Scientists find the culprit behind the outbreaks of hepatitis in children: A combination of two viruses that are usually harmless

Researchers insist that Covid itself is not the cause of a mysterious outbreak of hepatitis affecting children around the world.

However, lockdowns during the pandemic may have played a role.

Scientists today have pinpointed a normally harmless virus as the main culprit behind the unusual liver disease that has sickened 200 young people in the UK and left dozens in need of transplants.

Two separate studies concluded that adeno-associated virus 2 (AAV2) appeared to play an ‘important role’.

The virus, which usually doesn’t cause illness, infects most Britons by the age of 10.

But AAV2 cannot reproduce without a ‘helping’ pathogen, such as an adenovirus – which usually causes only cold-like symptoms. Adenovirus increased with hepatitis group when children returned to the pre-pandemic stage after Covid contained common viruses, leaving children with weakened immunity.

As a result, a group of academics backed by the UK’s Health Security Agency believe that dual infection of the two viruses may offer the best explanation for the outbreak.

So far, scientists have not found a cause, as Covid itself, a mutation in the adenovirus virus or weakened immunity due to viral restriction may be involved.

Overall, the two studies, which looked at dozens of children across the UK, found that 96 per cent of children with unexplained liver disease had ‘high AAV2 levels’. By comparison, only four percent of healthy young adults tested positive for AAV2 and to a much lower level.

Dr Antonia Ho, lead author of the study, said containment and restriction of Covid had resulted in a ‘much reduced circulation of the seasonal virus’.

An ‘equilibrium’ needs to be re-established as young people are mixing in pre-pandemic ways, which has led to ‘different types of circulation’ of the virus, she said. speak.

Those who differ were mainly juveniles, who had diarrhea, vomiting and stomach pain at first, followed by jaundice – jaundice.

Most were then hospitalized for hepatitis 1 to 11 weeks later, of which 40% were admitted to intensive care.

The World Health Organization (WHO) has reported at least 1,010 cases in 35 countries. Nearly 50 people need a liver transplant worldwide and 22 have died.

Preprints, which have not yet been peer-reviewed but have been published on the MedRxiv website, suggest that AAV2 is involved in hepatitis outbreaks.

The first study, conducted by the University of Glasgow’s MRC Center for Virus Research (CVR), examined nine children, average age 4, with hepatitis in Scotland.

They were all hospitalized between March 14 and April 4 and were cared for by the NHS for an average of 10 days. No liver transplant required.

Their DNA was extracted from blood, liver, stool and throat samples and compared the results with 58 healthy young men. The results showed that AAV2 was detected in all 9 hepatitis patients but none in the control group.

In a separate analysis, the researchers examined the genetics of patients with hepatitis.

They found that nearly 9 out of 10 young adults with hepatitis (89%) had the Human Leukocyte Antigen gene, compared with less than 2/10 (16%) in the general population.

The team says the findings may provide another part of the answer to why some children become severely unwell.

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

‘And so this suggests there may be a link to the viral cause of immune-mediated hepatitis.’

However, she said more studies are needed to confirm that the gene is involved.

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

Their analysis included liver samples from five children in need of a transplant and blood samples from the remaining children who did not.

Nearly all children tested positive for AAV2. By comparison, AAV2 is ‘rarely present’ outside of this group – only among 6% of healthy children and to a ‘much lower level’.

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

Both studies ruled out that recent or previous Covid infection caused hepatitis.

Tests showed that only two-thirds of people with hepatitis had Covid antibodies – similar to the prevalence among Scottish children at the time – and the virus was not present in any liver samples. None of the young people were vaccinated against Covid.

Researchers still don’t know why hepatitis flares occur.

However, they said the peak of adenovirus infections in the general population after the lockdown ‘may have contributed’.

Scientists have long warned that Covid would halt the spread of the virus as well as prevent other infections from circulating in the population, leaving people with lower immunity against them.

Prof Thomson said AAV2 itself could be the cause, or it could act as a ‘useful biomarker’ of a recent case of adenovirus infection, which could be the cause of cases of hepatitis.

She said: ‘There are many unanswered questions and larger studies are needed to investigate the role of AAV2 in cases of childhood hepatitis.

‘We also need to understand more about the seasonal circulation of AAV2, a virus that is not routinely monitored – it is possible that the peak of adenovirus infection coincides with the peak of AAV2 exposure, leading to aberrant presentation of the disease. hepatitis in susceptible young children. . ‘

Professor Judy Breuer, a virologist at GOSH, said the results could ‘reassure parents worried about Covid as neither group found any direct link to SARS infection. -CoV-2’.

‘However, our data suggest that AAV2 in the liver and blood of cases is the strongest biomarker for hepatitis,’ she added.

Source: | This article originally belonged to Dailymail.co.uk