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"Epstein-Barr Virus and the Origin of Myalgic Encephalomyelitis or Chronic Fatigue Syndrome"

Oliver3

Senior Member
Messages
846
Prophylactic vaccines (which they're working) on would be for those who haven't had the illness. We fall into another category. Many of these illnesses are especially bad for the human body (as we know).

As for us, we're still waiting for the magic bullet, so to speak. I knew they were working on these vaccines for common ailments that can kill or do great harm, but I'm glad to see that they're as advanced as they are.

These will be given longer trials than they had time for with the COVID vaccines. Yours, Lenora.
Thank you...I mean I was aware of the meaning of prophylactic but I was hoping beyond hope somehow it wouldn't matter!!
 

Oliver3

Senior Member
Messages
846
That's good news I'd say. It will be incredibly interesting to see how someone with ME would respond to an ebv vaccine. It could also not have much of an effect but hopefully it's strong enough to at least train the body to fight the virus for 12 months. I don't tolerate antivirals so for me this is likely my only route.

https://en.wikipedia.org/wiki/Epstein–Barr_virus_vaccine
Thats kinda what I was hoping...that there may be some effect
Kind of like those hear say reports about people improving after the covid shot
 

Oliver3

Senior Member
Messages
846
It sounds good news, but could take several years to get through the trials if it does at all. Then how does someone in the UK with ME/CFS get it prescribed? I'll keep my fingers crossed.
Most likely I'm sure.
I would've thought hiv was a much more tricky customer than ebv, but then I know nothing
 

godlovesatrier

Senior Member
Messages
2,545
Location
United Kingdom
Yes while we don't know what happens after covid or the ME triggering event, ebv seems to flare or replicate and cause issues for almost everyone (debatable I know). So I just saw this and thought fantastic news, it might fix a lot of the issues we're seeing. I suspect it will only fix a few symptoms though, but I bet there's a subset of patients who will respond dramatically to this.
 

lenora

Senior Member
Messages
4,913
Hello @Treeman. Have you had the newest shingles vaccine? It's supposed to be 95% effective and I certainly hope so as it's a nasty illness to have over and over again. Mind you, I guess that not all cases are equal, but still.

The last round I had (3 outbreaks one after the other) was before the antivirals were in full use. If nothing else, they'll shorten the outbreak and lessen the symptoms. Something to be grateful for.

But we ran to our pharmacy when we heard the newest vaccine was available. Two shots given over a few weeks. I was very nervous about causing another outbreak, but all was well.

I remember those horrid mushy peas well. Didn't they used to come with fish & chips? My mother was British as is my husband. I hadn't thought of them in years. Yours, Lenora.
 

Treeman

Senior Member
Messages
774
Location
York, England
Hello @Treeman. Have you had the newest shingles vaccine?

No, but the valacyclovir tablets are probably best for me at this time.

I remember those horrid mushy peas well. Didn't they used to come with fish & chips?

That's the ones, still a delicacy in the north of England. Some served at chippies are a bit tasteless, but I find the brighter the green (e.g. full of additives) the better they taste! Ask @YippeeKi YOW !! they love them.
 
Messages
68
Thank you for posting.

Does this apply to HHV6, cytomegalovirus, or zoster as well? Or HSV1 or 2?

My ME/CFS was triggered by chemotherapy for stage 3 uterine/ovarian cancer. My immunoglobulins and NK cell function dropped and I had PCR positive EBV (with only high VCA IgG antibodies) along with 6 other infections. Autoimmunity was triggered. Extended use of high dose Valcyte, along with IVIG, testing the other infections, then using Rituximab led to significant resolution of symptoms. Therefore, though this article is significant, I am concerned about the assertions it makes regarding these treatments. My doctor, an AIDS doctor for 30 years, has been very careful about identifying a subset of patients to try these strategies on.

Additionally, my 2 Moderna COVID vaccines reactivated my HHV6, but not EBV (I've had several tests confirming this) and this time Valcyte was not fully effective, but I have been successful with both Valcyte and Famvir taken concurrently.

I believe this is a very significant area of investigation as I have known MANY patients who, after years of suffering, have finally been adequately tested for EBV, HHV6 and CMV, found them active, and subsequently responded to treatment.

The paper suggests current antivirals are inadequate. Many of us would be most grateful to better understand the DNA demethylation agents discussed in the paper.

One of the main reasons why EBV is implicated in the disease is because it binds its glycoprotein 42 to the MHC class II of B lymphocytes and subsequently remains bound after its fusion with the plasma membrane. In addition, it is related to the DRB1 and DQB1 alleles because gp42 binds to the β1 domain of the β-chain of MHC-II. Therefore, if EBV-susceptible "old alleles" are present, since EBV has evolved over the years against these alleles, that is when EBV-associated disease develops.

In the article we mentioned that neither antivirals nor rituximab are fully effective because they do not eliminate all cells with EBV latency and therefore, would not serve to cure the pathology. Another thing is that these treatments are used chronically and they can reduce some symptoms by reducing the viral load and some B cells that could be infected. The problem with rituximab is that it is not specific for all cells with EBV latency, so it can also immunosuppress by eliminating healthy B cells.

Of the other pathogens you mention, it would be necessary to see if they have a similar mechanism of infection or if they alter the antigenic presentation in the same way as EBV does. For now I do not know since I am mainly focused on this virus.
 

Learner1

Senior Member
Messages
6,305
Location
Pacific Northwest
@Manuel Thank you for your thoughtful answer. It does seem like other herpes viruses behave in similar ways to EBV for many things. It would definitely be interesting to know if HHV6 and CMV behave in the same way as EBV in your work. Thank you for all your work and hope you feel better soon.
 

GlassCannonLife

Senior Member
Messages
819
One of the main reasons why EBV is implicated in the disease is because it binds its glycoprotein 42 to the MHC class II of B lymphocytes and subsequently remains bound after its fusion with the plasma membrane. In addition, it is related to the DRB1 and DQB1 alleles because gp42 binds to the β1 domain of the β-chain of MHC-II. Therefore, if EBV-susceptible "old alleles" are present, since EBV has evolved over the years against these alleles, that is when EBV-associated disease develops.

In the article we mentioned that neither antivirals nor rituximab are fully effective because they do not eliminate all cells with EBV latency and therefore, would not serve to cure the pathology. Another thing is that these treatments are used chronically and they can reduce some symptoms by reducing the viral load and some B cells that could be infected. The problem with rituximab is that it is not specific for all cells with EBV latency, so it can also immunosuppress by eliminating healthy B cells.

Of the other pathogens you mention, it would be necessary to see if they have a similar mechanism of infection or if they alter the antigenic presentation in the same way as EBV does. For now I do not know since I am mainly focused on this virus.

I believe there is a paper from 1997-1999 (can't recall exactly sorry!) that looked at long term, around 12 monthly, valaciclovir use in healthy people with prior EBV exposure (plus a placebo control). They saw that the proportion of latently infected B cells decreased over time, with an approximate half life of 8 months.

Wouldn't that suggest that long term use of antivirals can essentially "catch" the cells as they transition from latent to lytic periodically, slowly reducing the population of latently infected cells?