Article: Light on ME/CFS III: A Different Herpes Virus for CFS? - Varicella-Zoster, Shingles and ME/

Article: Light on ME/CFS III: A Different Herpes Virus for CFS? - Varicella-Zoster, S

You can view the page at http://forums.phoenixrising.me/content.php?449-Light-on-ME-CFS-III-A-Different-Herpes-Virus-for-CFS-Varicella-Zoster-Shingles-and-ME-CFS

 

these herpes viruses have lived in harmony with humans since the beginning..why would they be causing this disease now?

something wrong with this theory.

 

interesting, but wouldn't explain the brain inflammation that many of us have. I'm glad to have novel theories looked at (I hope there's enough funding to go around, though), but this one doesn't seem to have enough explanatory power. Something like this could be contributory, though.

 

Hi all, like Daffodil, I'm rather sceptical about this, as she says, whats suddenly changed to explain this new/increasing problem of ME?

You could speculate that the chickenpox vaccination is more likely to cause damage/reactivate/whatever than naturally caught chickenpox, which is a change, but too recent to explain outbreaks of ME which have been going on since the 1930s/1950s. Or are we further supposing that ME has always existed but was hidden by polio(atypical polio) until recently? Too speculative for me.

Having said all that I know I have poor ability to fight/suppress chickenpox. I got it 3 times when I was little, which my mother and doctor considered rather unusual. Perhaps in my case it has now reactivated as CFS and is insufficiently suppressed by aciclovir.

I have no argument with people making testable hypotheses (which this sounds like to me) and it has the advantage of being much less controversial than the retrovirus hypothesis.

Personally I think the retrovirus hypothesis fits the observations better as far as I can see, despite the hysteria which has dogged and fogged its investigation, I would hate to see that avenue closed down before its fully investigated.
OTH

ETA looks like willow and I were thinking roughly the same thing but I rambled and posted second. Now I'm wondering whether there is a chickenpox vaccination or I am confusing it with measles. Oh no, I blame the bronchitis brain fog which is a good excuse:In bed:.

 

these herpes viruses have lived in harmony with humans since the beginning..why would they be causing this disease now?

something wrong with this theory.

The whole herpesvirus theory with CFS is that yes, the herpesviruses do tend to live in harmony with humans much of the time but that is not because they are benign but because the immune system is able to keep them bottled up. In fact herpesviruses are kind of an odd man out in the viral world because usually our immune system is able to fight off and REMOVE the viruses our bodies encounter. With herpesviruses it is able to fight them off but it can't remove them - not a good thing.

When some latent herpesviruses become reactivated they're know to cause a wide variety of horrendous problems including meningitis and other nervous system disorders and shingles and other disorders. EBV causes lymphoma and nasal cancer. CMV causes retinitis, HHV8 causes karposi's sarcoma. They are being investigated in a wide variety of autoimmune diseases. People with immune suppression after cancer have to be very careful not to let the latent herpesviruses in their systems loose.

So, yes they are generally latent in healthy peoples bodies but tweak their immune systems the wrong way and let the herpesviruses out you have real problems.

 

interesting, but wouldn't explain the brain inflammation that many of us have. I'm glad to have novel theories looked at (I hope there's enough funding to go around, though), but this one doesn't seem to have enough explanatory power. Something like this could be contributory, though.

The problem with the brain inflammation is that there's just not enough of it to explain CFS. Brain inflammation studies have not found the high degrees of brain inflammation researchers feel is needed to account for the kind of debility found in CFS. If it had been there - our history would be very different.

MRI studies never showed large areas of inflammation in the brain in CFS. They showed, as I remember, areas of punctuated white objects or whatever they were, that were scattered across the brain in different areas in different individuals - making it difficult to state that these objects were causing CFS. If they had all been found in one area - that would have made a difference - but finding them in different areas made it difficult to say what they were doing. That doesn't say that some people don't have high levels of inflammation in the brain but the Incline Village studies did not find that consistently - at least as I remember.

One of the attractive aspects of this theory for me is that it doesn't rely on a brain infection - it relies on nervous system structures in the body that could effect the brain that have fewer viral defenses than the brain or other parts of the body and which are known centers of herpes virus infection.

Shapiro does note that these herpesvirus infections could ultimately result in brain infections in the most severe cases.

I also want to point out that both enteroviruses and HIV have been found in the basal ganglia- so if XMRV does work out for CFS - its presence there is a possibility as well.

 

Spot on - great article. Would explain almost everything for me (had fairly intense chickenpox as a kid), esp. the shingle-like FM symptoms without rash and the reaction to overstimulation through totally different kind of stressors (emotional vs physical).

