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Antiviral Antibodies against EBV and Neurotransmitters in Patients with Fibromyalgia

deleder2k

Senior Member
Messages
1,129
Antiviral Antibodies against EBV and Neurotransmitters in Patients with Fibromyalgia

Abstract
Fibromyalgia (FM) is characterized by chronic widespread pain lasting for a minimum of three months, and pain at mechanical pressure in at least 11 of the 18 tender points. The cause of fibromyalgia is unknown. Several hypotheses have been developed including "central sensitization". This theory proposes that fibromyalgia patients have a lower threshold for pain because of increased reactivity of painsensitive neurons in the spinal cord or brain. Some researchers supposed that different neurotransmitters (serotonin, catecholamine) could be involved in the pathophysiology of fibromyalgia-associated symptoms. The connection of FM to different viral infections has been proposed. Epstein Barr Virus (EBV) has been considered a possible cause of FM because of similarity of symptoms, but so far, the connection has not been proven. The objective of this study was to determine the prevalence of antibodies (Abs) IgM and IgG against EBV, and respectively the presence of a viral infection in a group of patients with FM. We also analysed the association between the titter of the antiviral antibodies, some neurotransmitters (serotonin, noradrenaline and adrenaline) and different clinical symptoms. The obtained results revealed that high EBV IgG concentrations in the serum of patients with FM correlated with pain intensity and associated clinical symptoms. This is consistent with the fact that FM is connected to the immune response to certain infectious agents (e.g. EBV, CMV).

http://www.jneuro.com/neurology-neu...rs-in-patients-with-fibromyalgia.php?aid=7360


Can one conclude that FM is connected to immune response to EBV based on this? @Jonathan Edwards, is this proper science, or is this what you refer to as 'immunobabble'?
 

halcyon

Senior Member
Messages
2,482
The connection of FM to different viral infections has been proposed. Epstein Barr Virus (EBV) has been considered a possible cause of FM because of similarity of symptoms
That seems like a very tenuous thread with which to connect the two things, especially when one of those things is a ubiquitous human virus. I wasn't aware that mononucleosis caused any pain more than abdominal pain due to organomegaly.

You'd have to go way farther to prove an association like this, such as demonstrating active presence of the virus in nerve centers associated with the painful areas, etc. Herpes viral titers are pretty close to being meaningless.
 
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SOC

Senior Member
Messages
7,849
Herpes viral titers are pretty close to being meaningless.
In healthy people perhaps. According to several of my doctors, including my GP, herpesviral titres are not meaningless in HIV patients, transplant patients, and others with immune dysfunction. The question for MS, ME, and other poorly-understood-illness patients, is whether herpesviral titres are meaningless in us.

There is also some question about the relevance of high herpesviral titres in patients who are decades from the original infection and whose antibody levels should have dropped. There's a reason they recommend the shingles vaccine (aka chicken pox booster) to older people -- our herpesviral (VZV/HHV3 in that case) antibody levels drop below safe levels over the years. High titres at that age are distinctly abnormal.

Additionally, herpesvirus titres should drop slowly after the initial acute infections. Herpesvirus titres that increase over time suggest an active infection against which the body is attempting to mount an increased antibody defence.

Over-simplified rules of thumb only apply to the very specific case for which they were designed -- in this case, healthy young people within a decade or so of the initial herpesviral infection. In that case, high antibody titres could be completely normal and no reason for concern. The problem arises when the rule of thumb is applied far outside it's range of applicability -- to increasing titres in seriously ill, immune disordered patients decades past their initial acute infection, for example.

Herpesviral antibody titres are far from a 100% perfect one-step diagnositic tool (What is?) There are a number of complications to take into consideration, so it's not a black/white, yes/no test. However, as a tool used along with other data about the entire clinical picture, it can be quite useful in a number of cases. It's only worthless to doctors who don't want to take the trouble to use their brains, look at the entire picture, and actually do a complete evaluation of the situation. Ya know, critical thinking.... evaluation, synthesis, that kind of thing.
 

halcyon

Senior Member
Messages
2,482
According to several of my doctors, including my GP, herpesviral titres are not meaningless in HIV patients, transplant patients, and others with immune dysfunction.
Those types of patients have clear signs of pathology due to the reactivation though, i.e. CMV retinitis/gastroenteritis/colitis, etc. There are no such clear signs in ME patients.
 

SOC

Senior Member
Messages
7,849
Those types of patients have clear signs of pathology due to the reactivation though, i.e. CMV retinitis/gastroenteritis/colitis, etc. There are no such clear signs in ME patients.
You mean currently known signs of pathology, I believe. We can't claim that we know everything yet. It seems this article is suggesting that there are additional signs of pathology in some patients/conditions that have not been recognized or acknowledged. This is quite possible. There's quite a lot we don't know about how herpesviruses affect the human body under different circumstances. Also, quite a few PWME do have symptoms very similar to acute EBV and HHV6 infection, so we can't say there are no signs of pathology in them, either.

