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Epstein-Barr virus behind the development of autoimmune diseases, cancer, ME/CFS and Long COVID

godlovesatrier

Senior Member
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2,545
Location
United Kingdom
Great article @Manuel . The problem really as I see it is the antivirals.

I've tried three so far and I feel like I'm getting nowhere. Valtrex seems to be best for ebv yet that gives my flank pain which I'm sure is kidney stone related. Famvir gives me terrible insomnia and angry episodes. TAF I took for 6 days but had to stop due to very bad brainfog and a worsening of my ME which I didn't experience on the previous two.

Famvir is the most tolerable but the insomnia ultimately causes ebv to reactivate through sleep deprivation.

I wish we had better alternatives. Valcyte is of course one of the most toxic ones to take. And the quality of the compounding that's affordable is terrible.

TAF is amazing for ebv but my ME seems to have worsened on it after only those 6 days at 12.5mg per day. I believe it was twice as strong as valcyte against ebv.

Wish I had more options. Im convinced Dr lerner was onto something and his supression of these viruses was why patients went into remission. However they only saw it with valcyte not valtrex so that's always been a conundrum. It's still very unclear to me what cmv virus actually does to ME patients and there is very little research around this pathogen. Although if you or anyone can point me to it or have thoughts would love to hear it. Thanks.

It seems clear the hhv-6 causes debilitation and terrible fatigue and loss of energy.
 
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68
As soon as I can I will respond to your comments. In the meantime, here are some of the answers I have posted on Twitter:

“After so many years of work and as a post Epstein-Barr virus infection ME/CFS sufferer it makes me really happy that they have put our article on the cover of the August issue of Pathogens journal:

https://www.mdpi.com/2076-0817/11/8

Until recently nobody talked about post-viral syndromes (actually they should be called chronic infectious syndromes) and they left all of us patients isolated both at a health and social level.

Unfortunately it took another virus like SARSCoV2 to show us how viruses are capable of developing chronic diseases like Long COVID. It is curious that for bacterial infections we use antibiotics but for viral infections we leave it to our immune system to manage to control it. This must change. We must prevent with antiviral treatments to prevent the development of chronic diseases such as Long COVID, ME/CFS, autoimmune diseases and even cancer. It is absurd to think that everyone's immune system can resolve most viral infections. Patients who develop diseases associated with these viruses were previously completely healthy. Having one or another type of MHC-II allele can make you weaker or more resistant to certain viruses. In the case of herpesviruses, it is not the viral particles that are the problem, but the latent cells that cause the immune disruption. The Epstein-Barr virus (EBV) is one of the oldest viruses with which humans have coexisted, even since we were apes. Living with this virus has led to the evolution of its evasion mechanisms and also of our resistance mechanisms (MHC-II alleles).

In the case of EBV, the patient only needs to have one of the "ancestral" alleles (the oldest) of the MHC-II weak against EBV, since one of the main reasons why this virus is related to the MHC-II alleles is because it infects cells through the interaction of its viral protein gp42 with the cell's MHC-II. In this way it fuses its membrane with that of the cell, forming a new gp42-MHC-II complex that alters antigenic presentation to CD4 T cells, since MHC-II is essential for the immune system to know what is foreign and what is not. By decreasing this antigen presentation to CD4 T cells, an acquired immunodeficiency develops that allows any inflammatory stimulus (other infection) in any tissue to lead to the formation of EBV-infected ectopic lymphoid aggregates. This, together with the altered immunosurveillance caused by the evasion mechanisms of these cells with EBV latency (increased Th2 and Treg), would lead to increased proliferation of these cells, which would increase the risk of neoplastic transformation or autoimmune disease in these tissues.

In the case of Long COVID two things can happen. That patients have other "weak" HLA alleles against that virus or that they are the same weak alleles against EBV, allowing SarsCov2 infection to cause recruitment of B cells with EBV latency and form these lymphoid aggregates. In other words, EBV is an opportunistic virus that takes advantage of the infection of other pathogens to settle in different tissues.

These tissues finally end up with chronic inflammation by activating receptors (TLRs) that continuously detect viral genetic material, causing an increase in the inflammatory and innate response but without the adaptive response being able to control the infection completely due to the decrease in the activation of CD4 T cells. This acquired immunodeficiency also causes reactivation of other latent pathogens such as other herpesviruses and Parvovirus B19, adding more problems and more inflammation. That is why it is common to have viral reactivations in all EBV-associated diseases.