 

Great article, thanks Cort. Seems so simple, yet so very possible! I've always thought it odd that so many people with me/cfs report having had some type of symptom years before onset, yet I had none. Perfectly healthy before me/cfs. But the itching is one I've had forever. Episodes of severe, tear the skin off itching on my shoulders and arms (yet able to run marathons). hmmm

 

MRI studies never showed large areas of inflammation in the brain in CFS. They showed, as I remember, areas of punctuated white objects or whatever they were, that were scattered across the brain in different areas in different individuals - making it difficult to state that these objects were causing CFS. If they had all been found in one area - that would have made a difference - but finding them in different areas made it difficult to say what they were doing. That doesn't say that some people don't have high levels of inflammation in the brain but the Incline Village studies did not find that consistently - at least as I remember.

One of the attractive aspects of this theory for me is that it doesn't rely on a brain infection - it relies on nervous system structures in the body that could effect the brain that have fewer viral defenses than the brain or other parts of the body and which are known centers of herpes virus infection.

Hi Cort. These statements underline the weakness of the Shapiro inflammation theory, because it rules out or ignores the brain pathology. There is mounting evidence that the UBOs are evident in me/cfs (even if only a subset) and that a defining CDC study that failed to find UBOs was deeply flawed. Simply saying that there is no current explanation for cause and effect is not evidence of no cause and effect.

It also ignores mounting evidence of brain abnormalities in SPECT and qEEG studies.

Furthermore, it ignores the considerable volume of work on intrinsic cellular dysfunction, particularly mitochondrial dysfunction and reduced ATP production.

As you say, Shapiro's work is currently just a theory (and also only applicable to a subset) with considerable less supporting research than already exists for the readily identifiable UBOs.

 

Not likely to be the cause for ME. It may be for a subset of CHF patients. Those punctate lesions in the brain are similar to AIDS dementia findings in the brain and to atypical MS. They indicate a more severe neurological disease. Much more similar to a pattern of retrovirus infection.

I guess it might not be a big deal if you don't have them in your brain. It takes on a whole new urgency when you know something is slowly destroying your brain and cognition.

 

Not likely to be the cause for ME. It may be for a subset of CHF patients. Those punctate lesions in the brain are similar to AIDS dementia findings in the brain and to atypical MS. They indicate a more severe neurological disease. Much more similar to a pattern of retrovirus infection.

I agree a retrovirus is the best fit so far, but that does not rule out all sorts of other things, such as VZV in the DRG as also part of the package for a subset.

The coming year/s will be interesting indeed for those who can find a way to hang on.

Most interestingly, my husband's new Doctor at a specialist clinic in Edmonton, Canada, treating only complex senior's health issues, figured out yesterday that the very painful rash John has had on his bum for 4 months is classic shingles. John started on Lyrica just yesterday and the pain has already subsided significantly.

I can't wait to share this thread with J's new doc in a couple of weeks. He is definitely NOT an ME/CFS specialist, but he is a guy who treats the whole body and is used to taking a very thoughtful, careful approach.

THANK YOU to all at Phoenix Rising for making this info available - years before the average Dr. would ever find it.

I guess it might not be a big deal if you don't have them in your brain. It takes on a whole new urgency when you know something is slowly destroying your brain and cognition.

Neurologists found those white spots in John's brain way back in 2003/4 when his headache issues were very severe - and attributed them to the number of falls John had had while bicycle racing. In watching John's cognition rather shockingly disappear since then I can't help but think they really are ME/CFS lesions. Too bad no one here, that I know of, knows much about what that looks like.

 

Hi Cort. These statements underline the weakness of the Shapiro inflammation theory, because it rules out or ignores the brain pathology. There is mounting evidence that the UBOs are evident in me/cfs (even if only a subset) and that a defining CDC study that failed to find UBOs was deeply flawed. Simply saying that there is no current explanation for cause and effect is not evidence of no cause and effect.

It also ignores mounting evidence of brain abnormalities in SPECT and qEEG studies.

Furthermore, it ignores the considerable volume of work on intrinsic cellular dysfunction, particularly mitochondrial dysfunction and reduced ATP production.

As you say, Shapiro's work is currently just a theory (and also only applicable to a subset) with considerable less supporting research than already exists for the readily identifiable UBOs.

The problem with the UBO's was that they were scattered across the brain (different sites for different people) - making it difficult to tie them to any one symptom or problem. Another problem is that while a big set of CFS patients had them - so do a significant number of healthy people. There seems to be something going on - because more people with CFS have them than do healthy controls but what they mean is really unclear. When you have people with the kind of lifelong and serious disability that you find in CFS I think researchers expect to find some really dramatic - like significant inflammation occurring in X area of the brain. So yes there is much more evidence that UBO's are present - but that hasn't, most unfortunately, lead anywhere that I know of. Perhaps in the future it will.

