Covid itself is not to blame for a mysterious hepatitis outbreak affecting children around the world, researchers stressed today.
However, pandemic-era lockdowns may have played a role.
Scientists today pinpointed a seemingly-harmless virus as the main culprit for an unusual liver disease, which has sickened 200 young people in the UK and left a dozen in need of transplants.
Two separate studies concluded that adeno-associated virus 2 (AAV2) appears to play an ‘important role’.
The virus, which usually causes no disease, 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 increasingly resembled the hepatitis cluster as youngsters reverted to the pre-pandemic mix after covid curbs suppressed common viruses, leaving children with weakened immunity.
Therefore, a team of UK Health Protection Agency-backed academics believes that dual infection with these two viruses may provide the best explanation for the outbreak.
Until now, scientists have flumoxed as the cause, the covid itself, may include mutations in the adenovirus or weakened immunity due to the virus curb.
Q&A: What is the mysterious global hepatitis outbreak and what is behind it?
What is hepatitis?
Hepatitis is an inflammation of the liver that is usually caused by a viral infection or liver damage from alcohol.
Some cases resolve on their own, with no ongoing problems, but a fraction can be fatal, forcing patients to undergo a liver transplant to survive.
What are the symptoms?
People with hepatitis usually experience fatigue, loss of appetite, nausea, vomiting, abdominal pain, dark urine, light-colored stools, and joint pain.
They may also suffer from jaundice – when the skin and whites of the eyes turn yellow.
Why are experts worried?
Hepatitis is usually rare in children, but experts have found more cases in the current outbreak than they would normally expect in a year.
According to the World Health Organization, the cases are of ‘unknown origin’ and are serious.
What are the top principles?
Adeno-associated virus 2 (AAV2)
Two separate UK studies, which involved dozens of children across the country, found that adeno-associated virus 2 (AAV2) was behind the hepatitis disease.
The virus, which doesn’t usually make people sick, often causes a flu-like illness with an adenovirus infection.
British experts tasked with investigating the spread of the disease believe the endless cycle of lockdowns may have contributed.
Restrictions may have weakened children’s immunity due to less social mixing, leaving them at higher risk of adenovirus.
This means that even a ‘normal’ adenovirus can have serious consequences, because children are not responding as they did in the past.
Other scientists said it could be an adenovirus that had acquired an ‘unusual mutation’.
This means it may be more widespread or better able to get around the child’s natural defenses.
In total, two studies looking at dozens of children across the UK found that 96 per cent of children with undiagnosed hepatitis had ‘high levels’ of AAV2. For comparison, only four percent of healthy young adults tested positive for AAV2 and at much lower levels.
Dr Antonia Ho, lead author of the study, said that the Covid lockdowns and restrictions ‘have greatly reduced the circulation of seasonal viruses’.
The ‘balance’ now needs to be re-established as young people are mixing in pre-pandemic ways, leading to ‘different types of circulation’ of viruses, she said.
Victims are mainly under-fives who initially experience diarrhoea, vomiting and abdominal pain, followed by jaundice – yellowing of the skin.
Most are hospitalized for liver inflammation after one to 11 weeks, with 40 percent admitted to the intensive care unit.
The World Health Organization (WHO) has reported at least 1,010 cases in 35 countries. Around 50 people worldwide have required a liver transplant and 22 have died.
The preprints, which have not yet been peer-reviewed but are published on the website MedRxiv, suggest that AAV2 is involved in hepatitis outbreaks.
The first study, led by the MRC-University of Glasgow Center for Virus Research (CVR), examined nine children in Scotland with an average age of four who suffered from hepatitis.
They were all admitted to hospital between March 14 and April 4 and stayed under NHS care for an average of 10 days. A liver transplant is not necessary.
Their DNA was extracted from blood, liver, stool and throat samples and the results were compared to 58 healthy young people. The results showed that AAV2 was detected in all nine hepatitis patients but none in the control groups.
In a separate analysis, the researchers examined the genetics of patients with hepatitis.
They found that nine out of 10 young people with hepatitis (89 percent) had the human leukocyte antigen gene, compared to less than two out of 10 (16 percent) in the general population.
The finding may provide another part of the answer to why some children become seriously ill, the team said.
Professor Emma Thomson, a clinical professor and consultant in infectious diseases at CVR and senior 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 a link to an immune-mediated cause of viral hepatitis.’
However, she said more studies are needed to confirm that this gene is involved.
The second study, led by Great Ormond Street Hospital (GOSH) and the UK Health Protection Agency, looked at 28 children in the UK with hepatitis.
Their analysis included liver samples from five children who needed transplants and blood samples from the remaining youngsters.
Almost all children tested positive for AAV2. For comparison, AAV2 was present ‘very rarely’ outside this group – in only six per cent of healthy children and at ‘very low levels’.
And sequencing of liver samples showed that AAV2 was present and spread within the organ.
Both studies ruled out that recent or previous Covid infection caused the hepatitis.
Tests showed only two-thirds of hepatitis sufferers had Covid antibodies – similar to the outbreak in Scottish children at the time – and the virus was not present in any of the liver samples. None of the youths had the covid vaccine.
Researchers still don’t know why hepatitis outbreaks are happening now.
However, they said it ‘may have contributed’ to the peak of adenovirus infections in the general population after the lockdown.
Scientists have long warned that the Covid curbs in place to stop the spread of the virus also prevent other infections from spreading in the population, leaving people with less immunity against them.
Professor Thomson said AAV2 itself may be the cause, or it may be acting as a ‘useful biomarker’ of recent adenovirus infections, which may be behind cases of hepatitis.
She said: ‘There are many unanswered questions and larger studies are urgently needed to investigate the role of AAV2 in pediatric hepatitis cases.
‘We also need to understand the seasonal circulation of AAV2, a virus that is not routinely monitored – it may be that the peak of adenovirus infection coincides with the peak in AAV2 exposure, which causes unusual manifestations of hepatitis in susceptible young children. .’
Professor Judy Breuer, virologist at GOSH, said the results could ‘reassure parents worried about Covid as neither team found any direct link to SARS-CoV-2 infection’.
‘Our data point to AAV2 in liver and or blood of cases as the strongest biomarker of hepatitis,’ he added.
Source: | This article is originally from Dailymail.co.uk