The internet has recently become gripped with the emergence of a new & mysterious hepatitis that has been plaguing an exceedingly small number of children around the world.
Naturally, some are using it as an opportunity to harp on their favorite boogieman. Some, who are vehemently opposed to this recent era of mass-experimentation with gene-therapy, will point to the mention of 'adenovirus' and think:
"Ah-ha! It is the adenovirus vectors being used to develop covid vaccines!"
Others, who aren't clinicians of any sort, signal how they regret not advocating for vaccinating children under 5, because there is a 'hypothesis' that the new cases of hepatitis may be related to SARS-CoV-2.
In my opinion, they are both wrong.
Hepatitis is inflammation of the liver. Inflammation can occur as a result of several factors. Alcohol abuse and infections are two of the most commonly discussed causes.
However, it can also occur secondary to toxic exposure, medications, autoimmune diseases, and even high fructose consumption - which in my opinion is one of the most under diagnosed causes of liver disease. I see fatty liver on imaging all the time, and unless the person is a known alcoholic, it often goes unaddressed.
Early on, the viral causes of Hepatitis were considered to be Hepatitis A and B. Which brings us to the first part of this story...
Isolation of Hepatitis C (?)
With the backdrop of Carleton Gajdusek's 'unconventional' slow virus hypothesis, virologists ramped up efforts in trying to blame known diseases on novel viruses.
In the 1970s, we observed cases of hepatitis that were negative for Hepatitis A and B - rather brilliantly, we called it non-A non-B hepatitis (NANBH). NANBH represented a small fraction of the number of people who died from acute hepatitis.
Several researchers decided that they would find the virus which caused NANBH - ignoring several other characteristics of this new disease entity. For example, NANBH was almost exclusively found in people who were alcoholics, heroin addicts, or received regular blood transfusions. At the time, the contents of blood transfusions were also different - particularly involving certain platelet factor proteins.
Researchers also ignored the other small problem - that NANBH was not infectious. It did not spread to the broader population, including the doctors who were taking care of these patients.
But, a new biotech firm in San Francisco, named Chiron Corp, began investigating NANBH in the 1980s.
They began by injecting chimpanzees with serum of patients with NANBH - which failed to elicit the disease. Next, they tested the liver of patients with NANBH to find a virus - again, failed.
Fortunately for Chiron, there was a new biomolecular technique in town, which is now familiar to most - PCR. Thus, they began amplifying random gene segments from the serum of patients with NANBH, in hopes of identifying DNA or RNA fragments which appear foreign.
Whatever these RNA fragments were, they were only seen in about half of the NANBH patients - and in barely detectable amounts. From these tidbits of amplified gene fragments, they claimed to have identified a new virus - which they called Hepatitis C.
Conveniently for Chiron, in the very same issue of Science (the very next page, in fact), they published their development of the antibody test which could identify patients who are 'infected' with this new 'virus.'
Digging into the paper, we uncover some strange findings when they test their own antibody against patients with reported NANBH.
For example, a higher proportion of people who received blood transfusions tested positive, versus patients with NANBH which were community-acquired.
Also, positive tests were seen in a higher proportion of people with 'chronic NANBH' compared to an acute infection (only 15%). Which is really strange. Because, if indeed an infectious agent is being tested, there is no time in which there is a higher viral load than in an acute infection.
One objection to this: "it is an acute infection, the body hasn't had time to generate antibodies."
Fair point, but the paper reveals that these "acute" infections were followed and tested for weeks. Ample time for any immune system to generate antibodies.
Unfortunately for Chiron, more inconsistencies came to light. First, many people who were testing positive for "Hepatitis C" antibody never developed hepatitis. And, some long-term observational studies found no difference in life expectancy between those 'infected' and those without infection.
Having invented the virus and the test, Chiron began with their marketing campaign. The first step was publication of their manuscript. As we saw above, they had no problem getting this published in Science - one of the most well known mainstream scientific journals in existence.
Chiron's CEO was Edward Penhoet - a professor of molecular biology at UC Berkeley. Luckily, the editor of Science was Dan Koshland Jr. - also a professor of molecular biology at UC Berkeley.
