Je signale un article remarquable publié par Lockdownsceptics (site anglais).
En partant de l’observation du variant indien… qui fait pschiit et qui se comporte désormais exactement comme… le variant anglais, avec une contagiosité dans les chaussettes, l’auteur élargit le débat avec des hypothèses foutrement intéressantes.
Il rappelle la théorie d’un épidémiologiste en 1981 qui s’interrogeait sur le comportement -étrange- de la grippe.
Hope-Simpson postula que le virus ne suivait pas le schéma classique (comme la rougeole ou les rhinovirus) : les malades infectent les non malades… Mais qu’il était plutôt “latent” chez certains porteurs… et ensuite “réveillé/activé” par des facteurs extérieurs (soleil, vitamine D, saison).
Son étude fut reprise par un groupe de scientifiques en 2008 qui résumèrent tout ce qui cloche avec le virus de la grippe :
- Why is influenza both seasonal and ubiquitous and where is the virus between epidemics?
- Why are the epidemics so explosive?
- Why do epidemics end so abruptly?
- What explains the frequent coincidental timing of epidemics in countries of similar latitudes?
- Why is the serial interval [the time it takes for secondary cases to appear] obscure?
- Why is the secondary attack rate so low?
- Why did epidemics in previous ages spread so rapidly, despite the lack of modern transport?
- Why does experimental inoculation [infection] of seronegative [without antibodies] humans fail to cause illness in all the volunteers?
- Why has influenza mortality of the aged not declined as their vaccination rates increased?
Retour au couillonavirus.
Whatever the underlying cause of the strange behaviour, though, some facts are clear. SARS-CoV-2 is not, by any reasonable definition, a highly transmissible virus – infected people on average only infect 10-15% of their close contacts, even at the height of the winter surge (and that is an upper bound as it assumes that all subsequent infections were caused by the index case rather than being co-index cases). This compares to 57% for rhinovirus and 70% for measles – those are highly transmissible viruses.
Voilà pourquoi tous les modèles mathématiques foireux se plantent systématiquement.
Et voilà pourquoi les confinements et autres mesures à la con… n’ont que peu d’effets.
Rather, COVID-19 is subject to the same kind of mysterious and explosive seasonal triggering as influenza is. This probably helps to explain why lockdowns make no clear impact on transmission or mortality, and why the virus does not immediately rebound when restrictions are lifted, as all the models keep wrongly telling us is going to happen.
