• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

Elevated EBV, HHV 6 -- what does this mean?

msf

Senior Member
Messages
3,650
Another explanation for individual patients testing positive for lots of different pathogens is that they harbour lots of different pathogens, which would explain why treating one of them would not have much effect. I do not want to turn this into a Lyme thread, but I think everyone who tests positive for Cpn and Mycoplasma should be aware that they are co-infections of Lyme.
 

Eeyore

Senior Member
Messages
595
My point with the VZV was mostly in response to @Valentijn, that at least in a few cases (HHV6 / VZV), I produce normal antibodies to herpes viruses. I would expect the general population to show similar results to mine. @Valentijn makes an interesting point though about whether it's possible that someone like me has EBV but isn't producing antibodies anymore - I suppose it's possible.

I don't believe there is anything really unique about us and herpes viruses. I think we just have the same viruses with the same frequency as everyone else.

My VZV titers didn't drop as far as I know - it's not something I've tested that much. They were normal though (although lab would say abnormal in that they indicate exposure to the virus, and "normal" would be no exposure, which by my age is almost unheard of).

My own belief is that herpes viruses are just red herrings for ME patients and have nothing to do with our illness. I think there are a few factors that led to this happening. First, I think it goes back to Dr. Strauss at the NIH not wanting to accept he had a brain tumor and experiencing seizures, instead trying to blame his CFS on EBV - he later died of that brain tumor though (read Byron Hyde's personal accounts of this).

The other factor is that we get a lot of blood tests. Most come back normal. The first things that will usually jump out as abnormal (and be flagged as such by the lab) are elevated titers for common herpes viruses like VZV and HHV6. As a result, patients think this is really abnormal, when what would be more abnormal is to have no evidence of exposure to VZV or HHV6 (although the lab would mark this as normal).

Lastly, EBV has long been associated with prolonged fatigue (with mono / glandular fever) lasting months after infection, and because our disease was so unfortunately named, many docs jumped to EBV as being the case of fatigue. It was a reasonable hypothesis, but over time, studies failed to show any connection with ME. Ultimately we must think scientifically and toss out theories that are scientifically refuted. Holding on to bad theories just hurts us because we can't get to the root of the problem.

In summary, I don't think herpes viruses are important to ME pathogenesis, other than that they, like other infectious and non-infectious causes, can serve as the initial trigger. I feel we've wasted too much time and too many resources hunting for a mystery pathogen that is not there.
 

Eeyore

Senior Member
Messages
595
Lots of people disagree. Nothing wrong with that. Since neither I, nor anyone else, definitively knows the cause of ME, we are all just offering opinions. What is above is my opinion, and some evidence which supports it (which is not the same as proving it).

Everyone is free to hold whatever opinion they like, but a problem, like ME, seems intractable, it is often useful to think out of the box and reexamine some of one's initial assumptions.
 

duncan

Senior Member
Messages
2,240
@Eeyore , you wrote "...there is no evidence that ME patients do have titers against anything at different levels or frequencies than the general population."

This runs contrary to what I have learned about ME over the years. It's not just a test here or there, it's about many tests for many pathogens over a sustained period, and this seems associated with ME patients.
 

Violeta

Senior Member
Messages
2,948
"Impaired ER function caused by factors such as inhibition of posttranslational modifications, altered ER Ca2+, increased protein synthesis, viral infection, temperature shock and energy depletion can lead to accumulation of unfolded or misfolded proteins in the ER, initiating ER stress."

It's good to try to understand the effects EBV has on the cell.
 

Mij

Senior Member
Messages
2,353
I tested negative for all herpes viruses with my sudden onset 24yrs ago. I also received several vaccinations during this viral period which may have caused a further down-regulation of my immune system.

I tested negative by PCR to many viruses 14yrs ago- nothing positive, but when I took immune modulators I got very ill and had extremely high titres to both HHV6 and EBV. It gave me a relapse. Dunno.
 
Last edited:

Violeta

Senior Member
Messages
2,948
What type of immune modulators did you take, @Mij ?

And do you think that means that the viruses were in you all along but your body wasn't fighting them?
 

Mij

Senior Member
Messages
2,353
What type of immune modulators did you take, @Mij ?

And do you think that means that the viruses were in you all along but your body wasn't fighting them?

I dont' know.

When I first became ill my CD4, CD8 and ratio were all in normal range. After the relapse they all dropped below normal range and my ratio increased.
 

Violeta

Senior Member
Messages
2,948
That's interesting, @Mij , did it happen after the transfer factor, or not until after the Immunovir? I am specifically wondering because I have a friend that's taking transfer factor with no improvement.

I wonder what happened?
 

Violeta

Senior Member
Messages
2,948
I dont' know.

When I first became ill my CD4, CD8 and ratio were all in normal range. After the relapse they all dropped below normal range and my ratio increased.
I had to look up Immunovir, and found this:

"A synthetic purine derivative it is a precursor to adenosine which modulates many physiological processes including inflammation."

From reading in the Unfolded protein thread and seeing the connection between protein misfolding, endoplasmic reticulum stress, heat shock protein 70/90, and viruses, I am wondering if the immunovir did something to affect protein folding.
 

Eeyore

Senior Member
Messages
595
Excellent question!

