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No serological evidence for a role of HHV-6 infection in chronic fatigue syndrome ?!

PhoenixBurger

Senior Member
Messages
202
Tried everything you've suggested plus a million more ideas.

Yes, I and several others dealing with benign fasciculation syndrome were sick with a flu-like illness prior to onset of symptoms. Do you know which enteroviruses are associated with fasciculations/spasms/twitching? Are there treatments in the form of antivirals?
 

Hip

Senior Member
Messages
17,824
Tried everything you've suggested plus a million more ideas.

Yes, I and several others dealing with benign fasciculation syndrome were sick with a flu-like illness prior to onset of symptoms. Do you know which enteroviruses are associated with fasciculations/spasms/twitching? Are there treatments in the form of antivirals?


Not sure, though the enteroviruses most commonly associated with long-term infection and long-term symptoms are coxsackievirus B and echovirus. These are also the enteroviruses strongly linked to precipitating ME/CFS. Dr John Chia is the world's leading clinical expert on enterovirus-associated ME/CFS, and he uses interferon therapy, ribavirin and oxymatrine as antiviral treatments. Oxymatrine you can buy online as a supplement.

Some Dr Chia weblinks for you:
Oxymatrine | Phoenix Rising
Dr. Chia On Oxymatrine, Autoimmunity, ME/CFS and FM | Phoenix Rising
Interferon | Phoenix Rising
NIH State of Knowledge Workshop: Pathogens II (EBV and Enteroviruses) | Phoenix Rising
An Interview With Dr. John Chia, M.D. Part I by Cort Johnson (8/08) | Phoenix Rising
An Interview With Dr. John Chia M.D. Enteroviruses and Chronic Fatigue Syndrome Part II: Persistence, Treatment and the Future by Cort Johnson. | Phoenix Rising
Ribavirin and Interferon- for the Treatment of Patients with Chronic Fatigue Syndrome Associated with Persistent Coxsackievirus B Infection: A Preliminary Observation
The role of enterovirus in chronic fatigue syndrome
Chronic fatigue syndrome is associated with chronic enterovirus infection of the stomach
Acute enterovirus infection followed by myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and viral persistence
 

PhoenixBurger

Senior Member
Messages
202
Thank you. This may sound absurd but I dated a girl several years ago who had polio as a child. She had some pretty bad disability even though she said the virus was long gone from her system. Is it possible that may not be the case, and I acquired something from her?
 

mellster

Marco
Messages
805
Location
San Francisco
Tried everything you've suggested plus a million more ideas.

Yes, I and several others dealing with benign fasciculation syndrome were sick with a flu-like illness prior to onset of symptoms. Do you know which enteroviruses are associated with fasciculations/spasms/twitching? Are there treatments in the form of antivirals?
Hi Phoenix, my onset in september 2009 was infectious for weeks then abated, then there was a 18 month period of recurring stomach cramps/gastritis and malabsorption during which twitching developed, first after workouts only, then constantly at least a couple of times per day, then I crashed in spring 2011 and remember sometimes waking up at night because my cheek was twitching. I stopped all exercise for 5 months and went onto heavy supplementation, then resumed slowly. I also got the MAF314 and can vigorously exercise again, but still have very mild occasional inflammation, a reactive lymph node and the twitching is almost completely gone, although it is still more frequent then before I got the infectious onset. I believe BFS is an expression of your immune system at work and there are a lot of papers on it. I think it can stay with you for years but should not become permanent. I should say I am still on the MAF314 and still heavily supplement which is a moving target. The only thing that was proven high in IGG was EBV, so I believe it may have been onset and/or reactivation and chronic. Hope this helps, all the best.
 

Hip

Senior Member
Messages
17,824
Thank you. This may sound absurd but I dated a girl several years ago who had polio as a child. She had some pretty bad disability even though she said the virus was long gone from her system. Is it possible that may not be the case, and I acquired something from her?

My view is that each person we kiss and/or have sex with, no matter how healthy they are, we probably pick up at least one chronic pathogen from them (and they probably pick up one or more bugs from us) if the relationship goes on for a while. The pathogen(s) transmitted could be viral, bacterial, fungal, protozoal, or a helminth.

It is only now, in hindsight, with my ME/CFS precipitated by a nasty chronic sore throat virus I picked up, that I have become very aware of the link between catching pathogens and these pathogens precipitating chronic diseases.

