Adenovirus infections are quite prevalent, particularly in youngsters.
In more than 35 nations, 1,010 instances of severe hepatitis in children without a known cause were reported between April and July of this year. Over a quarter of these cases—nearly half—occurred in the UK and in Europe.
The most common cause of childhood hepatitis is an infection with one of the hepatitis viruses (such as hepatitis A or hepatitis C). However, despite the fact that children were coming with elevated blood levels of hepatitis indicators, no signs of hepatitis viruses were found in these kids or in any subsequent cases that were connected to them.
Initial research revealed a potential connection between these hepatitis cases and viral infection. Adenovirus infections are quite prevalent, particularly in children. They frequently result in infections like minor colds, pink eye (conjunctivitis), or digestive issues. On rare occasions, nevertheless, they can occasionally cause hepatitis if they reach the liver.
It was challenging to determine that this was the most likely cause, given the prevalence of adenoviruses in youngsters and the rarity with which they cause hepatitis in healthy individuals.
Adenovirus, adeno-associated virus 2 (AAV2), and an underlying genetic propensity for the disease, according to a recent study, may be the cause of the recent surge in severe hepatitis cases reported in children.
In a pre-print study, which means it has not yet been peer-reviewed, a group of researchers examined nine of the initial hepatitis cases in April and ran a wide range of tests in an effort to identify any new or previously unidentified viruses or genetic factors that might have contributed to the children’s hepatitis.
The group discovered that all nine kids had adeno-associated virus type 2 infection. The results were then compared with those of 12 children who had adenovirus infections but no hepatitis, and 13 children who were healthy. None of these kids had Adeno-associated virus 2 found in them. This provided compelling evidence that these mysterious hepatitis cases were brought on by AAV2.
The virus known as Adeno-associated virus 2 is a member of the Dependoparvovirus family that affects both humans and some monkeys. AAV2 is particularly intriguing since it needs another virus to be infecting the host concurrently in order to infect it. In order to replicate itself within human cells, it makes use of this helper virus. Adenovirus and herpesvirus are the two most prevalent helper viruses for AAV2.
Six of the nine patients the researchers examined had an adenovirus, and three of them showed herpes virus symptoms. This suggests that AAV2 and one of these helper viruses likely worked together to create these hepatitis infections.
The research team next examined the children’s genomes in order to find particular immune system biomarkers known as human leucocyte antigens. Human leucocyte antigens are used by immune system cells to identify and engulf other viruses and pathogens. Other immune cells receive a signal from this and arrive to attack the infection. Human leucocyte antigens come in a variety of forms, and a person’s susceptibility to certain infections may depend on which form they have.
Eight of the nine kids, according to the study’s findings, had a greater genetic prevalence of a particular kind of human leucocyte antigen, possibly having elevated their risk of developing hepatitis symptoms as a result of these viral infections. People of European heritage are also more likely to have this type, which may help to explain why the majority of these hepatitis cases were in Europe.
Despite the fact that this study suggests a number of factors may be responsible for the sudden, acute hepatitis infections observed in youngsters, the study itself was modest in scope and only involved participants in Scotland. To properly understand the precise connection and determine the best ways to safeguard children moving forward, a far larger, peer-reviewed study will need to be conducted.
COVID-19 limits, which prevented many kids from getting exposed to these viruses and building immunity at the ages they typically would have, may also have contributed to this. As a result, when limits were eased, kids were suddenly exposed to these infections, which would overwhelm their immature immune systems and make them sick.
But more research is required to determine whether or not this actually contributed to the severe hepatitis cases.
Parvathy Sukumaran 