I believe that because it has generally been believed that ME is some form of chronic infection, and this has been the most widely researched area (perhaps after psychobabble!!!!), and no real progress has been made, the infectious thesis is more "in the box." i.e. If something is not working, don't keep doing it.
 

Eeyore

Senior Member
Messages
595
@Violeta - Actually, I do think the unfolded protein response is quite possibly very relevant in this disease, and have been looking at it. It probably plays a role in many diseases, especially autoimmune.
 

Violeta

Senior Member
Messages
2,948
Excellent question!

I believe that because it has generally been believed that ME is some form of chronic infection, and this has been the most widely researched area (perhaps after psychobabble!!!!), and no real progress has been made, the infectious thesis is more "in the box." i.e. If something is not working, don't keep doing it.

It's working for me, and several other people here have already stated that it's helping them. It might not be the complete picture, but if it is part of one's picture, why wouldn't they want to deal with it?

Even with respect to endoplasmic reticulum stress, if you have a virus and don't factor that in, you will most likely be unsuccessful in dealing with your issues. Actually, you could even make your issues worse.

Also, it's possible that when it is said that no real progress has been made, one might be only looking at it from the pharmaceutical point of view, because there does not seem to be answers available from the pharmaceutical companies. Many drugs have been hailed as being helpful for ME/CFS, only to prove a huge let down, not to mention making some much worse.
 

Violeta

Senior Member
Messages
2,948
My point with the VZV was mostly in response to @Valentijn, that at least in a few cases (HHV6 / VZV), I produce normal antibodies to herpes viruses. I would expect the general population to show similar results to mine. @Valentijn makes an interesting point though about whether it's possible that someone like me has EBV but isn't producing antibodies anymore - I suppose it's possible.

I don't believe there is anything really unique about us and herpes viruses. I think we just have the same viruses with the same frequency as everyone else.

My VZV titers didn't drop as far as I know - it's not something I've tested that much. They were normal though (although lab would say abnormal in that they indicate exposure to the virus, and "normal" would be no exposure, which by my age is almost unheard of).

My own belief is that herpes viruses are just red herrings for ME patients and have nothing to do with our illness. I think there are a few factors that led to this happening. First, I think it goes back to Dr. Strauss at the NIH not wanting to accept he had a brain tumor and experiencing seizures, instead trying to blame his CFS on EBV - he later died of that brain tumor though (read Byron Hyde's personal accounts of this).

The other factor is that we get a lot of blood tests. Most come back normal. The first things that will usually jump out as abnormal (and be flagged as such by the lab) are elevated titers for common herpes viruses like VZV and HHV6. As a result, patients think this is really abnormal, when what would be more abnormal is to have no evidence of exposure to VZV or HHV6 (although the lab would mark this as normal).

Lastly, EBV has long been associated with prolonged fatigue (with mono / glandular fever) lasting months after infection, and because our disease was so unfortunately named, many docs jumped to EBV as being the case of fatigue. It was a reasonable hypothesis, but over time, studies failed to show any connection with ME. Ultimately we must think scientifically and toss out theories that are scientifically refuted. Holding on to bad theories just hurts us because we can't get to the root of the problem.

In summary, I don't think herpes viruses are important to ME pathogenesis, other than that they, like other infectious and non-infectious causes, can serve as the initial trigger. I feel we've wasted too much time and too many resources hunting for a mystery pathogen that is not there.

Which part of this is "evidence"?
 

Eeyore

Senior Member
Messages
595
The evidence that herpes viruses are not important in the disease is that we have the same average titers, same levels of seropositivity, and same reactions in general. We don't all suffer unusual herpesvirus outbreaks. If immunity to herpes viruses were impaired, there would be an array of symptoms one would expect, such as lots of cold sores, high rates of shingles, etc.
 

Violeta

Senior Member
Messages
2,948
The evidence that herpes viruses are not important in the disease is that we have the same average titers, same levels of seropositivity, and same reactions in general. We don't all suffer unusual herpesvirus outbreaks. If immunity to herpes viruses were impaired, there would be an array of symptoms one would expect, such as lots of cold sores, high rates of shingles, etc.

What about epstein barr virus?
 

Eeyore

Senior Member
Messages
595
Also, it's possible that when it is said that no real progress has been made, one might be only looking at it from the pharmaceutical point of view

I'm not thinking about treatments when I say that. I'm thinking about understanding the basic cause of the illness. Trying to treat first is putting the cart before the horse. First, you have to know what you are dealing with.

That doesn't mean we shouldn't use a treatment if it's effective, although treatments should be rigorously tested - and the problem is that there just isn't money for it. Nancy Klimas has been trying to test anakinra for years, but it's too expensive (it's an immunosuppressant - specifically, it blocks interleukin 1). She can't get funding. Fortunately the rituximab trials seem to be going very well. The general efficacy of immunosuppressive drugs does suggest to me that the disease is more likely to be autoimmune than infectious, as treating a virus with rituximab or anakinra would make patients worse (and could even be life threatening). These drugs are known to cause serious viral illnesses not found in immunocompetent patients, such as JC virus, which can be fatal. It's common in the population but almost never causes issues in healthy people (maybe never).

I think the most useful part about the rituximab trial is that it can give us new understanding into the disease process. This is the only real hope of making us all feel better. In the mean time we are just using trial and error. Sometimes it works, and I do get why we do it (nothing better) - but the real solution comes from understanding the disease process, and right now, that is where our efforts should be directed.