Based on the hypothesis that the problem is EBV latency cells, there are few effective treatments. If you restore cortisol levels with corticosteroids you can further immunosuppress the Th1 response and therefore further proliferation of these latency cells. If you give antivirals against EBV you prevent viral replication but you do not eliminate the latent cells. If you only give antivirals against SarsCoV 2 you do not eliminate the ectopic lymphoid aggregates with EBV latency that have formed and therefore the problem will continue. And if you try to reduce the proinflammatory cytokines with some immunomodulatory therapy, the immunodeficiency caused by the gp42/MHC-II interaction is not eliminated, so the CD4 T cells will not recognize well the cells with EBV latency I. The treatment that would be useful would be a combination of antivirals and some treatment that would make the cells with latency move to the lytic phase or move to another type of latency that is recognized by the T cells. “

“DR2-DQ6, DR3-DQ2 and DR4-DQ8 are among the oldest haplotypes in existence. These haplotypes have survived over time because they are able to recognize a greater number of antigens compared to other haplotypes, allowing them to better eliminate some pathogens. For example, individuals carrying the HLA-DR4 allele were significantly associated with greater clearance of hepatitis B virus infection. The presence of HLA-DRB1*0401 and DRB1*1501 has been associated with greater clearance of hepatitis C virus infection. And so on with other pathogens. This means that these haplotypes have survived over time and have been inherited from population to population to this day. But they have a disadvantage and that is EBV.

Since EBV is the only member of the genus Lymphocryptovirus adapted to humans, transferred to a hominid ancestor millions of years ago, it could be hypothesized that EBV immune evasion mechanisms have evolved to evade these haplotypes. Furthermore, these haplotypes have the ability to generate strong Th1 responses, releasing IFN-γ. This provides a great advantage against many pathogens but not EBV. Since IFN-γ increases MHC-II expression in cells that previously did not express it, allowing the virus to infect even more cells through gp42-MHC-II interaction. This together with the altered antigenic presentation due to gp42, causes an increase in cells with EBV latency I and 0, increasing the evasion mechanisms of these cells (increased T-reg and IL-10) that generate an increased Th2 response and therefore a greater chronification of the infection.

But why is it EBV that generates all these diseases with these resistant haplotypes against other pathogens? Because not all individuals carrying these haplotypes have developed these diseases. Only a subset have developed them, indicating that there is an environmental factor (EBV infection) that is the origin of these diseases. Especially because it is closely related to the alleles of the beta domain of HLA-II, when infecting through this pathway.

Co-infections of other pathogens in individuals carrying these haplotypes and having EBV also play a role. Any tissue infected by another pathogen increases the inflammation of this tissue by recruiting cells. with EBV latency and forming ectopic lymphoid aggregates with EBV. Autoimmune diseases may develop in these tissues. This supports the fact that the likelihood of developing Long COVID increases the more reinfections they have had with SARS-CoV2.

So treatment against these EBV latency cells would help eliminate all EBV-associated diseases.”
 

godlovesatrier

Senior Member
Messages
2,545
Location
United Kingdom
Well that explains why antivirals don't generally low chronicly activated ebv levels @Shanti1 @DrUniverse

I guess for those of us unlucky enough to have ebv infect cells and not be cleared. Like myself. This keeps us in a constant state of sickness. I assume I now have more infected b cells than I did pre June 2020. And that's why I'm not currently healthier than I was before that time.

Really liked your write up of the treatment process. Don't think anyone else has explained it that well - that I know of. Would explain a lot because the virus pops straight back to life and reinvadss all the same tissues. I felt it leave my tonsils and neck glands when I started famvir and valtrex but I also noticed it creep back into these tissues after stopping the avs.

Very frustrating that there's no way to treat it.

Joshua liesk used beta glucans and reishi triterpenic acid. Triterpenic acid signals the immune system to kill infected ebv cells through apoptosis. The beta glucans stimulate the immune system to search for the infections. Of course the issue is it's not very potent and it seems to loose some efficacy with repeated use (from what I can tell).

I'd give anything to have a good treatment for ebv, would love to clear the infection from my b cells etc.
 

godlovesatrier

Senior Member
Messages
2,545
Location
United Kingdom
@Manuel

What are your thoughts on fasting with water only for a few days? To get round the issues mentioned in terms of treatment. Or would that not work? Supposedly the immune response is higher after 24 to 48 hours.

Joshua Liesk was quite fond of these three day fasts to reset the bodies energy dysfunction but also lower some viral load at the same time.

Just wondered what your thoughts are and whether it would impact ebv latency and infected b cells. As some people say that fasting effects b cells too.
 