I remember when I started going out with one girl (this was 20 years ago). Within the first two weeks of our relationship (which was sexual from day one), I suddenly started getting overactive bladder (a disease involving an uncontrollable desire to urinate). I never had any problems like that at all. Indeed, prior to that I had an excellent and very strong bladder. I could not figure out, at that time, why this overactive bladder condition had very suddenly happened to me. In retrospect, I think I must have picked up some pathogen from that girl, a pathogen that may have entered via my urinary tract, and then caused overactive bladder. Even today, I still have overactive bladder, even after all these years. Overactive bladder is a condition that may predispose you to getting fibromyalgia (it certainly is a common comorbid condition of fibromyalgia).

Then, some years later, from my next girlfriend, I suddenly had all the lymph nodes in my groin become swollen, weeks after commencing a monogamous sexual relationship with her. I think this was caused by me acquiring some pathogen in the groin area that caused lymph node inflammation. Sexual health tests at the time (and again later) found no sexually transmitted pathogens. But of course there are many other pathogens apart from the classic sexually transmitted ones. Antibiotics never helped. These groin lymph nodes are still swollen today.

In another relationship I had (which only involved kissing the girl), I suddenly developed IBS. Prior to that, my bowels and digestion were excellent. But almost overnight, I got IBS, within a month of that relationship starting. IBS has been linked to protozoal parasites such as Blastocystis hominis, and I think I may have picked up something like that from her.

Finally, the coup de grâce of my ill-health: I went on an evening date, only involving some kissing. On that fateful evening, I picked up a horrible sore throat through kissing (the sore throat appeared by the next day) — a vicious throat infection that would never go away. This sore throat virus rapidly spread to my stomach, intestines, lungs, sinuses, etc, and ended up precipitating ME/CFS, plus other ill-health conditions in me.

I have not had that many relationships in my life, but nearly all the ones I have had involved some completely new ill health condition starting very soon after the relationship commenced. And all the ill health conditions I have had started via relationships.

So that my story of the pathogens we can pick up from our amorous relationships. I should add that I am a romantic person, and I don't want to portray the seeking of a relationship sound like a medical risk. But I think picking up new pathogens this way does happen, even if we are not aware of it.
 
Messages
15,786
Magnesium has been a great help for me too, regarding spasms, twitching, and muscle cramps. And keeping my bowels moving :p

Not all forms of magnesium are as effective, so maybe a different type would be helpful?
 

mellster

Marco
Messages
805
Location
San Francisco
Hip - I agree that it is likely common bacteria, parasites and viruses not linked to common STDs that get frequently exchanged during sexual encounters that can start episodes of chronic illness. One more reason though to believe that there is either an underlying genetic predisposition and/or a sleuth of life stressors reigning in all at once, or (less likely IMO) a stealth pathogen making the patients more susceptible than the rest of the population.
 
Messages
15,786
Magnesium Citrate is supposed to be a good form, and works well for me. I use Jarrow's Magnesium Optimizer (Citrate), which also has a small amount of potassium citrate. Taking 2 per day seems to get rid of most of the twitching/spasms/cramps, though all bets are off when crashing.

Magnesium oxide is the cheap stuff, and will just give you diarrhea (or get things moving if taken when constipated). Chelated magnesium is supposed to be good, but just gave me diarrhea too.
 

AFCFS

Senior Member
Messages
312
Location
NC
Magnesium has been a great help for me too, regarding spasms, twitching, and muscle cramps. And keeping my bowels moving :p

Not all forms of magnesium are as effective, so maybe a different type would be helpful?
Magnesium orotate has been great for me. For me, it does not provide the more immediate bowel clearing of magnesium citrate and brings quite a bit of calm/relaxation in short order.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
There is nothing wrong with replication studies, but this has been studied before, ad nauseum. The authors don't review the literature on this topic- Dr. Knox and Dr. Ablashi have reviewed it before. See www.hhv-6foundation.org.

In short, the overwhelming majority of studies that use methods capable of distinguishing active and latent infections show a significant association between active HHV-6 and ME/CFS. Studies that do not use methods that distinguish active and latent infections, including serological studies, have failed to show an association.

The conclusion: ME/CFS patients are no more likely than healthy people to have been infected with HHV-6 at some point. Antibody titers alone, without showing recent 4-fold rise in titer, are not reliable indicators of active infection. But, ME/CFS patients are more likely to have this virus actively replicating in their blood and spinal fluid.

