Predictors for Developing Severe ME/CFS following acute EBV (Jason et al., 2022)

Pyrrhus

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Predictors for Developing Severe ME/CFS following Infectious Mononucleosis (Jason et al., 2022)
https://www.rehabiljournal.com/arti...drome-following-infectious-mononucleosis.html

A study from Lenny Jason that suggests that people who develop severe ME after infection with the herpesvirus EBV (AKA "mono" or "glandular fever") may have had a pre-existing gastrointestinal disease.

Background: About 10% of individuals who contract infectious mononucleosis (IM) have symptoms 6 months later that meet criteria for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Our study for the first time examined whether it is possible to predict who will develop ME/CFS following IM.

Methods: We have reported on a prospectively recruited cohort of 4,501 college students, of which 238 (5.3%) developed IM. Those who developed IM were followed-up at six months to determine whether they recovered or met criteria for ME/CFS. The present study focuses on 48 students who after six months had a diagnosis of ME/CFS, and a matched control group of 58 students who had no further symptoms after their IM. All of these 106 students had data at baseline (at least 6 weeks prior to the development of IM), when experiencing IM, and 6 months following IM. Of those who did not recover from IM, there were two groups: 30 were classified as ME/CFS and 18 were classified as severe ME/CFS. We measured the results of 7 questionnaires, physical examination findings, the severity of mononucleosis and cytokine analyses at baseline (pre-illness) and at the time of IM. We examined predictors (e.g., pre-illness variables as well as variables at onset of IM) of those who developed ME/CFS and severe ME/CFS following IM.

Results: From analyses using receiver operating characteristic statistics, the students who had had severe gastrointestinal symptoms of stomach pain, bloating, and an irritable bowel at baseline and who also had abnormally low levels of the immune markers IL-13 and/or IL-5 at baseline, as well as severe gastrointestinal symptoms when then contracted IM, were found to have a nearly 80% chance of having severe ME/CFS persisting six months following IM.

Conclusions: Our findings are consistent with emerging literature that gastrointestinal distress and autonomic symptoms, along with several immune markers, may be implicated in the development of severe ME/CFS.
 
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Predictors for Developing Severe ME/CFS following Infectious Mononucleosis (Jason et al., 2022)
https://www.rehabiljournal.com/arti...drome-following-infectious-mononucleosis.html

A study from Lenny Jason that suggests that people who develop severe ME after infection with the herpesvirus EBV (AKA "mono" or "glandular fever") may have had a pre-existing gastrointestinal disease.
Hectic.

Would it not be worthwhile to run valtrex when getting EBV for the first time? Why is this not standard practice? Especially considering how many cancers and autoimmune conditions are attributed to EBV.
 
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Pyrrhus

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Would it not be worthwhile to run valtrex when getting EBV for the first time?
Unfortunately, Valtrex appears to be only partially effective against EBV and CMV.

According to a 2019 review, Valtrex should work best for HSV and VZV, and is only partially effective against EBV and CMV. Valcyte should work best for HSV, VZV, EBV, CMV, but is only partially effective against HHV6. However, this 2019 review was mainly based on in vitro studies, and does not take into account dosage and dosing frequency.

In the below graph, Valtrex is represented by "ACV", and Valcyte is represented by "GCV". ("BCV" stands for Brincidofovir, a drug approved only for smallpox.)

1646776666483.png


Reference:
https://www.sciencedirect.com/science/article/pii/S0166354218306570?via=ihub
 
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Unfortunately, Valtrex appears to be only partially effective against EBV and CMV. According to a 2019 review, Valtrex should work best for HSV and VZV, while Valcyte should work best for HSV, VZV, EBV, and CMV. However, this was mainly based on in vitro studies.

In the below graph, Valtrex is represented by "ACV", and Valcyte is represented by "GCV":

View attachment 47168

Reference:
https://www.sciencedirect.com/science/article/pii/S0166354218306570?via=ihub
Hm true. I thought people have studied valtrex and EBV in humans and found it to be sufficient? I don't know any literature off the top of my head though.
 

CSMLSM

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If you are trying to clear EBV then you need to remove all infected cells because the latency states it goes into in the cells.
EBV infects at least B cells, astrocytes and Microglial cells. First these cells need to be able to be replaced so they really need to be a type of cell that can be lost.
Then you need to cause apoptosis in these cells so the latent stage cannot progress and you have neutralised the virus in that cell with no persistance of that instance of the infection (that individual cell).

