Scientists find culprit behind children’s hepatitis epidemic: Combination of two usually harmless viruses –

Researchers stated that Covid itself was not responsible for the mysterious hepatitis epidemic affecting children around the world today.

However, pandemic-era blockades may have played a role.

Today, scientists have identified a mostly harmless virus as the main culprit for the unusual liver disease that sickened 200 young people in the UK and required a dozen transplants.

Two separate studies concluded that adeno-associated virus 2 (AAV2) plays an “important role”.

The virus, which does not normally cause illness, infects most Britons by the age of 10.

However, AAV2 cannot replicate without a “helper” pathogen, such as an adenovirus, which usually only causes cold symptoms. Adenoviruses increased in line with the hepatitis cluster, which experts say is due to weaker immunity when they return to pre-pandemic mixing levels.

Therefore, a team of academics supported by the UK Health Security Agency believes that the dual infection of these two viruses may be the best explanation for the outbreak.

So far, scientists have been baffled as to what causes the disease, with theories blaming Covid itself or even a mutation in a type of adenovirus.

Overall, two studies examining dozens of children in the UK found that 96% of children with unexplained hepatitis had “high levels” of AAV2.

By comparison, only four percent of healthy teens tested positive for AAV2 and at much lower levels.

Dr. Antonia Ho, lead author of one of the studies, said that Covid blockades and restrictions have led to “significant reductions in seasonal virus circulation”.

He said a “balance” needs to be re-established as young people mix in pre-pandemic ways, causing “different types to circulate” of viruses.

Patients of the strange disease were under the age of five, initially with diarrhea, vomiting and stomach pain, followed by jaundice – yellowing of the skin.

Some are hospitalized with liver inflammation after 1 to 11 weeks, and 40% of them are admitted to intensive care.

The World Health Organization (WHO) has reported at least 1,010 cases in 35 countries. Worldwide, about 50 have required liver transplants and 22 have died.

Preprints that have not yet been peer-reviewed but have been published on the MedRxiv website indicate that AAV2 is implicated in the hepatitis epidemic.

The initial study, led by the MRC-University of Glasgow Virus Research Center (CVR), looked at nine children aged four, on average, suffering from hepatitis in Scotland.

All were hospitalized between 14 March and 4 April and spent an average of 10 days under the care of the NHS. There is no need for a liver transplant.

Their DNA was extracted from blood, liver, stool and throat samples and the results were compared to 58 healthy teenagers.

AAV2 was detected in all nine patients with hepatitis, but none in the control groups.

In a separate analysis, the researchers looked at the genetics of hepatitis patients.

They found that approximately nine out of 10 youth (89%) with hepatitis have the human leukocyte antigen gene, compared to less than two out of 10 youth (16%) in the general population.

The team said this finding may provide another part of the answer to why some children are seriously ill.

Professor Emma Thomson, clinical professor and infectious disease consultant at CVR and senior author of the Scottish study, explains: “The gene itself is important because it encodes a receptor that presents viruses or other pathogens to the immune system.

“And this suggests that there may be an association with an immune-mediated cause of viral hepatitis.”

However, more studies are needed to confirm that this gene is involved, he said.

The second study, led by Great Ormond Street Hospital (GOSH) and the UK Health Safety Agency, looked at 28 children with hepatitis in the UK.

Their analysis included liver samples from five children who needed transplants, and blood samples from other young people who did not.

Almost all children tested positive for AAV2. By comparison, AAV2 was present “only very rarely” outside this group, in only 6% of healthy children, and “at much lower levels”.

And sequencing of liver samples showed that AAV2 was present and spread throughout the organ.

Both studies excluded a recent or previous Covid infection causing hepatitis.

Tests showed that only two-thirds of hepatitis patients – comparable to the prevalence in Scottish children at the time – had Covid antibodies and the virus was not found in any liver samples. None of the teens had been vaccinated against Covid.

Researchers still don’t know why the hepatitis epidemic is occurring now.

However, they said, a spike in adenovirus infections in the general population after the blockades “may have contributed.”

Scientists have long warned that Covid measures to stop the spread of the virus are disrupting the circulation of other infections among the population and making people have lower immunity to them.

Professor Thomson said AAV2 may be the cause itself or act as a “useful biomarker” of a new adenovirus infection underlying hepatitis cases.

There are many unanswered questions and larger studies are urgently needed to explore the role of AAV2 in pediatric hepatitis cases.

“We also need more information on the seasonal circulation of AAV2, a virus that is not routinely monitored: an increase in adenovirus infection may coincide with an increase in AAV2 exposure and lead to an unusual manifestation of hepatitis in young children who are susceptible.”

GOSH virologist Professor Judy Breuer said the findings “may reassure parents of their concerns about Covid, as neither team found a direct link to SARS-CoV-2 infection.”

“However, our data point to AAV2 in the liver and/or blood of cases as the strongest biomarker for hepatitis.”