Scots scientists identify new virus behind mystery child hepatitis

The cause of the liver inflammation was unknown, with medics investigating Covid-19 among a range of potential origins.

Glasgow scientists identify virus behind acute child hepatitis, saying there is no evidence of Covid-19 link iStock

Scientists in Glasgow have identified the virus thought to be behind a mysterious outbreak of severe hepatitis in young children.

Many youngsters with the condition have had to be hospitalised for several days, with 11 children in England and one in Scotland requiring a liver transplant.

The cause of the liver inflammation was unknown with medics investigating Covid-19 among a range of potential origins.

On Monday, researchers revealed the findings of two new studies linking the acute hepatitis cases to the virus AAV2, saying there was no evidence of a direct connection to coronavirus infection.

AAV2 (adeno-associated virus 2) is not known to normally cause disease and often accompanies infection with adenoviruses, the scientists said. It is not an adenovirus – which had been considered a possible source for the illness – but a member of the parvovirus family.

Researchers found the virus at very high levels in the blood and liver of patients sampled, and it was also found to be replicating in the liver.

In the UK, the majority of the 268 cases have been found in children under the age of five, with nearly 40% of hospitalised cases (74 of 189) requiring admission to intensive care.

One of the studies examining cases from Scotland was carried out by the MRC-University of Glasgow Centre for Virus Research and the Royal Hospital for Children in Glasgow, in partnership with Public Health Scotland and international bodies.

Professor Emma Thomson, clinical professor and consultant in infectious diseases and senior author of the Scottish study said: “The presence of the AAV2 virus is associated with unexplained hepatitis in children. This virus can only infrequently in the presence of another virus (usually an adenovirus).

“AAV2 may cause disease itself or it may be a useful biomarker of recent adenovirus infection which may be the main underlying pathogen, but which can be harder to detect. There are many unanswered questions and larger studies are urgently needed to investigate the role of AAV2 in paediatric hepatitis cases.

“We also need to understand more about seasonal circulation of AAV2, a virus that is not routinely monitored – it may be that a peak of adenovirus infection has coincided with a peak in AAV2 exposure, leading to an unusual manifestation of hepatitis in susceptible young children.”

The Scottish study also looked at the genetics of the children to identify whether any of them had underlying susceptibility to acute hepatitis.

Using detailed genomic testing of the patients, researchers were able to identify differences in the Human Leukocyte Antigen gene, that were not commonly found in the control groups of healthy children, or in the genes of children with other forms of hepatitis.

The team believe these genetic sequences may offer another part of the answer as to why some children have become seriously unwell.

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