In 1988, an opportunity arose - the Emperor of Japan (Hirohito) was quite sick and needed regular blood transfusions. Chiron decided to solidify their name by testing the blood for 'Hepatitis C.' Within a year, Japan approved the new test - and used it to screen their blood banks, bringing Chiron tens of millions of dollars.
Soon after, the FDA approved the test and also recommended universal testing of blood donations. Thereafter, the American Association of Blood Banks mandated the screening of all blood donations. Cha-ching!
With their recent financial success, Chiron bought Cetus - another biotech firm. Cetus was founded by Donald Glaser - yet another professor in the same department of the same university. It also happens that Chiron made a large donation to the same department at around the same time.
Surely, this has been corrected...
When I learned of this, my first thought was "there is no way that hepatitis C has never been isolated. The medical industry around hep C is massive."
Not only do we regularly screen people for hepatitis C, but we've also blamed it as the cause of liver cancer - amongst other things. In addition, there are very expensive drug cocktails that are used to 'cure' people of hepatitis C.
Instead of question these claims, we most recently celebrated the 'groundbreaking' work of the original team from Chiron. This article published in the Lancet in October 2020, celebrates The Nobel Prize in Physiology or Medicine awarded to the pioneering scientists who 'isolated' hepatitis C.
The New Childhood Hepatitis
Some of the most detailed work on this new phenomenon seen in a handful of children comes from the UK Health Security Agency:
Let's take a closer look at their technical briefing...
- Cases of acute hepatitis in children - no association with travel or known hepatitis viruses
- 163 cases as of May 3, 2022 - "non-A to non-E hepatitis"
- No deaths - 11 liver transplants
- Most have been discharged from hospital or fully recovered (88/163)
- Only 13 are still in hospital
- The often mentioned adenovirus cause is detected in 72% - mostly from blood
- Problem: adenovirus is extremely common, and you can PCR adenovirus from many people's blood at any given time
What about in the liver itself?
- 14 total liver biopsies
- Adenovirus detected in 9/14, but only in the lumen of sinusoids - which are contiguous with blood supply
- Testing of the liver tissue itself (hepatocytes) was negative on immunohistochemistry
- PCR of liver tissue was also negative
Finally, the UK HSA report mentions that these cases have no known epidemiological link - so how could this be infectious?
The obvious conclusion would be that it is not of an infectious cause. But, try telling that to virologists and the Public Health Enterprise.
Other possible cause?
- Approximately 75% of patients mentioned in a survey that they had taken Tylenol
- Although the UK HSA has seemingly dismissed this as a possible cause - they note that further investigation into toxic causes is still underway...
Toxic Exposure Hypothesis
From my reading of virology history, it is clear that the field has a tendency to invent viral causes of disease without substantive evidence. The analogous case of hepatitis C, having occurred decades earlier, adds fuel to the fire of this skepticism.
Several drugs can cause liver damage. Alcohol and some foods, particularly those high in fructose, can cause hepatitis.
Tylenol in high doses is toxic to the liver. Most people do not overdose on Tylenol (especially the adult population). However, of all the over-the-counter medication, it is probably one of these easiest to accidentally overdose on. The reason is simple: it is found in many formulations which are used to treat pain & inflammation.
Some people may not know that there are about 600 over-the-counter drugs which contain acetaminophen/paracetamol (Tylenol). This makes it quite easy to take high doses inadvertently. Especially in children.
Need not be Tylenol
I am not entirely set on this 'accidental Tylenol OD' hypothesis. Although, it is certainly a possibility.
I am more concerned about the following question:
"Did these kids intentionally overdose on anything, at all?"
Why might children intentionally OD? Well...
- Mass hysteria surrounding covid
- Social isolation
And, most importantly:
As if the wave of anxiety & depression amplified by the ubiquity of social media was not enough, we have seen a large increase in drug abuse, depression, anxiety, and suicidal ideation in recent years.
It is the perfect storm. Whether intentional or accidental, there are several non-infectious factors which could lead to hepatitis in an exceedingly small number of people.
And, in case you need a reminder, this wouldn't be the first time a microbe was blamed for the toxic effects of drugs:
Unfortunately for the English children, the UK HSA is still pending a toxicology report...