Ongoing research: Identifying viruses in tissue and nerve samples from ME/CFS patients

[Shanti1]

I'm the same too. The antivirals help but don't eradicate the viruses. If there was an antiviral to eradicate the particular virus troubling us, we still need some way to fix our immune system, eg if it was ebv, we could potentially catch ebv again.

Also, a 'normal' person gets ebv mono, than recovers and their immune system keeps it suppressed. I think fixing the immune system is closer to a real cure than an antiviral that could eradicate a virus, but I'd take either.

For now, I have to stay on antivirals to maintain my level of function as well as a few other things. Just using what's available for now. I think even with a cure, age is going to make it harder to recover???

I'm in the same boat. My offenders are EBV and Candida krusei and if I stop the antivirals or antifugals, I get MUCH worse. But it begs the question, why are these pathogens gaining the upper hand when most people who are exposed manage to keep them in check?

In his recent thread on his article on the connection between EBV, long-Covid, and ME/CFS, Manuel mentions, "This review suggests that in individuals with certain genetic characteristics - specifically those with "weak" HLA-II haplotypes against EBV - this virus can become more easily established"

The HLA I and HLA II regions of chromosome 16 code for MHC I and II receptors on our cells. These receptors help us to distinguish self from non-self and to recognize intracellular (MHC I/ TH1) and extracellular (MHC II /TH2) pathogens. Allele variants in both HLA I and HLA II are associated with varying autoimmune conditions and pathogen susceptibility. I wouldn't be surprised if part of the answer lies there.

 

[Wishful]

But it begs the question, why are these pathogens gaining the upper hand when most people who are exposed manage to keep them in check?

Why is one person active at 100, and another one is sickly and dies at 21? We're all different. I expect we have quite different immune cells and immune support systems and levels of support chemicals in our serum, so we do respond differently to different invaders. Maybe having a certain strain of viral infection at age 7 makes for a different immune response to EBV at age 28 than if it was a different strain at 7. For that matter, maybe it makes a difference if you had chicken soup on the third day or on the fourth day. Our bodies are not like consumer products, built from near-identical parts in identical configuration.

Also, while we may know that our cells involve HLA or whatever, there are probably other critical factors that we still don't know about (and have acronyms for). Even if you studied all there is known about immune cells, there's no guarantee that you could find the answer, because it might still be unknown.

Why did I suddenly lose a critical gut bacterial strain? I didn't take antibiotics or any other obvious cause. It's just one of those mysteries. Hey, maybe I picked up a virus that attacked that bacterial strain ... and the virus died out after eliminating its host. How to prove it? Actually, I don't really care, since the problem is now fixed.

 

[Forummember9922]

Dr. Chia is doing research right now that is showing enterovirus protein in the peripheral blood leukocytes. They are testing the samples then incubating and testing them again. His lab found enterovirus protein in my sample pre-incubation then much more enterovirus protein post-incubation, indicating an active infection.

This is remarkable research, IMO. I'm glad to see more researchers starting to take enteroviruses more seriously.

What we need is a polarizing statistic IE observations seen in 100% of CFS patients but 0% of Controls, or at least 80%. The polarizing observations we have so far is fibronectin observations, butryrate-producing bacteria observations, tryptophan/serotonin observations. Enteroviruses certainly come up enough to deserve new research and godspeed to chia.

Any links on this that you can provide? Or is this unofficial speculation

 

[Rufous McKinney]

I have a vague notion.
In both cases, the spine and CSF are involved if there is inflammation.

agree...very likely in my case....

The thoracic duct is the largest lymphatic vessel in the body, and it ascends through the chest, alongside the spine. It continues upwards, eventually reaching the neck.

I need to further investigate this.

I knew the thoracic area is important to the lymph system. And I have spinal defects all over the place including there. Tai chi directly works this area: sure wish I could get that happening effectively.

I continue to feel at least some of us have structural issues that / contribute or worsen things. CCI.

