Hepatitis Cases Mount, And So Do The Theories
Hepatitis Cases Mount, And So Do The Theories
Yet The Answer To The Question Of Cause Remains "I Do Not Know"
It has now been a month since the start of a global outbreak of hepatitis in a cohort of patients with the lowest incidence of liver disease, very young children. If anything, less seems known now than at the start of the outbreak.
While adenovirus has been detected in a majority of US cases identified by the CDC, and sequencing has indicated the particular strain to be type 41, known to cause gastrointestinal symptoms, doctors are far from certain it is the cause of the liver disease.
Nearly half of the children identified by the CDC also have tested positive for adenovirus, a common bug among kids that usually causes severe stomach illness and pink eye. CDC officials are casting a wide net as they search for a cause but on Wednesday the agency said that adenovirus infection “continues to be a strong lead.”
Adenovirus has also been detected in around 70% of cases identified in the UK, yet even in the UK doctors are refraining from asserting a clear causative role for adenovirus in the hepatitis cases.
"Over the last week, there's been some important progress with the further investigations and some refinements of the working hypotheses," Philippa Easterbrook, from the WHO's global hepatitis programme, told a press conference.
One reason doctors are uncertain about adenovirus type 41: known indicators of adenovirus-related liver damage or disease are not being found in this cases linked to this hepatitis outbreak.
None of the U.K. liver samples " … show any of the typical features you might expect with a liver inflammation due to adenovirus but we are awaiting further examination of biopsies," Easterbrook added.
COVID Related?
Even though only around 18% of patients have tested positive for an active SARS-CoV-2 infection, doctors are taking a closer look at a possible role for COVID, perhaps in the form of a lingering “long COVID” effect of a prior and no longer active infection.
"At present, the leading hypotheses remain those which involve adenovirus, with also still an important consideration about the role of Covid as well, either as a co-infection or a past infection," Easterbrook said.
One hypothesis for the involvement of past COVID infection described in The Lancet centers on a residual presence of virus in the intestines—what researchers are labelling as “viral reservoirs”.
SARS-CoV-2 has been identified in 18% of reported cases in the UK and 11 (11%) of 97 cases in England with available data tested SARS-CoV-2 positive on admission; a further three cases had tested positive within the 8 weeks prior to admission.2 Ongoing serological testing is likely to yield greater numbers of children with severe acute hepatitis and previous or current SARS-CoV-2 infection. Eleven of 12 of the Israeli patients were reported to have had COVID-19 in recent months,3 and most reported cases of hepatitis were in patients too young to be eligible for COVID-19 vaccinations. SARS-CoV-2 infection can result in viral reservoir formation.4 SARS-CoV-2 viral persistence in the gastrointestinal tract can lead to repeated release of viral proteins across the intestinal epithelium, giving rise to immune activation.5 Such repeated immune activation might be mediated by a superantigen motif within the SARS-CoV-2 spike protein that bears resemblance to Staphylococcal enterotoxin B,6 triggering broad and non-specific T-cell activation. This superantigen-mediated immune-cell activation has been proposed as a causal mechanism of multisystem inflammatory syndrome in children.4, 7
The reference to Israeli patients is particularly noteworthy, owing to recent research from Israel of wastewater data regarding levels of fecal shedding of the SARS-CoV-2 virus. While that study’s conclusions were considered specious and probably wrong by no less a viral authority than Geert Vanden Bosche, the data gathered was not entirely without value. As fellow Substack writer Igor Chudov has detailed, the data confirmed an ongoing presence of the virus in the gut, indicating an inability of COVID patients to fully clear the virus.
… highly vaccinated Israel is beset with Chronic Covid, and that people who seem to have recovered from Covid, are still sick and have ongoing active Covid infections that they picked a long time ago.
I myself had significant criticisms of the Yaniv wastewater study, owing to methodological defects and questionable base assumptions.
Yet, to the extent the data can be trusted, the presence of SARS-CoV-2 virus in wastewater confirms the virus does express itself within the GI tract, and, as Igor demonstrated, can reside there for some time, leading to gut-related “post-acute COVID-19” gastrointestinal symptoms.
We report expression of SARS-CoV-2 RNA in the gut mucosa ∼7 months after mild acute COVID-19 in 32 of 46 patients with IBD. Viral nucleocapsid protein persisted in 24 of 46 patients in gut epithelium and CD8+ T cells. Expression of SARS-CoV-2 antigens was not detectable in stool and viral antigen persistence was unrelated to severity of acute COVID-19, immunosuppressive therapy and gut inflammation. We were unable to culture SARS-CoV-2 from gut tissue of patients with viral antigen persistence. Post-acute sequelae of COVID-19 were reported from the majority of patients with viral antigen persistence, but not from patients without viral antigen persistence.
Thus COVID infection may yet prove to play a role in the hepatitis outbreak, although not from an active infection but from post-acute persistence of the virus within the intestines. Hepatitis arising from such “long COVID” phenomena would mark a major increase in the potential severity and seriousness of lingering post-acute COVID infection.
Still No Correlation To COVID Inoculation
While there continues to be a level of suspicion on social media that the much-maligned (and justly so!) COVID inoculations are somehow involved, the reported clinical data has yet to yield evidence of any demonstrable link between the inoculations and the hepatitis outbreak. The stumbling block is simple: by far the majority of pediatric hepatitis cases are in patients too young to receive the inoculations.
Because adenoviruses are used in some of the COVID-19 vaccinations, one theory on social media suggested a link between the jab and the hepatitis outbreak in the U.K., where most of the cases have been reported, according to Reuters.
But these adenoviruses in the vaccines are "harmless transporters which have been modified so they cannot replicate or cause infection," according to BBC News.
"There is no evidence of any link to the coronavirus (COVID-19) vaccine. The majority of cases are under 5 years old, and are too young to have received the vaccine," the U.K. Health Security Agency (UKHSA) said.
The eternal caveat remains that absence of evidence is not evidence of absence. While the possibility of the inoculations playing a role is at this point increasingly unlikely,
However, the possibility of the lunatic lockdowns having stunted immune system development among children due isolation and social distancing limiting otherwise routine exposure to environmental pathogens remains an actively considered hypothesis.
Prof McConkey told Pat Kenny he believes social distancing, as a result of the pandemic, may have played a part.
"It could be a link to the social distancing we've all had.
"We've all been sort of not physically interacting with as many people for the last couple of years.
"So little children haven't been getting their usual childhood exanthems - their fevers, and snotty noses that children normally get in the first couple of years of life.
We need a deep dive into data the mRNA manufacturers haven't yet released.
With all we have seen, it makes you wonder about what we haven't.
I still suspect it is some kind of auto immune reaction from the actual viral exposure, perhaps potentiated by spike protein shedding from the vaccinated.