This are the key arguments that I am thinking about at the moment. Latent enteroviral infections ... latent is a poor word. It turns out enteroviruses have three lifecycles, and only one of those shows up in serological testing (probably). The other two are tissue based lifecycles, and do not induce viremia and only rarely induce cell lysis. Data from Lerner suggests the same thing might happen with herpes viruses ... which could explain a lot. Without blatant viremia it is less likely that antibodies will be made, so antibody data is suspect. What Lerner recently showed though is we have unique herpes antibodies. We have antibodies to the inside of these viruses, not the capsid. This fits the alternate lifecycle hypotheses.

The big question for me though is whether this represents opportunistic infections, where weaknesses in our immunity mean that alternate viral lifecycles cannot be removed, or whether it is causal.

Bye, Alex
 

heapsreal

iherb 10% discount code OPA989,
Messages
10,089
Location
australia (brisbane)
I think when it comes to the herpes viruses and probably other viruses the terms reactivate and replicate get mixed up. replicate is when more virus are being made where reactivate the viruses are just doing their job of making us feel like crap. This is also why one can still feel crappy on antivirals as antivirals just stop replication, not reactivation and is why one has to be on avs for a long time as we have to wait for the viruses to die out or for viral load to be low enough that the immune system can take care of it.

So i think the so called latent virus is still reactivating(maybe at a lower level) but just not replicating, if that makes sense??
 

Butydoc

Senior Member
Messages
790
I think when it comes to the herpes viruses and probably other viruses the terms reactivate and replicate get mixed up. replicate is when more virus are being made where reactivate the viruses are just doing their job of making us feel like crap. This is also why one can still feel crappy on antivirals as antivirals just stop replication, not reactivation and is why one has to be on avs for a long time as we have to wait for the viruses to die out or for viral load to be low enough that the immune system can take care of it.

So i think the so called latent virus is still reactivating(maybe at a lower level) but just not replicating, if that makes sense??
I believe reactivation of a virus does imply that it has gone from a latent phase to a replicating phase. I also believe what makes us feel sick is the immune response to the virus. I asked the same question to Dr. Montoya and was given this answer.

Gary
 

heapsreal

iherb 10% discount code OPA989,
Messages
10,089
Location
australia (brisbane)
I believe reactivation of a virus does imply that it has gone from a latent phase to a replicating phase. I also believe what makes us feel sick is the immune response to the virus. I asked the same question to Dr. Montoya and was given this answer.

Gary
I could be wrong but my thinking is that reactivation is that the virus is no longer dormant and is then living off the host, us. I suppose the virus has to be reactivating to replicate but i think the two are still seperate. I make this assumption as antivirals stop viruses from replicating but the active virus is whats making us feel unwell and also like u mentiuon the immune response makes us feel unwell through inflammatory cytokines etc etc

On antivirals we still 'crash' but the severity of the crashes are reduced. I feel that the crashes still occurr because of viruses reactivating but the severity is lessening due to the replication being interrupted by antivirals and viral load reduces???? Also lerner i think has mentioned that parts(lytic)of the viruses can still cause immune responses making us feel unwell. I suppose antivirals can still affect these part of viruses??

Hopefully there are more scientists working on this then just us having a guess. As mentioned earlier about the different life cycles of viruses, once they work it out maybe they can then treat the viruses at the different life cycles it has and possibly irradicate the viruses all together, i hope.
 

AFCFS

Senior Member
Messages
312
Location
NC
I will need to ask my doc this, but am interested in knowing how others may have had LabCorp HHV6 interpreted with the HHV 6 IgG Antibodies with a HIGH index score, where the ranges are identified as:

Negative < 0.76
Equivocal 0.76 - 0.99
Positive > 0.99
And
HHV 6 IgM is Negative:
Negative < 1:10