 

[Shanti1]

I expect we have quite different immune cells and immune support systems and levels of support chemicals in our serum, so we do respond differently to different invaders. Maybe having a certain strain of viral infection at age 7 makes for a different immune response to EBV at age 28 than if it was a different strain at 7. For that matter, maybe it makes a difference if you had chicken soup on the third day or on the fourth day.

I agree that HLA genes aren't by any means the only factor that can cause our immune system to function or malfunction. Nonetheless, HLA and the MHC receptors they code for are responsible for pathogen recognition by T and B cells, giving them a central and important role and their variations have been tightly associated with susceptibility or resilience to many different autoimmune diseases and pathogens.

I'm not sure to what degree HLA genes factor in susceptibility to other pathogens associated with ME/CFS, but for EBV, Manuel's paper identifies an observed mechanism through which EBV interacts with a specific HLA/MHC type, allowing it to suppress immune function and proliferate.

I'm not saying that this is the only way EBV hijacks the immune system or that is the issue in all people, just that in my view, it is a good candidate as an important factor in those of us who have identified EBV as a problem.

Our bodies are not like consumer products, built from near-identical parts in identical configuration.

Exactly my point, we all have different genetics and this makes us different. HLA genes in particular have great variation, which often confer resistance or susceptibility to conditions and pathogens (Human Leukocyte Antigen (HLA) System: Genetics and Association with Bacterial and Viral Infections). In my mind, genetics are about probability. For example, nearly 100% of celiac patients have a specific HLA allele, if you don't have that allele, you don't get celiac, but for most HLA associations, the HLA type confers risk, not destiny, probably because most conditions are multifactorial.

Obviously, sometimes HLA may be not involved and a whole multitude of other factors, often working in tandem are responsible for ME/CFS pathology.

 

[Oliver3]

Why is one person active at 100, and another one is sickly and dies at 21? We're all different. I expect we have quite different immune cells and immune support systems and levels of support chemicals in our serum, so we do respond differently to different invaders. Maybe having a certain strain of viral infection at age 7 makes for a different immune response to EBV at age 28 than if it was a different strain at 7. For that matter, maybe it makes a difference if you had chicken soup on the third day or on the fourth day. Our bodies are not like consumer products, built from near-identical parts in identical configuration.

Also, while we may know that our cells involve HLA or whatever, there are probably other critical factors that we still don't know about (and have acronyms for). Even if you studied all there is known about immune cells, there's no guarantee that you could find the answer, because it might still be unknown.

Why did I suddenly lose a critical gut bacterial strain? I didn't take antibiotics or any other obvious cause. It's just one of those mysteries. Hey, maybe I picked up a virus that attacked that bacterial strain ... and the virus died out after eliminating its host. How to prove it? Actually, I don't really care, since the problem is now fixed.

Science is based on trying to unravel these complexties. It doesn't make sense not to understand the intricacies.
To ignore evidence of a phenotype would also be detrimental.
Hopefully, the oft talked about era of personal medicine will answer many questions and provide solutions.

 

[heapsreal]

I'm in the same boat. My offenders are EBV and Candida krusei and if I stop the antivirals or antifugals, I get MUCH worse. But it begs the question, why are these pathogens gaining the upper hand when most people who are exposed manage to keep them in check?

In his recent thread on his article on the connection between EBV, long-Covid, and ME/CFS, Manuel mentions, "This review suggests that in individuals with certain genetic characteristics - specifically those with "weak" HLA-II haplotypes against EBV - this virus can become more easily established"

The HLA I and HLA II regions of chromosome 16 code for MHC I and II receptors on our cells. These receptors help us to distinguish self from non-self and to recognize intracellular (MHC I/ TH1) and extracellular (MHC II /TH2) pathogens. Allele variants in both HLA I and HLA II are associated with varying autoimmune conditions and pathogen susceptibility. I wouldn't be surprised if part of the answer lies there.

The main reason antivirals don't clear the virus is because they don't actually kill the virus but just stop them reproducing.

