Their findings reveal it is likely a combination of 3 elements — co-infection with two different viruses and genetic susceptibility
Representative photo by iStock Two new preprints published this month by researchers from the United Kingdom shed some light on what might be causing the paediatric hepatitis outbreak which has many scientists perplexed. Their findings reveal it is likely a combination of three elements: co-infection with two different viruses and a genetic susceptibility.
Probable cases of paediatric hepatitis, whose cause remains unknown, have risen to over a thousand. Some 22 deaths and 46 liver transplants have also been reported from 35 countries, according to World Health Organization (WHO) data as of July 8, 2022.
Hepatitis A-E has been ruled out following laboratory testing. While the data is incomplete for now, pathogens like adenovirus 41 and SARS-CoV-2 have been repeatedly reported among these cases.
The latter has been detected in more than half the cases in Europe — the region with the highest prevalence of paediatric hepatitis of unknown aetiology.
One study found adeno-associated virus 2 (AAV2) in the plasma and liver of all nine children the authors did a detailed investigation on. Across both studies, it was found in 96 per cent of the cases.
AAV2 is a dependoparvovirus which means it “typically requires a co-infecting ‘helper’ virus to replicate,” the authors noted.
This is where the second virus comes into the picture. While it’s unclear for now as to what this could be, the possibility of adenovirus 41 cannot be ruled out.
The two studies, while independent of each other, were conducted simultaneously. One looked at nine cases and was carried out in Scotland by the MRC-University of Glasgow Centre for Virus Research (CVR) and the Royal Hospital for Children in Glasgow.
The second assessed 28 cases from all four UK nations at Great Ormond Street Hospital and the UCL Great Ormond Street Institute of Child Health, in partnership with the UK Health Security Agency.
Judy Breuer, senior author of one of the papers and a clinical virologist at University College London and a consultant at Great Ormond Street Hospital for Children, believes adenovirus 41 is involved.
“We feel very certain that the adenovirus is playing a role in some way,” she was quoted as saying by health news website STAT. Herpes virus HHV6 is the second theory of the other helper virus.
Both studies have ruled out the possibility of a SARS-CoV-2 infection having any role here. The authors also note that the outbreak occurred after lockdown restrictions were relaxed and “represented one of many infections, including other enteric pathogens such as norovirus, that occurred in UK children following return to normal (social) mixing,” Breuer and authors wrote.
Emma Thomson, clinical professor and consultant in infectious diseases at the MRC-University of Glasgow Centre for Virus Research and senior author of the Scottish study said a lot remained to be unanswered and larger studies were needed to establish concrete evidence.
“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,” she said, University of Glasgow reported.
The preprints are yet to be peer reviewed, the cohorts of both studies are small and even the authors have maintained that further investigations need to be conducted to understand the link between adenovirus / HHV6 and AAV2 infections.
Data from the United States’ Centers for Disease Control and Prevention found no increase in hepatitis-associated emergency department visits or hospitalisations, liver transplants, or adenovirus infections as compared to pre-COVID levels. This only complicates matters.
The WHO has now launched a “global survey with an aim to estimate the incidence of severe acute hepatitis of unknown aetiology in 2022 compared to the previous five years.”
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