically rigorous level, why and how. It’s a wake up call to do better, even if — as always — doing better means abandoning what we know for certain from our hard-earned experience, just as the bleeders and purgers had to give up on their centuries of accumulated wisdom.

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Computational Semantics

Meaning elaborated through Transactional Understanding