Actually if you put Shapiro's theory in tandem with the Lights theory (see part II) it can account for those things. THe DRG don't just send signals to the brain (that should be enough to alter brain activity) they also interact with the sympathetic nervous system. THe mitochondrial problems could be explained by a dysfunctional sympathetic nervous system that is not shuffling blood to the muscles - causing mitochondrial problem and cellular dysfunction. This is not to say as well that cellular (immune) dysfunction didn't allow pathogens egress to the DRG in the first place.

Viral presence in the DRG also gives the viruses an easier shot into the brain - which Shapiro acknowledges - so her theory doesn't necessarily negative brain abnormalities either.

This is not to say that Shapiro but there are possibilities.

 

I guess it might not be a big deal if you don't have them in your brain. It takes on a whole new urgency when you know something is slowly destroying your brain and cognition.

Agreed

 

I agree a retrovirus is the best fit so far, but that does not rule out all sorts of other things, such as VZV in the DRG as also part of the package for a subset.

The coming year/s will be interesting indeed for those who can find a way to hang on.

Most interestingly, my husband's new Doctor at a specialist clinic in Edmonton, Canada, treating only complex senior's health issues, figured out yesterday that the very painful rash John has had on his bum for 4 months is classic shingles. John started on Lyrica just yesterday and the pain has already subsided significantly.

I can't wait to share this thread with J's new doc in a couple of weeks. He is definitely NOT an ME/CFS specialist, but he is a guy who treats the whole body and is used to taking a very thoughtful, careful approach.

THANK YOU to all at Phoenix Rising for making this info available - years before the average Dr. would ever find it.

Neurologists found those white spots in John's brain way back in 2003/4 when his headache issues were very severe - and attributed them to the number of falls John had had while bicycle racing. In watching John's cognition rather shockingly disappear since then I can't help but think they really are ME/CFS lesions. Too bad no one here, that I know of, knows much about what that looks like.

What a timely report. That rash must have been really painful. Sorry to hear about your sons reduction in cognition - that must be a difficult thing to see. One of the more interesting things I found about Shapiro's paper was that VZV requires high doses of antivirals to be effective - just as is true for some people with CFS. Montoya, I believe, is also looking at other herpes viruses (herpes simplex - a very dangerous virus when it gets to the brain) and we'll see how that goes.

I want to note again that HIV is found in the dorsal root ganglia as well so retroviruses do hang out there and this theory does not preclude that possibility.

 

I thought they had found many years ago the UBO's to be transient rather than any kind of permanent lesions, which may decrease, but shouldn't negate all significance. Haven't followed anything on this for years. Maybe it is very significant for a subtype. My Spect and MRI showed no UBO's, and this during a prolonged severe phase.

 

herpes viruses dont live in harmoney with us. Normal people are able to keep them supressed where cfsers have poor nk function and nk cells are one of our prime immune defences against viruses, so with this guard down these herpes viruses are able to run wild. Thats why some thing cfs is an immune defiency, possibly a secondary immune defiency from xmrv or maybe a primary immune defiency. So with these viruses reactivating all the time we are in a constant state of glandular fever/mono.

cheers!!!

 

I thought they had found many years ago the UBO's to be transient rather than any kind of permanent lesions, which may decrease, but shouldn't negate all significance. Haven't followed anything on this for years. Maybe it is very significant for a subtype. My Spect and MRI showed no UBO's, and this during a prolonged severe phase.

Not so transient really. They just have tried to ignore them because they show a biological basis for ME rather than a psychological one. I don't understand why researchers don't look into these lesions more. Most with the more neurological type of ME have them.

Normal people do not usually have them except for some older folks. These lesions are being found it children and young adults in ME.

 

The problem with the brain inflammation is that there's just not enough of it to explain CFS. Brain inflammation studies have not found the high degrees of brain inflammation researchers feel is needed to account for the kind of debility found in CFS. If it had been there - our history would be very different.

MRI studies never showed large areas of inflammation in the brain in CFS. They showed, as I remember, areas of punctuated white objects or whatever they were, that were scattered across the brain in different areas in different individuals - making it difficult to state that these objects were causing CFS. If they had all been found in one area - that would have made a difference - but finding them in different areas made it difficult to say what they were doing. That doesn't say that some people don't have high levels of inflammation in the brain but the Incline Village studies did not find that consistently - at least as I remember.

One of the attractive aspects of this theory for me is that it doesn't rely on a brain infection - it relies on nervous system structures in the body that could effect the brain that have fewer viral defenses than the brain or other parts of the body and which are known centers of herpes virus infection.

