Covid itself is not to blame for the extraordinary outbreak of hepatitis affecting children around the world, researchers insisted today.
However, pandemic-era lockdowns may have played a role.
Scientists today identified a harmless virus as the main cause of the rare liver disease, which 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) appears to play a ‘significant role’.
The virus, which usually does not cause any illness, infects most Britons by the age of 10.
But AAV2 cannot replicate without a ‘helper’ pathogen, such as adenovirus – which usually causes cold-like symptoms. Adenoviruses increased in parallel with the cluster of hepatitis when the young returned to the pre-pandemic mix after Covid suppressed the normal virus, leaving children with weak immunity.
Therefore, a team of academics supported by the British Health Security Agency believe that two infections with these two viruses may provide a better explanation for the outbreak.
Until now, scientists have been confused about the cause, considering that Covid itself, changes in the adenovirus or weakened immunity due to viral barriers may have been involved.
Overall, the two studies, which looked at dozens of children across the UK, found that 96 per cent of children with unexplained hepatitis had ‘high levels’ of AAV2. In comparison, only four percent of healthy young adults tested positive for AAV2 and at much lower levels.
Dr Antonia Ho, the study’s lead author, said the Covid-19 lockdown and restrictions had led to a ‘decrease in the seasonal virus cycle’.
The ‘balance’ 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, he said.
The worst sufferers have been under five years of age who initially experience diarrhoea, vomiting and abdominal pain, followed by jaundice – yellowing of the skin.
Most are hospitalized with liver tumors one to 11 weeks later, with 40 percent in intensive care.
The World Health Organization (WHO) has reported at least 1,010 cases in 35 countries. About 50 have required liver transplants worldwide and 22 have died.
Previous publications, not yet peer-reviewed but published on the MedRxiv website, suggest AAV2 is involved in hepatitis outbreaks.
The first study, led by the MRC-University of Glasgow Center for Virology Research (CVR), looked at nine children, aged four years on average, with hepatitis in Scotland.
All admitted to hospital between March 14 and April 4 stayed under NHS care for 10 days, on average. None required a liver transplant.
Their DNA was extracted from blood, liver, stool and throat samples and compared the results against 58 healthy young people. The results showed AAV2 was detected in all nine hepatitis patients but in none of the control groups.
In a separate analysis, the researchers examined the genes of patients with hepatitis.
They found that nearly nine in 10 young people with hepatitis (89 percent) had the Human Leukocyte Antigen gene, compared to less than two in 10 (16 percent) in the general population.
This finding may provide another part of the answer to why some children have become so sick, the team said.
Professor Emma Thomson, clinical professor and consultant in infectious diseases at CVR and lead author of the Scottish study, explained: ‘The gene itself is important because it encodes a receptor that presents viruses or other pathogens to the immune system.
“And so this suggests that there may be a link to an immune-mediated cause of viral hepatitis.”
However, he said more studies are needed to confirm that this gene was involved.
The second study, led by Great Ormond Street Hospital (GOSH) and the UK’s 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 the remaining teenagers who did not.
Almost all children tested positive for AAV2. In contrast, AAV2 was ‘rarely present’ outside this group – among only six per cent of healthy children with ‘very low levels’.
And sequencing of the liver samples showed that AAV2 was present and had spread throughout the organ.
Both studies showed that recent or previous Covid infections caused hepatitis.
Tests showed only two-thirds of hepatitis patients had antibodies to Covid – similar to the prevalence in Scottish children at the time – and the virus was not present in any of the liver samples. None of the young people had the Covid vaccine.
Researchers still don’t know why the outbreak of hepatitis is happening now.
However, they said a spike in adenovirus infections in the population after the lockdown ‘may have contributed’.
Scientists have long warned that Covid curbs in place to prevent the spread of the virus also prevented other infections from circulating in the population, leaving people with low immunity to them.
Professor Thomson said AAV2 itself could be the cause, or could act as a ‘significant biological marker’ of recent adenovirus infections, which could be behind cases of hepatitis.
He said: ‘There are many unanswered questions and larger studies are urgently needed to investigate the role of AAV2 in cases of hepatitis in children.
“We also need to understand more about the seasonal cycle of AAV2, a virus that is not routinely monitored – it could be that the peak of adenovirus infection coincided with the peak of AAV2 exposure, leading to an unusual manifestation of hepatitis in susceptible young children. ” .’
Professor Judy Breuer, virologist at GOSH, said the findings could ‘reassure parents worried about Covid as no teams have found any direct link to SARS-CoV-2 infection’.
“Our data, however, point to AAV2 in the liver and, or blood of the case as a stronger indicator of hepatitis,” he added.
Source: | This article is originally from Dailymail.co.uk