Fasting (not eating) can achieve this (in certain circumstances) and certain molecules (drugs) can trigger appotosis in these cells.
Taking one of these substances with having previously stimulated these cells to reactivate EBV from latency, you start to clear infected cells.

From what I can tell from my research.
 
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If you are trying to clear EBV then you need to remove all infected cells because the latency states it goes into in the cells.
EBV infects at least B cells, astrocytes and Microglial cells. First these cells need to be able to be replaced so they really need to be a type of cell that can be lost.
Then you need to cause apoptosis in these cells so the latent stage cannot progress and you have neutralised the virus in that cell with no persistance of that instance of the infection (that individual cell).

Fasting (not eating) can achieve this (in certain circumstances) and certain molecules (drugs) can trigger appotosis in these cells.
Taking one of these substances with having previously stimulated these cells to reactivate EBV from latency, you start to clear infected cells.

From what I can tell from my research.
How do you stimulate reactivation? Fasting as well?
 

CSMLSM

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How do you stimulate reactivation? Fasting as well?
Anything that triggers ME/CFS basically.

Example- do some exercise, go on a treadmill or exercise bike and start to trigger yourself as hard as possble. This is dangerous if you do not have a way to shut it down please do not do this. I have had experience that it works for me, had an experience the other day. Was much better following. Opposite to normal with ME/CFS

If you Fast enough (currently I do for approx 12h on 12h off, not strict) and for long enough (at least 4 day ish) your body starts to breakdown unneccessary and old cells. The cells we want to neutralise are these cells I believe.
Drugs/molecules substances are available that will do the same.

I am onto something. I can manage this condition for sure now but being able to cure myself would be the dream.

Daniel
 

CSMLSM

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Its mild Fasting, but has metabolic significance for a healthy homeostasis.

The effect I mention is thought to not occur at this level though, sorry for not making clearer.

Daniel
 

CSMLSM

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Pretty much I do that now.
I used to find starving myself would help with somethings. Presumable this was reducing the number of infected cells and limiting my underlying immune dysfunction.

Advice for everybody-
I do not recommend starving yourself. If your depressed please talk to someone if you can. Do not hurt yourself.

Daniel
 

CSMLSM

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Hi everyone sorry,

meant Fast for a full 4 days to achieve the desire affect. Do not try this. I will experiment on myself when strong enough.
Working on physical fitness first and reducing atrophy. Building muscle and strength. Can go on tredmill and will start exercise bike soon.

Daniel
 

Shanti1

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I thought people have studied valtrex and EBV in humans and found it to be sufficient?
The section of the below 2019 paper titled, "Antivirals Against EBV Evaluated in the clinic" goes through the evidence for valganciclovir and valacyclovir. In the human trials, they both appear to be effective. While it is possible that valga may be more effective than valac, based on the in Vitro data, this was not called out in the clinical trials reviewed in this paper.
Novel Therapeutics for Epstein–Barr Virus - MDPI

How do you stimulate reactivation?
Stimulating reactivation is a bad idea. Valacyclovir (or similar meds) does not eliminate the virus, the viral plasmid in the cell remains intact. It only stops the replication ie the production of additional viruses. Inducing replication by inducing PEM through intense exercise may increase viral load, decrease immune function, and possibly cause harm. It wouldn't reduce baseline viral load or the number of cells infected. I've been on valacyclovir for 8 months now and pushing and getting PEM sets me back, it does not help me clear viruses and improve.

An example is mono. While acyclovir, may reduce viral shedding during Mono, it doesn't eliminate the virus from cells (just the replication), alleviate symptoms, or shorten the course of the disease. This is because the symptoms are an immune response to EBV-infected B-Cells.

EBV infection can be latent, abortive lytic, and lytic reactivation. It has been proposed that abortive lytic may be a common finding in ME/CFS, the virus still produces immuno-suppressive proteins, and symptoms, but is not susceptible to antivirals.

If symptoms are being caused by active EBV, there is no need to try to activate further. To me, the role of antivirals is in eliminating active viral replication, maintaining latency, and possibly lowering viral load over time (as we know, EBV can not be eliminated). As cells divide and die and the virus is not able to replicate due to the antivial, the viral load may also decrease (not certain on this). Some have postulated that the reason some do not respond to antivirals but are still symptomatic is because of the abortive lytic phase (HIP has some great posts on this). Dr. Lerner found people sometimes had to be on antivirals for extensive time to get benefit. For me, oxymaitrine paired really nicely with valacyclovier because it boostes TH1 response to help the body control the virus while the antiviral inhibits replication.

