A few months ago, cases of a severe acute hepatitis of unknown origin affecting young children around the world began to appear. It is estimated that more than 1,000 children – many of them under the age of five – living in 35 countries have been affected. Cases have also been detected in Europe, especially in the United Kingdom, and also in Spain. Now, two studies carried out by scientists from London and the University of Glasgow (United Kingdom) could have identified the probable cause of this disease, and the main suspect is not the coronavirus, as was pointed out until now, but another virus that was thought harmless, adeno-associated virus 2 (AAV2).
And it is that, the researchers have ruled out any connection with the coronavirus infection or with the vaccines against COVID-19, and have attributed these liver problems to the presence of two common viruses that have reappeared after the imposed restrictions ended. to stop the pandemic. Specifically, they say that babies who were exposed to these pathogens later than normal due to COVID-19 restrictions lost some early immunity against:
In the opinion of the researchers, this could explain why some children developed rare and serious liver complications. They have stated that coinfection with AAV2 and adenoviruses or, less frequently, the herpes virus HHV6, were a probable cause of cases of hepatitis of unknown origin among children, although they warn that more research is needed to confirm this, since In fact, the information that is published to support this idea is made up of two preprints. In addition, it has also not been clear why some of the children affected by this mysterious hepatitis develop inflammation of the liver, but these scientists point out that genetics could play an important role.
Coinfection with AAV2 and adenovirus or, less commonly, the herpesvirus HHV6, was a likely cause of hepatitis of unknown origin among children
Both studies also found that all but two of the 14 sick children studied had a specific mutation in a type of gene called HLA that is involved in the body’s response to pathogens, causing their immune system to overreact to a Viral infection. This mutation is quite common in northern Europeans: 11% of Britons have it and it is known to be related to certain autoimmune pathologies, said Emma Thompson of the Glasgow Virus Research Center.
The researchers found no AAV2 proteins or actual copies of the virus in the patients’ liver cells, suggesting that instead of directly damaging liver cells, AAV2 may trigger an immune response that causes liver damage. That hypothesis is supported by the HLA type link and the fact that some children had gastrointestinal illness many weeks before developing hepatitis, a leader of the London team, virologist Judy Breuer, of Great Ormond Street Hospital, said in a statement. a press conference.
Less childhood immunity against adeno-associated virus AAV2
AAV2 was found in 96% of cases in both studies. AAV2 is not an adenovirus, but belongs to the parvovirus family. This virus was found at very high levels in the blood and liver of the patients tested, and it was also found to be replicating in the liver. However, AAV2 was absent, or only at very low levels, in the blood and liver of control groups consisting of children who did not have acute hepatitis.
The Scottish study, published in the MedRxiv repository (not yet peer-reviewed), included nine cases and 58 control subjects. Using next-generation sequencing and real-time PCR, the group of scientists compared samples and found the presence of AAV2 in the plasma and liver of the nine cases, while no AAV2 was found in any of the individuals in the study groups. control.
The London team studied 28 cases, including liver samples from five children who needed a transplant and blood samples from the rest; residual samples were sufficient to test 17 cases of AAV2, 16 of which were positive. RNA sequencing of liver samples confirmed the presence of AAV2 replication in the livers of children with unknown hepatitis. Patient samples were compared to 132 controls from immunosuppressed and immunocompetent patients. The London study showed that AAV2 was rarely present in children who did not have hepatitis (six out of 100), and at much lower levels even in immunocompromised children (11 out of 32).
One of the researchers, Professor Judith Breuer, an expert in virology at University College London and Great Ormond Street Hospital, said: “During the lockdown period, when children did not mix, they did not transmit viruses to each other.” Because of this, she adds, “they weren’t developing immunity to the common infections they would normally encounter.” “When the restrictions were lifted, kids started mixing, viruses started circulating freely, and suddenly they were exposed with this lack of prior immunity to a whole battery of new infections.”
“We also need to better understand the seasonal circulation of AAV2, a virus that is not routinely monitored. It could be that a peak of adenovirus infection coincided with a peak in exposure to AAV2, which would have led to an unusual manifestation of hepatitis in susceptible young children, concluded Emma Thompson, who considers it urgent that “larger studies be carried out to investigate the role of AAV2 in pediatric hepatitis cases”.
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