- Researchers now think they may know why some young children developed serious hepatitis or liver inflammation.
- Over 1,000 cases have been reported worldwide according to the WHO.
- At least 22 deaths have been reported.
Research teams in the U.K. think they may have discovered what’s caused an outbreak of unexplained hepatitis infections in young children.
Over 1,000 cases have been reported worldwide according to the
Two teams of researchers, from Glasgow and London, found that COVID-19 lockdown restrictions delayed babies’ exposure to adenovirus and adeno-associated virus 2 (AAV2), preventing them from developing an early immunity to infection.
Adenovirus normally causes colds and upset stomachs, but AAV2 typically doesn’t cause symptoms and needs another virus (like adenovirus or herpes) to replicate.
Researchers suggest when these two common viruses began circulating again after pandemic restrictions were lifted, some children who had no immunity ended up with hepatitis cases.
Although one researcher believes that AAV2 might have been a cause of some children’s hepatitis before the lockdowns. Many of the children also had genetic mutations that could affect their immune systems.
Both teams of researchers found that children’s livers were infected with AAV2, a type of herpes virus, and an adenovirus – which was initially believed to cause the hepatitis or inflamed liver.
“The potential that AAV2, although not previously associated with disease, may, together with AdV-F41 (adenovirus) and/or HHV-6 (herpes virus), be causally implicated in the outbreak of unexplained hepatitis, requires further investigation” the London study authors wrote.
The Glasgow-based team investigated any potential link to COVID-19, but found no evidence that the disease was linked to the mysterious hepatitis cases.
“It’s quite likely that there’s been a trickle of cases before that we haven’t [noticed],” Emma Thomson, PhD, a professor of infectious diseases at Glasgow University and a senior author of the Scottish study, told The Herald.
“So we don’t think that lockdown necessarily precipitated this but that the patterns may have changed so that we’ve seen the cases come all at once instead of a steady trickle,” she continued.
Both studies are still in preprint and have not been peer-reviewed.
Dr. Dolly Sharma, director of pediatric infectious diseases at Staten Island University Hospital, part of Northwell Health in New York told Healthline that AAV typically requires a ‘helper virus,’ either adenovirus or human herpes virus (HHV) to replicate.
“Preliminary data from studies have identified the presence of AAV with these other viruses in children presenting with pediatric hepatitis from non-typical hepatitis viruses (A through E),” she said.
Sharma said it’s unclear whether the presence of AAV is representative of co-infection with these other helper viruses.
“Or if reactivation of AAV from primary infection is contributing to current pediatric hepatitis cases,” she said.
Asked if AAV2 might have caused hepatitis indirectly through an immune reaction, Dr. Ilan Shapiro, chief health correspondent and medical affairs officer at AltaMed Health Services said, “It can happen.”
“The interesting thing would be to see if they actually replicate the same type of results in other publications, in larger scale,” he said.
“This can actually give us more information if it was AAV2 that was actually causing the hepatitis when you get infected with adenovirus, or there’s a synergy there between both of them,” Shapiro continued.
Dr. Diego R. Hijano, a pediatric infectious diseases expert at St. Jude Children’s Research Hospital said adeno-associated viruses are a type of virus that haven’t been clearly associated with any diseases previously.
“These viruses are widespread and have been found in humans, other primates, sheep, cows, birds and horses and birds,” he said. “No negative consequences of AAV infection have been demonstrated in humans and they have not been considered harmful.”
However, Hijano explained that AAV can establish a “latent infection,” which is also the hallmark of certain other viruses, like herpes.
Hijano said that after an initial infection, they may go ‘dormant’ and ‘wake up’ (reactivate) in certain situations.
“A common example is herpes simplex I (HSV-1), that causes cold sores,” he said. “Most individuals acquire HSV-1 while growing up, and many developed cold sores throughout their life under certain situations such as stress, hot sun, cold weather.”
He pointed out that if those cells with “dormant” AAV are infected with a helper virus, AAV can be “rescued” from them.
Shapiro said measures like barriers, filters, masks, and hand washing can make it more difficult for AAV2 to cause an infection that ends up as hepatitis.
He also thinks more research is needed before we can be sure that AAV is to blame.
“At this moment with the numbers that are presented,” he said, “it gives us a clue and we need to follow that to see if these other cases and other information can help us out.”
He cautioned that compared to the total of cases we’re seeing worldwide, “It’s still a small amount of numbers to create an expectation that this will be the solution or the culprit of it.”
Two research teams working independently in the U.K. have concluded that two common viruses along with potential genetic mutation is likely what is causing unexplained cases of hepatitis in children worldwide.
They also say that the infection prevention measures we’re familiar with, like masks and handwashing, are ways we can reduce a child’s risk of experiencing this type of hepatitis.
