SARS-CoV-2 found in vagus nerve of deceased COVID patients, supporting Michael VanElzakker's vagus nerve infection hypothesis of ME/CFS

[Hip]

A 2023 German study examined the vagus nerves of 23 patients who died of COVID, and found in every case, the vagus nerve was infected with SARS-CoV-2.

The authors believe this infection may be responsible for the dysautonomia observed in long COVID.

Furthermore, it seems to me this finding of an infected vagus in COVID patients supports Dr Michael VanElzakker's chronic vagus nerve infection hypothesis of ME/CFS.

This vagus nerve infection theory of ME/CFS was discussed on these forums when it was first published in 2013. Though oddly, the German authors do not make any reference to Dr VanElzakker's theory in their paper.


Dr VanElzakker's vagus nerve infection theory states that a vagus infections could cause the symptoms of ME/CFS by constantly triggering what is known as the sickness behaviour response.

Sickness behaviour is an orchestrated symptomatic response that is built in to the body, designed to help overcome infections. This response is triggered when we catch infections. All the miserable symptoms you get during an infection such as the flu come from the sickness behaviour response springing into action.

It is the vagus nerve which is responsible for detecting infections in the body, and when detected, this nerve will trigger the sickness behaviour response until the infection is cleared. But if the vagus nerve is itself chronically infected, then this response is constantly triggered, with no end. And this is what causes the ongoing symptoms of ME/CFS, in VanElzakker's theory.

The PolyBio Research Foundation are planning further studies to see if they can find viruses in the nerve tissues of ME/CFS patients.

In terms of treatment, Michael VanElzakker says that antiviral drugs have poor penetration into such nerve tissue. So this could be why antivirals are often of limited benefit in ME/CFS.

 

[Husband of]

But Is COVID 19 also found in the vagus nerve of people that survived acute COVID and got long COVID, or who did survived acute COVID and did not get long COVID?

 

[Hip]

But Is COVID 19 also found in the vagus nerve of people that survived acute COVID and got long COVID, or who did survived acute COVID and did not get long COVID?

My understanding is that you can only test the vagus nerve for viral infections post mortem. You cannot test in live patients. So vagus nerve tissue samples from ME/CFS patients or long COVID patients are therefore hard to come by.

Same with the brain: you can only test for viral infections in brain tissue once the patient is deceased. The 3 brain studies which found enterovirus in the brain were on ME/CFS patients who committed suicide, and their relatives agreed to the study. But each of those 3 studies found enterovirus in the brain.


The German study did examine the vagus nerves of 5 controls, whose cause of death was not COVID, and found no sign of SARS-CoV-2 in their vagus nerve tissue.

 

[Rufous McKinney]

This makes considerable sense to me.

I've had increasing trouble with the vagus nerve and stomach emptying. Many severe folks seem to have j-tubes and no stomach emptying at all. I noticed these emptying issues weren't mentioned in a very long discussion of SIBO. That surprises me.

Also, Sickness Behavior is really a big deal in my opinion.

Because I can stop down Sickness Behavior by changing my body chemistry. Sort of like nearly instant remissions.

 

[Hip]

In terms of a treatment for a chronic vagus nerve infection, Michael VanElzakker in his paper says antivirals have poor penetration into such nerve tissue.

So I was thinking about what could be done to get antivirals into the vagus. Well it is known that certain proteins are carried along the vagus nerve, by the mechanism of retrograde axonal transport (RAT). For example, tetanus toxin protein is able to travel along nerves by RAT.

It is RAT which also carries viruses along the vagus nerve. Dr Chia says enterovirus can enter the vagus nerve in the stomach, and travel along the nerve by RAT, reaching the brain in just 3 days.

If you had a benign protein which could travel along the vagus nerve by RAT, and you bonded that protein to a potent antiviral like say interferon, then maybe just by orally consuming this treatment, it should enter the vagus in the stomach, and perhaps clear viruses from the vagus.

I don't know if this is feasible, but just thinking out loud.

 

[Rufous McKinney]

@Hip I saw the patent pending for a University / b-caryophylene delivery systems.

Maybe you could team up with some lawyer and try to patent this idea/ which might someday BE feasible.

Then, your descendants, could be rich.

 

[Alvin2]

This is very interesting.

I remember also reading that Parkinsons may be caused by something travelling up the vagus nerve into the brain, there was a study that found cutting the vagus nerve prevented or treated Parkinsons, i forget the details.

 

[bertiedog]

I am wondering if the following might be helpful regarding where is the inflammation in ME patient's coming from. The following is part of a blog from the Biomesight website regarding Proteobacteria which cause high amounts of LPS -

Overgrowth of Proteobacteria in the large intestine is one of the most clinically significant imbalances in the microbiome. This is due to one molecule—lipopolysaccharide (LPS). LPS is a structure composed of fat and sugar rings found in the cell wall of specific types of bacteria (Gram negative bacteria). LPS is considered a type of toxin (endotoxin) because of its interactions with the host’s immune system. For the bacteria, LPS provides structural integrity and protection, but for the host, LPS causes inflammation. Different bacteria have different LPS and Proteobacteria have the most inflammatory LPS.

LPS interacts with the immune system via TLR-4, which increases inflammatory cytokines like TNF-⍺, NK-κβ, IL-6, and IL-8. This results in low grade inflammation throughout the body. High levels of LPS can damage the lining of the digestive tract, resulting in gastrointestinal inflammation and digestive symptoms. It may also increase risk of autoimmune diseases in the digestive tract, like inflammatory bowel disease (IBD). In the immune system in the digestive tract (GALT), we see a decrease in balancing immune cells (T regulatory cells) and an increase in autoinflammatory immune cells (Th17 lymphocytes).

The low grade systemic inflammation may result in brain inflammation, influencing depression, cognitive dysfunction, brain fog and fatigue. LPS also causes inflammation in the blood vessels, increasing risk for atherosclerosis and congestive heart failure. High blood levels of LPS are also associated with endometriosis, metabolic syndrome, obesity, type II diabetes and liver disease.

The more research we do, the more we are finding LPS may play a role in many, many different diseases throughout the body. So decreasing your inflammatory LPS levels by decreasing Proteobacteria may be extremely important to your health.

If you currently have elevated Proteobacteria, there are a few considerations to reduce how much LPS gets into your bloodstream. Limit or avoid saturated fat and alcohol since they both increase absorption of LPS. LPS absorption is also enhanced when the permeability of the small intestine is increased (aka leaky gut). So consider limiting your use of NSAIDs as they increase intestinal permeability."

These are my latest results from Biomesight regarding Proteobacteria which produce large amounts of LPS. They are very bad and somehow I cannot seem to improve my symptoms no matter how careful I am about my diet. I also don't have a clue where I got all these bacteria from!

I

 

[bertiedog]

Sorry about the bottom files I couldn't delete them!