I think we can agree that there's no certainty whatsoever about how various herpesviruses play into the pathology of poorly understood conditions like ME, fibro, and MS. They could play no part, or a significant part. We simply don't have the data to say for sure one way or the other. There's definitely no reason to dismiss herpesviruses out of hand. Plenty of researchers are looking into herpesviruses as a contributing factor in neurological and neuroimmune conditions. Time will tell, one way or another. I just hope I'm still around when we find out, because I'm very curious to know how that particular line of research plays out.
 

Jonathan Edwards

"Gibberish"
Messages
5,256
Antiviral Antibodies against EBV and Neurotransmitters in Patients with Fibromyalgia

http://www.jneuro.com/neurology-neu...rs-in-patients-with-fibromyalgia.php?aid=7360

Can one conclude that FM is connected to immune response to EBV based on this? @Jonathan Edwards, is this proper science, or is this what you refer to as 'immunobabble'?

The abstract does not contain the basic elements I would consider necessary to call this a scientific communication. God knows why journals publish things like this now. It looks entirely unsubstantiated. I think I might classify as immunoamateur rather than immunobabble. Or maybe flogging a dead horse.
 

SOC

Senior Member
Messages
7,849
The symptoms of FM are nothing like acute EBV.
Did anyone say they are? o_O They found some symptoms of FM that correlated to high EBV IgG titres so they might be previously unrecognized symptoms of chronic EBV pathology. A number of symptoms of ME/CFS (not FM) are similar to acute EBV and/or HHV6.
 

barbc56

Senior Member
Messages
3,657
@Jonathan Edwards

Is Fibromyalgia now considered a neurological disorder or does it depend or not answered at thisvtimea.? Mine started with a complicated broken arm and wrist and then about two (?), possibly less, months later the "pain" which feels like you have the flu, a vampire sucking out your bone marrow while running a fever of 106 but with no fever, no vampire.;)

I sometimes call FM the Princess and the Pea syndrome.

I see a neurologist and he tends to think this, but then he IS a neurologist.

Barb
 

Jonathan Edwards

"Gibberish"
Messages
5,256
@Jonathan Edwards

Is Fibromyalgia now considered a neurological disorder or does it depend or not answered at thisvtimea.? Mine started with a complicated broken arm and wrist and then about two (?), possibly less, months later the "pain" which feels like you have the flu, a vampire sucking out your bone marrow while running a fever of 106 but with no fever, no vampire.;)

I sometimes call FM the Princess and the Pea syndrome.

I see a neurologist and he tends to think this, but then he IS a neurologist.

Barb

Dear Barb,
I am beginning to get an idea of ME/CFS but so far I have not got my head around fibromyalgia. Part of the problem is that a lot of doctors use the term just to have a clever word to say. In my medical career I never met a patient with a condition that I think deserved being called fibromyalgia - but then maybe people with FM were never referred to me. I did not get many people with ME referred to me.
 

A.B.

Senior Member
Messages
3,780
@Jonathan Edwards

Alan Light has found receptor antibodies in ME/CFS patients with POTS and orthostatic intolerance, similar to the ones reported by Scheibenbogen.

At 24:30.

 

Hip

Senior Member
Messages
17,824
For both fibromyalgia and ME/CFS, I'd like to see a high throughput sequencing study that determines the genetic strains of EBV (and other viruses like enteroviruses) present in patients. A recent study found multiple sclerosis was strongly associated with specific genetic strains of EBV.
 
Messages
2,087
@Jonathan Edwards

Alan Light has found receptor antibodies in ME/CFS patients with POTS and orthostatic intolerance, similar to the ones reported by Scheibenbogen.

At 24:30.

Just watched this briefly, is the following correct :
All these CFS patients had POTS or OI yet a similar % had the elevated autoantibodies that were in the Scheibenbogen paper. Does this imply there is no relationship between POTS, OI and these autoantibodies?
 

halcyon

Senior Member
Messages
2,482
Just watched this briefly, is the following correct :
All these CFS patients had POTS or OI yet a similar % had the elevated autoantibodies that were in the Scheibenbogen paper. Does this imply there is no relationship between POTS, OI and these autoantibodies?
This is the part I'm not understanding. Non POTS/OI patients and some controls have the same autoantibodies.
 
Messages
1
It was indeed a mistake. I have uploaded a pdf with the correct figure. It was my fault since I make all my own slides. I was using the BR2A as a template and forgot to copy in the M2R values to replace the template.
 

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