Violeta

Senior Member
Messages
2,895
Manuel, does echinacea do what we are looking for, or is the B cell proliferation counterproductive?

Echinacea purpureaExtract Enhances Natural Killer Cell Activity In Vivo by Upregulating MHC II and Th1-type CD4+ T Cell Responses

https://www.liebertpub.com/doi/abs/10.1089/jmf.2021.K.0064

Oral Echinacea intake increased levels of MHC II, CD4+ T cells, Th1 cytokines, and NK cell activity. In addition, E treatment increased B cell proliferation, leukocyte counts, and immunoglobulin levels. Taken together, these results suggest that the chicoric acid of E can improve immune response by controlling NK cell activity, which may be a useful function for immunomodulation systems.
 

godlovesatrier

Senior Member
Messages
2,545
Location
United Kingdom
Life extension reishi seems to increase the t cells, increase the nk cell counts and make nk cells more cytotoxic (better function). Seems to do everything basically, but it's expensive, the study I found said you need to dose 5.5g a day. I was almost taking that much, going to attempt to do a before and after blood test to prove the NK cells actually go up.
 

Violeta

Senior Member
Messages
2,895
Life extension reishi seems to increase the t cells, increase the nk cell counts and make nk cells more cytotoxic (better function). Seems to do everything basically, but it's expensive, the study I found said you need to dose 5.5g a day. I was almost taking that much, going to attempt to do a before and after blood test to prove the NK cells actually go up.

That's amazing info about reishi, I am going to be more consistent with it.

I buy reishi powder and put it in capsules.
 

godlovesatrier

Senior Member
Messages
2,545
Location
United Kingdom
That won't work I'm afraid.

Only alcohol extracted forms were found to be bioavailable. The raw powder doesn't get extracted by gastric juices at all. Also Joshua liesk tested loads of powders and only Life Extension Reishi showed any medicinal components. Specifically triterpenes. Whereas in all the other samples tested the triterpenes were so low as to be negligible.
 

Violeta

Senior Member
Messages
2,895
That won't work I'm afraid.

Only alcohol extracted forms were found to be bioavailable. The raw powder doesn't get extracted by gastric juices at all. Also Joshua liesk tested loads of powders and only Life Extension Reishi showed any medicinal components. Specifically triterpenes. Whereas in all the other samples tested the triterpenes were so low as to be negligible.

That's unfortunate. But Life Extension reishi does work even though it's a powder?
 

godlovesatrier

Senior Member
Messages
2,545
Location
United Kingdom
It's the extraction process that helps - the paper I read didn't specifically say why though.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4684115/

When Ganopoly was studied in late-stage cancer patients, it was found that a dose of 5.4 g/d increased IL-2, IL-6, and IFN-γ and decreased TNF-α and IL-1. This dosage also increased NK cells (CD56+ cells) and NK activity.

https://pubmed.ncbi.nlm.nih.gov/12916709/

The mean absolute number of CD56+ cells was significantly (P < 0.05) increased after 12-week treatment of Ganopoly, whereas the numbers of CD3+, CD4+, and CD8+ were just marginally increased compared to baseline levels, with the CD4:CD8 T cell ratios unchanged.

and specifically:

1800 mg Ganopoly PO TID × 3 mo; hot water extraction, then 75% ethanol extraction, then purified by gel filtration

However Josh got the mass spectrometry done in an official lab, I've seen the report showing a clear spike for triterpenes, that ONLY Life Extension Reishi showed, so I know what I will continue to buy with all this in mind.

I feel much worse when I stop this product, it's the one thing I have not been able to stop without becoming much sicker. I've taken it for 18 months without any real side effects. Apart from the first 3 weeks where it made me feel pretty unwell, no doubt due to the large boost in NK cell function.
 

Violeta

Senior Member
Messages
2,895
It's the extraction process that helps - the paper I read didn't specifically say why though.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4684115/



https://pubmed.ncbi.nlm.nih.gov/12916709/



and specifically:



However Josh got the mass spectrometry done in an official lab, I've seen the report showing a clear spike for triterpenes, that ONLY Life Extension Reishi showed, so I know what I will continue to buy with all this in mind.

I feel much worse when I stop this product, it's the one thing I have not been able to stop without becoming much sicker. I've taken it for 18 months without any real side effects. Apart from the first 3 weeks where it made me feel pretty unwell, no doubt due to the large boost in NK cell function.

Where is the report that only Life Extension reishi showed? I would like to see what other brands they tested.