Fri, 04/24/2020 - 17:40
Dear colleagues,
- Follow-up on “L’exception suédoise”: As I had hoped, I received quite several reactions from you. You find them anonymized in the first attachment. An important element of course is the registration of mortality, which differs according to the country. Two colleagues sent me an analysis of the New York Times https://www.nytimes.com/interactive/2020/04/21/world/coronavirus-missing-deaths.html?smid=em-share
The most important element is indeed the difference between the actual excess deaths and the reported COVID deaths. As you can see in the Table (attach 2), in most countries the COVID deaths underestimate the real excess deaths, except in Belgium and ….Sweden, where a slight over reporting was noted.
Some reactions in a nutshell:
- To have a fair comparison, one should carefully align according to the actual start of the epidemic (bc deaths only start to be seen several weeks after the epidemic starts)
- Population density is an important parameter: It is probable higher in Belgium than Sweden; higher in Flanders than Wallonia, Higher in Lombardy than Sooth of Italy, higher in NYC than Oklahoma….
- The Swedes didn’t go skiing in Northern Italy, the Belgians did
- Sweden has a good system of contact tracing.
- (see attachment for more) ….
In the meantime, it seems that there is a European (ECDC) initiative to harmonize the epidemiological parameters (in retrospect?)
WHY did we not have a good test-and-trace system in place? It is only NOW that policy makers start talking about it, in the context of relaxing the restrictions Sorry, it is even not urgent any more, but MUCH TOO LATE, because they seem to think that you can take the hundreds of well-trained “tracers” that we need just from a shelve in a warehouse !
- The origin of SARS-CoV-2: in follow up of the claim by Luc Montagner and others that it wasz “created” in a lab. A nice analysis in Nature Merdicine, with as a major conclusion: “Our analyses clearly show that SARS-CoV-2 is not a laboratory construct or a purposefully manipulated virus.”
- The Receptor Binding Site mutations suggest that the virus has evolves in a human or human-like environment (I.e. an enigmatic intermediate host between the bat and the human that has an human-like ACE2…)
- The polybasic cleavage site between S1 and S2 (to enhance fusion) is another adaptation to the human host that is also needed in f.i. avian influenza to turn it into a high pathogenicity form for humans.
- Regarding the prevailing hypothesis that the pangolin is the “intermediate host”, they presume that other SARS-like CoV are circulating in China and that human-to-human transmission has optimized especially the polybasic cleavage site.
→ The authors conclude that the adaptations are “logical”, but the precise mutations, elaborated by the virus, are rather unexpected, not derived from any lab virus backbone and therefore not the result of human manipulation.
I guess this settles the discussion. The explanation of Prof Montagner was difficult to follow, as he presumed that this virus was created in an attempt to make an HIV vaccine. But why would one then start from a highly pathogenic SARS-like virus and not a more innocent viral vector?
I feel it is useless to argue with people who think that COVID is caused by 5G networks, but investigating this kind of more sophisticated “fake news”, supported by prominent people, is important, because it may be perceived as truth by a part of the intellectual or political elite. And we need to be ready to give scientific arguments.
- As you know, I’m puzzled by the role of children in this epidemic and you hear various opinions from our own experts these days, with even contradictory advices to the general public. Therefor I keep looking for literature, but I fail to find good evidence until now. I add this paper on Tranmission patterns in EClinicalMedicine. It doesn’t provide an answer to my question, but it is a nice illustration in (unfortunately a bit fuzzy) summary graphs how the epidemic evolved in several areas and what the presumed effect of interventions has been. Fig 4 (P. 18) is particularly interesting, because it analyzes the epidemic according to age groups and “social contact pattern” (site). It seems evident that the age groups between 24-44 and 45-64 on one hand, and households and “public places/community” (but less so schools and workplaces) on the other are “drivers”. But especially the latter has to be put into perspective, because schools and workplaces were closed at an early stage. So, we’ll have to wait whether re-opening of those places will lead to a second wave….?
Best wishes,
Guido