Abstract and chapter 1 of “Follow the Sun”
Seán Ó Nualláin & David Bernal-Casas (2020)
We start with the basic science. Covid-19 is an extremely nasty and extremely transmissible coronavirus. Except in summer in the northern hemisphere is it not a good idea to have mass assemblies. It is about to wreak havoc all over the Northern Hemisphere . There will be a lot more illness and death this autumn and winter then there was in spring. However the Southern Hemisphere will see an attenuation of its effects as it goes through its own spring and summer.
One of the main receptors of covid-19 seems to be ace 2. Receptor ace2 is an antagonist to Ace which is related to hypertension but ace2 has many many other roles in human physiology. The coronavirus itself used by covid-19 once this receptor has been accessed is itself extraordinarily nasty.
However the intellectual virus which caused the world economy to lose literally trillions of Dollars was much worse. Sir and its variants which was the epidemiological Model used does not have a variable corresponding to the number of virus particles! But covid-19 is even more vulnerable to daylight and temperature than most viruses. The model used by the governments all over the world can only work near the equator and even then in a very limited way
Our first discovery was to use publicly available data about daylight hours to compare to decay of covid-19 exemplified as number of transmissions in Ireland and Spain. We got an extraordinary result from these two very different countries with the exponents and intercepts converging all the way up the solstice. We extended the methodology to include temperature and humidity and successfully modelled the epidemic in both these countries from the start in January and February.
But these results were minor compared to the true Revelations. When we examined the data about Transmissions from Arizona we found that temperature humidity and daylight hours explained over 99% of the variability. In short human interventions like lockdown and change of behaviour had no effect whatsoever. This let us to ask the question of questions which was whether lockdown in spring in the Northern Hemisphere any good effect whatsoever.
Our answer was a categorical no. Heaviside not Maxwell was the physicist who wrote the formulation of the equations we use in college. We used his stair function and boxcar function to find the the amount of variability explained by lock down was between 0 and 1%. It is also fair to say that locking people in doors almost certainly caused a significant number of illnesses and deaths.
As we approach what will be perhaps the worst winter in Ireland since 1850 there are some Solutions we can use. We have found that ultraviolet light and dehumidification used in doors can sterilise spaces. We have to hang in there until April next. However there is a much bigger question to be asked about why two independent neuroscientists who were unfunded and just doing this out of concern for the fellow citizens solved this problem first despite billions been thrown at conventional science. There are also questions to be asked about why Shi Zhengli was allowed continue her experiments when it was clear they were extraordinarily dangerous. Finally we have to ask whether the virus was released accidentally or deliberately and if deliberately for what purpose. It is noticeable that around 100 elections have been postponed and in Ireland at deeply unpopular government which had never been elected has now gotten a full-time 9 years in office as a result
Finally, the go-to paper (Andersen et al, 2020) which “established” that sars-cov-2 is not a lab artefact needs to be addressed. Their arguments are the following and we have put the following counters to
them in writing without any reply ;
1. The RBD (receptor binding domain used by covid-19 is non-optimal so it cannot be engineered.
Counter; “passaging” which is a form of directed evolution will give this type of result as we show in the book
2 There is no evidence showing the elaboration of “passaging” from the Menachery, Baric and Zhengli work.
"Subsequent generation of a polybasic cleavage site would have then required repeated passage in cell culture or animals with ACE2 receptors similar to those of humans, but such work has also not previously been described.”
Counter; but of course there isn't! Zhengli refuses to share her lab books. This has now become particularly important since the first vaccine by Pfizer – almost certainly one of dozens available within a year – uses the spike protein, leaving intact the claim that no vaccine for a coronavirus has yet been developed
3. This blatant contradiction does not require a counter
"Polybasic cleavage sites have not been observed in related ‘lineage B’ betacoronaviruses, although other human betacoronaviruses, including HKU1 (lineage A), have those sites and predicted O-linkedglycans"
but in the conclusion
" However, since we observed all notable SARS-CoV-2 features, including the optimized RBD and polybasic cleavage site, in related coronaviruses in nature, we do not believe that any type of laboratory-based scenario is plausible."
4. RATG13 – which appeared in the literature only after the pandemic began – is not close enough to sars-cov-2
"Furthermore, a hypothetical generation of SARS-CoV-2 by cell culture or animal passage would have required prior isolation of a progenitor virus with very high genetic similarity, which has not been described."
Again, we need to see those lab books – particularly as RATG13 was itself new to us, and we suspect the lab books might reveal a successor
5. Sars-cov-2 did not mutate quickly as one would expect and was therefore in contact with human immune systems before the pandemic.
Counter; while sources like Latham generously point to the possibility of an inadvertent release due to the exhumation of 3 miners clearly victims of RATG13 in 2012, the Chinese have shown no hesitation in experimenting on the Uighurs, often with bizarre traditional Chinese therapies
Andersen, K.G., Rambaut, A., Lipkin, W.I. et al. The proximal origin of SARS-CoV-2. Nat Med 26, 450–452 (2020). https://doi.org/10.1038/s41591-020-0820-9