I know this has been tossed around before, and have read this (http://www.hhv-6foundation.org/patients/patient-faq):
Dr. Jose Montoya, an infectious disease specialist at Stanford University, uses IgG antibody tests done by IFA to determine whether patients qualify for antiviral treatment since PCR DNA tests are insensitive. (This virus is found mostly in the tissues and not in the blood, so it is more productive to look for indirect evidence of HHV-6 in the form of unusually elevated antibody levels). Montoya uses the HHV-6 IgG test at Focus Diagnostics Laboratory. Other labs that offer the IFA test (which is reported as a titer such as 1:160 instead of a single number) include Specialty Laboratories and Medical Diagnostics Laboratory. Quest Diagnostics owns Focus Diagnostics so you may be able to get the Focus test through Quest. (Ask your local Quest office if they send their HHV-6 testing to Focus.) For more information about testing options, please refer to the Testing page on our website.
and this (http://www.hhv-6foundation.org/patients/hhv-6-testing-for-patients):
Overview on Testing for HHV-6 infection
Nearly 100% of us are infected with HHV-6 by early childhood. This initial infection has caused our bodies to develop HHV-6 antibodies to fight against future HHV-6 viral infection or reactivation. In addition, at least 30% of us have small but consistently detectable levels of inactive (latent) HHV-6 virus that persist harmlessly in the blood into adulthood—many times never reactivating or becoming active over the course of a lifetime. Therefore, the relevant question when testing for HHV-6 infection is not whether you have HHV-6 virus or antibodies present in your blood, but rather is the virus active or latent? Unfortunately, this is not an easy question to answer. Two signs of an active infection are (1) viral DNA in your plasma or serum (as opposed to blood), and (2) unusually elevated antibody titers, on an IFA test. A PCR test on blood identifies both latent and active infections, so it is not helpful in answering this question unless it is a quantitative test.

TEST
Can it differentiate active from latent infection?
Comments
ELISA IgG test
Example: “positive >1.0″ No. These results are intended to give only “yes/no” answers to whether you are exposed to the virus in the past. An ELISA> 5 in an adult MIGHT be a clue of an active infection, but only the antibody tests done by IFA can tell you with precision how elevated the antibodies are.
IFA IgG test
Example: Titer 1:640 Sometimes! If the titer is highly elevated, it means that the patient has had a recent infection or currently has a chronic infection. Titers vary by laboratory. Focus Diagnostics (Quest) has a median antibody titer between 1:80 and 1:160 for controls. Other labs have much lower control titers. If the patient has an immune deficiency with low total IgG, then the antibody titer will not be elevated. If HHV-6 is the only antibody titer out of five viruses to be elevated above average, then this indicates possible HHV-6 infection.
IgM test
(ELISA or IFA) Yes. IgM only appears during an active infection or for 2-3 months after an active infection. The absence of an IgM antibody does not mean you do not have a active infection. Low level infections can perist with no evidence of IgM.
PCR DNA test on plasma or serum
(qualitative or quantitative) Yes. HHV-6 is never found in plasma or serum unless there is an active infection. However, the absence of HHV-6 DNA in the plasma/serum does not mean that there is no active infection. HHV-6 does not circulate in the plasma/serum except during the initial infection and transiently during an acute infection. Any positive test result should be repeated with a quantitative test. Also, a whole blood test should be ordered to rule out chromosomally integrated HHV-6 which occurs in 1% of the population. (See CIHHV-6) Someone who inherits HHV-6 in the chromosome will always be positive in the serum, whether the HHV-6 is active or not.
Quantitative PCR DNA test on whole blood
Example: 1200 copies/ml Yes. If the viral load is >200 copies per ml or 20 copies per microgram of DNA then this is an active infection. Healthy persons will have very low viral loads, typically less than 20 copies/ml in the whole blood.
Qualitative PCR DNA test on whole blood
Example: “Positive” with no numerical value given No. This test is useless for differentiating active from latent infection, and should be avoided. Most healthy individuals have small levels of latent HHV-6B in the blood. This test can be useful for determining if you have HHV-6A or HHV-6B Finding HHV-6A DNA is unusual and follow up testing might be worthwhile.

