Scientists find the reason for the outbreak of hepatitis in children: a combination of two normally harmless viruses

Covid itself is not to blame for the mysterious hepatitis outbreak affecting children around the world, researchers are responding today.

However, pandemic-era lockdowns may have played a role.

Today, scientists have identified a normally harmless virus as the main cause of the unusual liver disease, which has infected 200 young people in the UK and left dozens needing transplants.

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

The virus, which usually does not cause any disease, infects most Britons by the age of 10.

But AAV2 cannot reproduce without a “helper” pathogen, such as adenovirus – which usually causes cold-like symptoms. The number of adenoviruses rose in line with the group for hepatitis, which experts believe the children had weaker immunity when they returned to pre-epidemic levels of adenovirus.

Therefore, a team of academics backed by the UK’s Health Security Agency believes that the double infection with these two viruses may provide the best explanation for the outbreak.

So far, scientists have been confused about the root cause of the disease, with theories blaming Covid itself or even a mutation in a strain of adenovirus.

Q&A: What is the mysterious global hepatitis outbreak and what’s behind it?

What is hepatitis?

Hepatitis is inflammation of the liver usually caused by a viral infection or liver damage from drinking alcohol.

Some cases resolve on their own, with no persistent problems, but some of them can be fatal, forcing patients to need a liver transplant to survive.

What are the symptoms?

People with hepatitis generally 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 do experts care?

Hepatitis is usually rare in children, but experts have already detected more cases in the current outbreak than they would normally expect within a year.

The cases are of “unknown source” and are also serious, according to the World Health Organization.

What are the most important theories?

Adeno-associated virus 2 (AAV2)

Two separate studies in the UK, which looked at dozens of children across the country, found that adeno-associated virus 2 (AAV2) appears to be behind hepatitis.

The virus, which usually does not infect people, often accompanies infection with a flu-like illness.

weak immunity

British experts tasked with investigating the wave of disease believe the endless cycle of lockdowns may have played a contributing role.

The restrictions may have weakened children’s immunity due to reduced social contact, making them more at risk of contracting adenovirus.

This means that even “natural” adenoviruses can cause dangerous outcomes, because children do not respond to them as well as they did in the past.

adenovirus mutation

Other scientists said it may have been the adenovirus that had acquired the “unusual mutations”.

This means that it could be more transmissible or more able to get around children’s natural immunity.

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.

For comparison, only four percent of healthy young adults have tested positive for AAV2 and at much lower levels.

Dr Antonia Ho, lead author of the studies, said the COVID-19 lockdowns and restrictions had led to a ‘significant reduction in the spread of seasonal viruses’.

She said the “balance” needs to be re-established now that young people have mixed in pre-pandemic ways, leading to “different types of circulation” for viruses.

Most sufferers of this strange disease are children under the age of five who initially have diarrhea, vomiting and stomach pain, followed by jaundice – yellowing of the skin.

Some were then hospitalized with hepatitis 1 to 11 weeks later, with 40 percent of them admitted to intensive care.

The World Health Organization (WHO) has reported at least 1,010 cases in 35 countries. It required nearly 50 liver transplants worldwide and 22 people died.

Prior publications, which have not been peer-reviewed but have been published on the MedRxiv website, indicate that AAV2 is involved in the outbreak of hepatitis.

The first study, led by the University of Glasgow’s Virus Research Center (MRC), examined nine children, on average, aged four, with hepatitis in Scotland.

All were hospitalized between 14 March and 4 April and remained in NHS care for an average of 10 days. Nothing requires a liver transplant.

Their DNA was extracted from blood, liver, stool and throat samples and the results were compared with 58 healthy young men.

AAV2 was detected in all nine hepatitis patients but was not detected among anyone in the control groups.

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

They discovered that nearly nine in 10 children with hepatitis (89 percent) had the human leukocyte antigen gene, compared to less than two in 10 (16 percent) in the general population.

The team said this finding may provide another part of the answer as to why some children become seriously ill.

Professor Emma Thompson, 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 exposes viruses or other pathogens to the immune system.

Thus, this suggests that there may be a link to an immune cause of hepatitis caused by viruses.

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’s Health Security Agency, looked at 28 children with hepatitis in Britain.

Their analysis included liver samples from five children who requested a transplant and blood samples from the remaining young adults who did not.

Almost all children have tested positive for AAV2. For comparison, AAV2 was present ‘extremely rarely’ outside this group – among only six percent of healthy children and at ‘significantly lower levels’.

Sequencing of liver samples showed that AAV2 was present and spread within the organ.

The two studies ruled out that a recent or previous infection with Covid caused hepatitis.

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

Researchers still don’t know why the hepatitis outbreak is occurring now.

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

Scientists have long warned that Covid restrictions in place to stop the spread of the virus have also halted the spread of other infections in the population, lowering people’s immunity to it.

Professor Thompson said that AAV2 itself may be the cause, or may serve as a “useful biomarker” of recent adenovirus infection, which could 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 more about the seasonal cycle of AAV2, a virus not routinely monitored—the peak of adenovirus infection may have coincided with peak exposure to AAV2, resulting in unusual manifestations of hepatitis in susceptible young children. “.

Professor Jodi Brewer, a virologist at GOSH, said the findings could “reassure parents worried about Covid as neither team has found any direct link to SARS-CoV-2 infection”.

“However, our data suggest that AAV2 is present in the liver, or that the blood of cases is the strongest biomarker of hepatitis,” she added.

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