@GlassCannonLife No need to respond to this post. I know you aren't feeling well Please rest and take care of yourself.

file:///C:/Users/revot/Desktop/molecules-24-00997.pdf
https://ar.iiarjournals.org/content/33/12/5693
https://www.frontiersin.org/articles/10.3389/fimmu.2021.656797/full
 
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CSMLSM

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The section of the below 2019 paper titled, "Antivirals Against EBV Evaluated in the clinic" goes through the evidence for valganciclovir and valacyclovir. In the human trials, they both appear to be effective. While it is possible that valga may be more effective than valac, based on the in Vitro data, this was not called out in the clinical trials reviewed in this paper.
Novel Therapeutics for Epstein–Barr Virus - MDPI



Stimulating reactivation is a bad idea. Valacyclovir (or similar meds) does not eliminate the virus, the viral plasmid in the cell remains intact. It only stops the replication ie the production of additional viruses. Inducing replication by inducing PEM through intense exercise may increase viral load, decrease immune function, and possibly cause harm. It wouldn't reduce baseline viral load or the number of cells infected. I've been on valacyclovir for 8 months now and pushing and getting PEM sets me back, it does not help me clear viruses and improve.

An example is mono. While acyclovir, may reduce viral shedding during Mono, it doesn't eliminate the virus from cells (just the replication), alleviate symptoms, or shorten the course of the disease. This is because the symptoms are an immune response to EBV-infected B-Cells.

EBV infection can be latent, abortive lytic, and lytic reactivation. It has been proposed that abortive lytic may be a common finding in ME/CFS, the virus still produces immuno-suppressive proteins, and symptoms, but is not susceptible to antivirals.

If symptoms are being caused by active EBV, there is no need to try to activate further. To me, the role of antivirals is in eliminating active viral replication, maintaining latency, and possibly lowering viral load over time (as we know, EBV can not be eliminated). As cells divide and die and the virus is not able to replicate due to the antivial, the viral load may also decrease (not certain on this). Some have postulated that the reason some do not respond to antivirals but are still symptomatic is because of the abortive lytic phase (HIP has some great posts on this). Dr. Lerner found people sometimes had to be on antivirals for extensive time to get benefit. For me, oxymaitrine paired really nicely with valacyclovier because it boostes TH1 response to help the body control the virus while the antiviral inhibits replication.

@GlassCannonLife No need to respond to this post. I know you aren't feeling well Please rest and take care of yourself.

file:///C:/Users/revot/Desktop/molecules-24-00997.pdf
https://ar.iiarjournals.org/content/33/12/5693
https://www.frontiersin.org/articles/10.3389/fimmu.2021.656797/full
While I agree completely with what you are saying, hence why I stated clearly do not try this and said I am going to experiment on myself. I also made it clear that if you do not have a way to shut it down it is dangerous. I was very clear.
The reason for stimulating the virus is because when activated these cells are able to be triggered into apoptosis but only while activated. I believe I have such a molecule able to do this is all.

But you are correct completely though so thank you for adding this to make it more clear to those that may have gotten confused :)

Daniel
 
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I had a strange issue when I was younger where I would sometimes get a bit nervous and I would have to go to the toilet a lot, this happened with some of my A-level exams but not others e.g. GCSE or A2 level, it also happened when I went to work just after leaving school, but was never an issue at university, it didn't correlate with general anxiety or panic attacks or anything like that, I don't know if it would be considered I.B.S. Also always had quite strong hayfever around may, june, july and i'm allergic to some cats, seems to depend on how long their hair is. My mother also is diagnosed with ME/CFS though I can't tell whether its the same, I can tell that she doesn't have multiple chemical sensitivity. We both have a tendency towards OCD behaviours but my mother doesn't realize that she has it, I also have autism disorder but I didn't realize until I was over 30 years old.
 

CSMLSM

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I had a strange issue when I was younger where I would sometimes get a bit nervous and I would have to go to the toilet a lot, this happened with some of my A-level exams but not others e.g. GCSE or A2 level, it also happened when I went to work just after leaving school, but was never an issue at university, it didn't correlate with general anxiety or panic attacks or anything like that, I don't know if it would be considered I.B.S. Also always had quite strong hayfever around may, june, july and i'm allergic to some cats, seems to depend on how long their hair is. My mother also is diagnosed with ME/CFS though I can't tell whether its the same, I can tell that she doesn't have multiple chemical sensitivity. We both have a tendency towards OCD behaviours but my mother doesn't realize that she has it, I also have autism disorder but I didn't realize until I was over 30 years old.
That is unfortunate maybe someone here might be able to help you :)