While both LabCorp and Quest laboratories offer a basic qualitative ELISA test for HHV-6, additional testing is necessary to determine a proper diagnosis of HHV-6 infection for the reasons listed above. FOCUS Diagnostics, a division of Quest Laboratories, offers many of the above tests that may help to properly identify an HHV-6 infection. Patients may have blood drawn at any Quest laboratory, and request that these specific testing inquiries be forwarded to FOCUS Diagnostics to ensure proper results.
***************************************************************************************************************
As mentioned, mine was done by LabCorp, so not sure if that means another test is needed if HHV 6 IgG Antibodies with a HIGH index score.....
 

heapsreal

iherb 10% discount code OPA989,
Messages
10,089
Location
australia (brisbane)
I will need to ask my doc this, but am interested in knowing how others may have had LabCorp HHV6 interpreted with the HHV 6 IgG Antibodies with a HIGH index score, where the ranges are identified as:

Negative < 0.76
Equivocal 0.76 - 0.99
Positive > 0.99
And
HHV 6 IgM is Negative:
Negative < 1:10

I know this has been tossed around before, and have read this (http://www.hhv-6foundation.org/patients/patient-faq):

and this (http://www.hhv-6foundation.org/patients/hhv-6-testing-for-patients):

***************************************************************************************************************
As mentioned, mine was done by LabCorp, so not sure if that means another test is needed if HHV 6 IgG Antibodies with a HIGH index score.....

Trying to not sound like a broken record but another test to help verify active infection is a lymphocyte subset test where cd t cells are measured, cd8 t cells are commonly high in active herpes infections.
http://www.sydpath.stvincents.com.au/tests/ImmunoFrames/lymphocytosis.htm
unsure if cd8 t cells high in hhv6 but they are high in ebv and cmv so one would think also high in hhv6??
 

AFCFS

Senior Member
Messages
312
Location
NC
Trying to not sound like a broken record but another test to help verify active infection is a lymphocyte subset test where cd t cells are measured, cd8 t cells are commonly high in active herpes infections.
http://www.sydpath.stvincents.com.au/tests/ImmunoFrames/lymphocytosis.htm
unsure if cd8 t cells high in hhv6 but they are high in ebv and cmv so one would think also high in hhv6??
Thanks, sometimes if we hear the record enough it may sink in :).

I did have the % CD8-/CD57+ Lymphs and Abs. CD8-CD57+ which were both relatively low in the reference interval (think this is in line with what was being referenced. Lacking the CMV and the EBV in any signifcant results, just thinking that also with chlamydia pneumoniae igg high, mycoplasma pneumoniae igg abs high, hhv 6 igg antibodies high and the assoiated IgM values negative, if it start to looks more like the body is just hammering away at something that is not there anymore but sees as a threat or if there is another interpretation.

Had two docs suggest, without knowing any lab results, that a run of antibiotics would likely not hurt anything but may help, or at the very least give a better clinical picture.
 

heapsreal

iherb 10% discount code OPA989,
Messages
10,089
Location
australia (brisbane)
if u have myco and cpn then a few weeks of doxy could be diagnostic for you, although 2 things can say its working, 1 u will feel like crap as u having a die off reaction and 2 u will feel better. Treating these could be enough to take the load off your immune system and allow it to go after the viral stuff like hhv6??
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
One of the reasons I don't like talking of latent vs. reactivating any more is that this is all within the framework of a viral lytic lifecycle. What about the minimally lytic and non-lytic lifecycles? Viruses can be active in those, and reactivate, without inducing viremia and therefore showing normal in serological testing. Only a biopsy has a chance of seeing what is really going on. So far this is only strongly supported for enteroviruses so far as I am aware, but the a lot of findings by Lerner fit with this.

So it is entirely possible to have a reactivated virus that shows no viremia. What it does mean though is the virus is again affecting cellular chemistry.

So far as I am aware all of this research is still inside virology. I do not know if there would be many doctors who are aware of it. I hope to investigate this more in the coming months.
 
Messages
88
Location
Canada Niagara Falls
This are the key arguments that I am thinking about at the moment. Latent enteroviral infections ... latent is a poor word. It turns out enteroviruses have three lifecycles, and only one of those shows up in serological testing (probably). The other two are tissue based lifecycles, and do not induce viremia and only rarely induce cell lysis. Data from Lerner suggests the same thing might happen with herpes viruses ... which could explain a lot. Without blatant viremia it is less likely that antibodies will be made, so antibody data is suspect. What Lerner recently showed though is we have unique herpes antibodies. We have antibodies to the inside of these viruses, not the capsid. This fits the alternate lifecycle hypotheses.

The big question for me though is whether this represents opportunistic infections, where weaknesses in our immunity mean that alternate viral lifecycles cannot be removed, or whether it is causal.

Bye, Alex
Alex I am very interested in this line of thinking it really starts to make sense. If you could point me in the right direction for lerners info on herp viruses I would be greatful...thank you
Gary K