If most of the hepatitis suffered by children remains unexplained, the multiplication of mysterious pediatric hepatitis in the spring (1,010 cases in 35 countries) mobilized the WHO. 5% of children underwent liver transplants, at least 22 died.
In two independent studies, English and Scottish researchers (it is in Great Britain that the majority of cases have been detected) found high levels of a virus (AAV2) in the liver cells of sick children.
The viral track had been put forward from the start of the outbreak, but raised questions, the initially suspected adenoviruses being considered non-pathogenic. According to the researchers, the co-infection by adenoviruses and this AAV2 (which needs the presence of an adenovirus to multiply) could explain the disease.
This co-infection would not be enough. Most sick children would be carriers of the same variant of a gene that conditions our reaction to external pathogens. Hepatitis would be the consequence of an immune runaway.
On the other hand, the track of a deleterious effect linked to exposure to the Covid-19 virus seems to have been ruled out, the proportion of sick children previously infected with SARS-CoV2 not being higher than the control group.
The confinements in question
If the track is credible, the two studies, of which only one has been published, relate only to a limited number of cases. They leave open the question of the most serious cases as well as the chronology of this outbreak (which has slowed down since June). Have lockdowns diminished the effectiveness of children’s defences? Did the sudden exposure to a large number of viruses overwhelm them?