An abnormal reaction of the immune system that normally occurs in the presence of the AAV2 virus is the cause of acute hepatitis that has affected more than a thousand children in 35 countries in the past year and whose origin has, until now, been a mystery.
However, three independent and separate investigations conducted in the United Kingdom and the United States of America, the two most affected countries, today, are presented in Article published in the journal Natureits results AAV2 has been shown to be present in almost all infected children and only in a small percentage of healthy children.
AAV2 must be associated with infection with other viruses and, in many cases, with a genetic predisposition to trigger hepatitis, according to the analysis. The coincidence between the increase in hepatitis cases in children with the end of epidemic restrictions, and their decline in the following months, suggests that Covid-19 may have contributed to this phenomenon.
AAV2 may be necessary but not sufficient to trigger hepatitis. “New cases stopped appearing months ago,” Maria Botti, a hepatologist at Val d’Ebron Hospital in Barcelona, was quoted by La Vanguardia newspaper.
The first cases became known in April last year, when children under the age of five were admitted to UK hospitals with abnormally elevated transaminases, often with jaundice, sometimes with vomiting and some progressing to acute liver failure.
Of the 1010 cases reported to WHO by July 8, 2022, 46 had had liver transplants and 22 had died. In Spain, 40 cases had been reported, one of which had undergone a transplant.
The first hypothesis indicated that adenovirus 41 is a possible cause of these hepatitis cases after analyzing the presence of this pathogen in infected children, however, this possibility was not confirmed.
The three new investigations performed a metagenomic analysis, which consists of sequencing all the genetic material of a sample without assuming which pathogens could be found, making it possible to identify viruses that were not previously suspected.
In a first study by the University of Glasgow, AAV2 virus was detected in 81% of infected children and 7% of healthy children, proving that the fact that there were cases with AAV2 and without hepatitis shows that the microorganism is not. enough to cause disease.
About 93% of sick children have a genetic variant that predisposes them to T-cell-associated autoimmune diseases, and the presence of AAV2 virus in altered hepatocytes surrounded by immune T cells suggests that the virus plays a major role in acute hepatitis.