From scientific fraud to the ruin of nations: the myth of asymptomatic transmission

Have excessive measures been taken, with devastating consequences, based on wrong assumptions? How did we allow this to happen without ever having proper scrutiny?

How likely is asymptomatic transmission of the SARS-Cov2 virus? And how relevant is that possibility today and in the near future? These two questions are absolutely essential and it is therefore necessary to rescue them for a broad and plural debate.

The potential transmissibility of SARS-CoV-2 through asymptomatic individuals has become one of the pillars of last year’s plans to “combat” the health crisis, and since then little or nothing has been discussed. It was on this premise that extremely costly efforts were made to track down asymptomatic individuals, in the belief that they were a relevant enough driver of the spread of the pandemic to justify the brutal cost imposed on society – not only directly, but also indirectly, as a result of the policies adopted.

In this article we will review the events and the main scientific articles that have addressed this issue, absolutely central to the unfolding of the putative pandemic.

On the epidemiology of influenza

The epidemiology of influenza swarms with incongruities, incongruities exhaustively detailed by the late British epidemiologist, Edgar Hope-Simpson. He was the first to propose a parsimonious theory explaining why influenza is, as Gregg said, “seemingly unmindful of traditional infectious disease behavioral patterns.” Recent discoveries indicate vitamin D upregulates the endogenous antibiotics of innate immunity and suggest that the incongruities explored by Hope-Simpson may be secondary to the epidemiology of vitamin D deficiency. We identify – and attempt to explain – nine influenza conundrums:

1. Why is influenza both seasonal and ubiquitous and where is the virus between epidemics?
2. Why are the epidemics so explosive?
3. Why do they end so abruptly?
4. What explains the frequent coincidental timing of epidemics in countries of similar latitude?
5. Why is the serial interval obscure?
6. Why is the secondary attack rate so low?
7. Why did epidemics in previous ages spread so rapidly, despite the lack of modern transport?
8. Why does experimental inoculation of seronegative humans fail to cause illness in all the volunteers?
9. Why has influenza mortality of the aged not declined as their vaccination rates increased?

We review recent discoveries about vitamin D’s effects on innate immunity, human studies attempting sick-to-well transmission, naturalistic reports of human transmission, studies of serial interval, secondary attack rates, and relevant animal studies. We hypothesize that two factors explain the nine conundrums: vitamin D’s seasonal and population effects on innate immunity, and the presence of a subpopulation of “good infectors.” If true, our revision of Edgar Hope-Simpson’s theory has profound implications for the prevention of influenza.