Shapiro does note that these herpesvirus infections could ultimately result in brain infections in the most severe cases.

I also want to point out that both enteroviruses and HIV have been found in the basal ganglia- so if XMRV does work out for CFS - its presence there is a possibility as well.

So you're saying we do have brain inflammation, just not enough to cause our symptoms? Hmm. Or not enough, in most patients, to cause the symptoms?

Because I can sense a significant amount of inflammation in my brain (MRI was supposedly clear 4 years ago [although I'd like a second opinion on that since they made a judgement call about something they saw and I didn't trust them], but the inflammation is worse now). Topiramate (an anti-seizure medicine prescribed as an adjunct medicine in seizure therapy or, as in my case, primary medicine for migraine... also used in ME), NSAIDs, and gabapentin (originally an anti-seizure medicine, but now, as I'm sure you know, used for pain in fibromyalgia) all help (especially combined), but don't resolve the problem. I don't think I have many symptoms I didn't have at my last MRI, so that's a possibility that the brain inflammation isn't causing the bulk of my disability.

The other possibility is that we have brain inflammation of a different type than is viewable on MRI. Complex migraine can cause symptoms very much like ME and MS (or rather, like a stroke, since migraine is generally an acute condition), and migraine is not viewable on MRI, but is thought to be caused by inflammation of the blood vessels (rather than demyelination of the nerves, which is what MS has which you see with MRI).

note (Internet disclaimer): the personal information herein is private information posted here only for ME/CFS patients, carers, and their families, and is not to be posted elsewhere or used for purposes other than to directly benefit individual ME/CFS patients. Please respect my privacy. Thank you.

 

Curious for a bit of a refresher, I looked at UBO's in Oslers Web index. It lists many pages focused on UBO's, some are just detailing all the bantering on their importance, but others are quite clear explaining the significance, such as these (paraphrasing of course),

On page 123, a Reno Radiologist says that the brain scans of the majority of the patients became negative for UBO's after Acyclovir treatment. The UBO's reappeared after stopping the Acyclovir.

Then on page 562, Anthony Komaroff says that even though approx 22% of the healthy controls had the UBO's, the Tahoe cohort was close to 80%, suggesting a genuine pathological process, not yet presented in some. The symptomatic patients also had larger and deeper lesions than the healthy controls. Also, some patients exhibited a clear correlation between lesion position in the brain and clinical symptoms. They could see a relation between position of some lesions and autonomic function, balance, vision, etc.

been a long time with much progressive fading memory, I should re-read the book.

 

So you're saying we do have brain inflammation, just not enough to cause our symptoms? Hmm. Or not enough, in most patients, to cause the symptoms?

Because I can sense a significant amount of inflammation in my brain (MRI was supposedly clear 4 years ago [although I'd like a second opinion on that since they made a judgement call about something they saw and I didn't trust them], but the inflammation is worse now). Topiramate (an anti-seizure medicine prescribed as an adjunct medicine in seizure therapy or, as in my case, primary medicine for migraine... also used in ME), NSAIDs, and gabapentin (originally an anti-seizure medicine, but now, as I'm sure you know, used for pain in fibromyalgia) all help (especially combined), but don't resolve the problem. I don't think I have many symptoms I didn't have at my last MRI, so that's a possibility that the brain inflammation isn't causing the bulk of my disability.

The other possibility is that we have brain inflammation of a different type than is viewable on MRI. Complex migraine can cause symptoms very much like ME and MS (or rather, like a stroke, since migraine is generally an acute condition), and migraine is not viewable on MRI, but is thought to be caused by inflammation of the blood vessels (rather than demyelination of the nerves, which is what MS has which you see with MRI).

When you look at the MRI's of some disorder the inflammation just jumps out at you - my recollection is that that has not happened in CFS studies. I think that must be right because if it had happened then researchers would have jumped on it - and they haven't.

My guess is that its very possible that MRI's aren't picking up what's going on - and there is a good amount of indirect evidence that the blood vessels are involved (thanks for reporting that MRI's don't pick that up - I didn't know that). It's interesting that you mention migraine because some researchers think CFS is related in some way to migraine and Baraniuk recently came out with a paper indicating that migraine is substantially increased in CFS. Baraniuks proteome paper suggested that blood vessel problems in the brain are key to CFS; his second study should be out in the next couple of months (hopefully); it'll be very interesting to see what it says. My guess is that someone is going to develop some sort of scan that picks up what's going on - and everyone's jaws will drop.

On the other hand it could be the dorsal root ganglia - part of the nervous system - but just outside of spinal cord that are dysregulating things in the brain and the body (via the blood vessels)