I think the virus will just go into a dormant state or in healthy people the viral load drops low enough that the immune system can control it.

Another reason is as we mentioned is the virus is in certain tissue the antivirals can't reach.

Another point is the initial trigger for cfsme has damaged the immune system and somehow stopped our natural killer cells from working properly. This can then allow other infections. There's older studies showing the longer one is sick with cfsme, the more infections one is likely to have.

We often forget the cns and the hpa axis which can effect the immune system and other symptoms like sleep issues, pots/oi etc. I think there is a subset where the initial infection has left them but they are left with severe symptoms from the cns/hpa dysfunction with pots/oi so severe they can't sit up for more than a minute or less and other cns symptoms. For these people Anti infection meds and immune meds are useless. They get left behind alot in the research and seem to be some of the sickest cfsme patients.

 

[heapsreal]

What we need is a polarizing statistic IE observations seen in 100% of CFS patients but 0% of Controls, or at least 80%. The polarizing observations we have so far is fibronectin observations, butryrate-producing bacteria observations, tryptophan/serotonin observations. Enteroviruses certainly come up enough to deserve new research and godspeed to chia.

Any links on this that you can provide? Or is this unofficial speculation

Low natural killer cell function. Many studies on this. Nothing done on it other than acknowledge it. At a minimum it could be helpful to use as a biomarker for diagnosis along with the traditional cfsme criteria.

 

[SWAlexander]

I uploaded a summary of my collection:

HLA I and HLA II are associated with?​

https://swaresearch.blogspot.com/2023/11/hla-i-and-hla-ii-are-associated-with.html

 

[SWAlexander]

Restoring the infected powerhouse: Mitochondrial quality control in sepsis
https://www.sciencedirect.com/science/article/pii/S2213231723003695

Highlights​

• •
  Mitochondrial dysfunction drives inflammation and organ damage.
• •
  Early biogenesis and maintained mitochondrial mass are associated with sepsis survival in observational studies.
• •
  Mitophagy and biogenesis can be induced pharmacologically, and hold promise for future therapeutic avenues.
• •
  The key lies in the timing of the interventions promoting mitochondrial quality control in sepsis.
• •
  Induction of mitophagy and mitochondrial fusion during sepsis improves outcomes in pre-clinical models.
• •
  Induction of mitochondrial biogenesis after sepsis improves cognition in rats.

 

[SWAlexander]

Preprint

IgG Antibody Responses to Epstein-Barr Virus in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Their Effective Potential for Disease Diagnosis and Pathological Antigenic Mimicry​

Excerpt:
"When we compared data of all ME/CFS patients or data of a subgroup of these patients with non-infectious or unknown disease trigger to the dataset of HC, we could not find an antibody-based classifier that would meet the desired accuracy in the test dataset. In contrast, we could identify a 26-antibody classifier that could distinguish ME/CFS patients with an infectious disease trigger from HCs with 100% and 90% accuracies on the train and test sets, respectively. We finally performed a bioinformatic analysis of the EBV peptides associated with these 26 antibodies. We found no correlation between the importance metric of the selected antibodies in the classifier and the maximal sequence homology between human proteins and each EBV peptide recognized by these antibodies. In conclusion, these 26 antibodies against EBV have an effective potential for disease diagnosis of a subset of patients, but they are less likely to trigger pathological autoimmune responses that could explain the pathogenesis of ME/CFS."
https://www.preprints.org/manuscript/202311.1523/v1

PDF file 11 pages.

 

[Wishful]

It doesn't make sense not to understand the intricacies.

I'm not arguing against research. I'm just pointing out that the research isn't complete yet, so any theories are based on limited knowledge, and thus the truth might not be available at this time. I do appreciate reports about new discoveries in how our bodies work. Eventually we'll be able to figure out mysterious diseases faster.

 

[Oliver3]

Indeed. I'm hoping these supercomputers can really ramp up our understanding of disease

 

[Wishful]

We have impressive knowledge of some parts/functions of the body, but in others I think we're really not much more advanced than the middle ages. Serotonin reuptake drugs were probably considered a miracle of modern science, but isn't the theory for how they actually work now in question? I'm sure there are plenty of other drugs prescribed based on a theory that isn't actually valid.

