A possible connection between COVID-19 contagion and the mysterious liver damageseen in children around the worldhas been put forward by   a squad of scientist inThe Lancet .

Since January , hospital have seen unusually high numbers of previously intelligent child patients with acute hepatitis ( knockout and with quick onset liver scathe ) . The case were first report in the UK , before spreading around Europe , the US , Japan , and around the world .

In April , a likely perpetrator emerged :   adenovirus F case 41.Adenoviruseshave been witness   in at least 74 case consort to the World Health Organization ( WHO ) , with 18 identified as adenovirus F case 41   – a type that has n’t been link with liver terms previously . In the UK , where most cases have been report , adenovirus has been found in75 percentof those children tested . Sixteen percent also tested positive for COVID-19 , though the UK Health Security Agency stressed that COVID-19 was prevalent during the clip of price of admission , so this was not unexpected .

However , as   Professor Will Irving of the University of Nottinghamexplained in April , this still leaves the puzzle as to why the adenovirus could be causing liver harm when it had n’t done previously .

" The link with adenovirus infection rest tantalising – a definite possibility but not yet proven , " Irving   said .

" There are very few pillow slip reports in the global literature of adenovirus contagion being associated with hepatitis in immunocompetent children ( or adults ) – so if it transpire that adenoviral infection is regard in get this disease outbreak , there will be a need to explicate why the rude account of adenovirus infection has changed so dramatically in 2022 . "

The new proportionateness piece published in The Lancet suggests   a potential solvent : premature COVID-19 infection , lurking in the intestines . " SARS - CoV-2 viral persistence in the gastrointestinal parcel can lead to repeated waiver of viral proteins across the enteral epithelium , giving rise to resistant activating , " theteam wrote .

They explain that when the resistant system is also converge with adenovirus infection , this could trigger an over - reaction to the contagion , release orotund sum of inflammatory proteins and inflaming the liver .

" We suppose that the late report cases of severe penetrating hepatitis in children could be a consequence of adenovirus infection with intestinal trophism in child previously infect by SARS - CoV-2 and hold viral reservoirs , " they posit .

" We suggest that children with acute hepatitis be inquire for SARS - CoV-2 tenacity in stool , metric ton - cell receptor skewing , and IFN - γ upregulation , because this could provide evidence of a SARS - CoV-2 superantigen mechanism in an adenovirus-41F - supersensitised innkeeper . "