Medicine: great progress, but much more is needed.

 

[SWAlexander]

For anybody who has the stamina, there is a very long and multi layer thread by Manuel Ruiz in regards to the link: https://www.preprints.org/manuscript/202311.1523/v1

𝐃𝐢𝐝 𝐲𝐨𝐮 𝐤𝐧𝐨𝐰 𝐭𝐡𝐚𝐭 𝐄𝐬𝐩𝐭𝐞𝐢𝐧-𝐁𝐚𝐫𝐫 𝐯𝐢𝐫𝐮𝐬 𝐜𝐨𝐮𝐥𝐝 𝐛𝐞 𝐚 𝐭𝐫𝐢𝐠𝐠𝐞𝐫 𝐟𝐨𝐫 𝐬𝐲𝐦𝐩𝐭𝐨𝐦𝐬 𝐢𝐧 𝐌𝐄/𝐂𝐅𝐒 𝐚𝐧𝐝 𝐋𝐨𝐧𝐠 𝐂𝐎𝐕𝐈𝐃?

https://twitter.com/i/web/status/1708786834409451832

https://twitter.com/manruipa

 

[Aidan Walsh]

agree...very likely in my case....


I need to further investigate this.

I knew the thoracic area is important to the lymph system. And I have spinal defects all over the place including there. Tai chi directly works this area: sure wish I could get that happening effectively.

I continue to feel at least some of us have structural issues that / contribute or worsen things. CCI.

I just saw some MRI Contrast Scans she had compression of her Spine with the renal vein & aorta vein, it was different to the aorta & renal vein & the SMA vein. Rufous, see Jayne Flanders post 5 hours ago on Facebook, Renal Nutcracker Syndrome Support Group she had numerous MRI Contrast scans although not diagnostic but I think better than doppler or venous scans

 

[Oliver3]

We have impressive knowledge of some parts/functions of the body, but in others I think we're really not much more advanced than the middle ages. Serotonin reuptake drugs were probably considered a miracle of modern science, but isn't the theory for how they actually work now in question? I'm sure there are plenty of other drugs prescribed based on a theory that isn't actually valid.

Medicine: great progress, but much more is needed.

That goes without saying tho. Baffled by the obviousness.
Its all we've got.
Science is never resolved because always there will be new " truths".
Ssris do work tho, to some extent. Perhaps it's their antihistemic properties. But we used them for better or worse and learn from them . That's the scientific method.
Machine learning will speed this up.

 

[Wishful]

Baffled by the obviousness.

Baffled by the obliviousness to the obviousness by all too many people in society.

 

[Oliver3]

Not people on here tho

 

[Methyl90]

I have a vague notion.
In both cases, the spine and CSF are involved if there is inflammation.

Microglia are a type of glial cell located throughout the brain and spinal cord. They act as the first and main form of active immune defense in the central nervous system (CNS). In response to certain brain injuries or diseases, microglia can change their behavior, becoming activated. This activation plays a key role in the brain's inflammatory response, which can be both protective and, if excessive, potentially harmful. One other theory is, that an overload of spinal or brain inflammation could exhaust microglia activity.

Inflammatory Conditions: Diseases like sarcoidosis, tuberculosis, or certain forms of arteritis can lead to lymphatic obstruction or dysfunction. Even chyle enters the thoracic duct and flows upwards into the thoracic duct. The thoracic duct is the largest lymphatic vessel in the body, and it ascends through the chest, alongside the spine. It continues upwards, eventually reaching the neck.

I like it when I have the possibility of passing a wooden stick throughout the spine but I focus a lot on the thoracic part in each vertebral space... I think and hope it can be useful but I have never noticed obvious improvements, either in the short term or in the long term period... probably if the cervical part is also congested the information, hormones etc will struggle to go up and down... this is why alignment is important.