Are Infections Just a Trigger of ME/CFS, or an Ongoing Cause of ME/CFS?

[Sidereal]

I'm not sure I agree with this if you are defining ME/CFS tightly -- as with the CCC (well-admininistered) or the ICC. Yes, there may be ME-similar illnesses that include fatigue and neurological problems and were initiated by things like TBI, trauma, or overtraining, but I'm not ready to say those conditions are equivalent to ME/CFS. I suspect that many of those cases are wastebasket diagnosis cases -- people with unexplained fatigue and some other symptoms are given the CFS diagnosis because doctors can't explain the symptoms.

Of course we don't know for certain what ME/CFS is and we can't separate out different groups until we have biomarkers that can distinguish them, so I won't say it's absolutely not true that ME/CFS can be triggered by TBI or overtraining. But I'm certainly not taking it as a given.

No, I am defining ME/CFS tightly. It's just that the TBI cases get told they have post-concussive syndrome so they don't flock to CFS doctors. The usual rehabilitation attempts do not help or make things worse.

 

[SOC]

No, I am defining ME/CFS tightly. It's just that the TBI cases get told they have post-concussive syndrome so they don't flock to CFS doctors. The usual rehabilitation attempts do not help or make things worse.

I disagree that they are the same illness. There's some overlap in symptoms between post-concussive syndrome and ME/CFS, but they are certainly not identical. Some ME/CFS symptoms overlap with some symptoms of many different conditions, particularly ones with neurological symptoms, but that doesn't make them the same illness.

 

[Snow Leopard]

With regards to the enterovirus stuff, they seem to be common triggers right behind EBV and CMV. But I don't believe that ME/CFS is due to chronic 'low level' (or whatever you want to call it) enterovirus infection. Or EBV for that matter. If there were say, subgroups - one due to chronic enterovirus, the other chronic herpesvirus, why can't we tell which patient is which?

 

[halcyon]

If there were say, subgroups - one due to chronic enterovirus, the other chronic herpesvirus, why can't we tell which patient is which?

The British seemed to be able to back in the day. In Mowbray's cohort, the patients with VP1 positive blood samples or persistent enterovirus IgM did not overlap with those with elevated EBV EA IgG. He also states that the EBV group did not display the same extent of muscle fatigue on exercise as the enteroviral group.

 

[Mij]

• Enteroviral infections can trigger dormant viruses to reactivate, such as HHV6, Epstein Barr Virus, CMV, and chickenpox– all herpes viruses.

http://www.enterovirusfoundation.org/symptoms.shtml

 

[rosie26]

I think some subgroups are post intracellular infections that has taken on a new disease caused by genetics and I question mark also the interaction of antibiotics in the mix as well as another combination that could cause a switch of some kind? But the antibiotic scenario is a big question mark and may not be involved. I think flu, EBV, are more progressers of the underlying illness and changes the disease into ME and also locks us in to a more severe form of ME? I think we have switches and changes, possibly from one disease into a next more severe form? It's all very complicated.

 

[heapsreal]

If one has low nk function, it makes sense that different viruses can reactivate especially if one has high viral igg titres.

I dont understand why its a hard concept to understand , especially when the role of nk cells are to fight viruses.

It might not be the be all and end all but there are enough mecfsers that fit this profile. Maybe we need better more effective antivirals as current antivirals cant fully eradicate viruses.

Also what comes first , the low nk function or the viruses . We need ways to increase nk function .

I also think the longer one is ill the more damage and or more infections one can have.

I also think the immune system is in overdrive trying to clear infections and causes alot of inflammation etc. Also possible the immune system is still switched on even after the infections are cleared, but this could also be another sub group.

 

[Valentijn]

About 18 days later, I experienced the sudden onset of ME symptoms, which began very distinctly with a "dizzy spell" that would not go away.

This reminds me ... prior to the leg pain starting after my flu ended, I went on a bicycle ride to a movie theater during the break between Dutch language courses. I had trouble keeping my balance, slowing falling over on to the ground when we stopped at our destination, then repeatedly veering off the path on the way home a couple hours later.

I didn't feel obvious dizziness or vertigo, but must've had a bit of something going on. My sense of gravity was not quite matching up with reality

 

[Mij]

Mine started with severe vertigo.

The equilibrium and sense of gravity loss started after I was vaccinated (a couple of months after the vertigo) when I would exert myself. I kept feeling as though I needed to hold on to the wall or lie down, but I wasn't fatigued.

 

[redaxe]

One of the things I find curious is that we tend to speak of EBV, HHV6 etc... as something you get exposed to in childhood and that's it.... apart from the rare instance of EBV associated cancer it's not deemed a high risk pathogen.

But how do we know we are not being exposed to new strains of these viruses throughout our lifetimes? All viruses are constantly evolving - some reduce in virulence over time, other viruses can mutate and form rare nasty strains like that H1N1 flu virus that caused the narcolepsy in a subset of affected people.

These viruses like EBV and HHV6 etc do spread quickly in close communities. If rogue strains of EBV, HHv6 or enteroviruses do surface from time to time it could explain some of the cluster outbreaks that are reported and the occasional tendency for families to get hit by ME simultaneously.

These cases of teenage or early adult mono. Are these the primary EBV infection for these people or do they have some prior exposure/immunity but they just get hit by a virulent rogue strain at an age when their CD8+ cell function is not as robust as it was at infancy? Has anyone actually attempted to study this?
It shouldn't be too hard. You have to take regular EBV serology from a large group from birth to age 20 and record instances of mono/glandular fever and whether those events occur in patients with prior EBV immunity. That can then record instances of ME associated with EBV. A study like this would finally answer the question if an 18 year old gets ME after mono (the classic route to entering this disease) have they had EBV antibodies beforehand (i.e. at infancy). Ideally too we'd be able to sequence the genomes of multiple viral strains to see if some rare mutant strains are common in teens/adults with glandular fever and ME/CFS.

One thing is - there is no doubt we can carry multiple EBV and presumably other viral strains.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC155020/

I really think this is going to be a minefield to work through. In the end what we need (and this was flagged by the IOM authors I believe) is better testing for NK and CD8+ cell function (right now it's pretty poor apparently so this weakens any attempt to associate ME with low NK function) - ultimately the theories and the science is only ever as good as the diagnostic tools available.

And we need better antivirals, more targeted and safer immuno-suppression drugs and better immuno-stimulant drugs. In the long term is that viruses will always continue to evolve - we will probably never be able to protect ourselves against every damaging viral strain out there but we can and should work out this NK cell issue and work out why an otherwise healthy persons immune system goes down.

 

[MeSci]

There's something called post-concussion syndrome where a range of symptoms persist long after the mild traumatic brain injury 'should have' healed. The symptoms (and the reactions of the medical profession) are very similar to ME/CFS.

There are some threads on this topic, for example this one.

 

[Tammy]

@redaxe...............really like your post above................(except for immune-suppression drugs......never liked those). For my case of CFS.............it started with EBV and I think this beast has been an ongoing cause for my CFS. I think a lot of your comments on EBV are interesting and thought provoking. What are your thought's on the current EBV testing....(I think it's a cluster ****)....do you think we're missing something? It always bothered me when Dr's say the results show that EBV was a problem in the past but not now. I don't buy it. I feel that something's awry.

 

[MeSci]

• Enteroviral infections can trigger dormant viruses to reactivate, such as HHV6, Epstein Barr Virus, CMV, and chickenpox– all herpes viruses.

http://www.enterovirusfoundation.org/symptoms.shtml

I wonder what has happened to that organisation? The latest news seems to be from 2008 - when it was set up!

 

[Marco]

There are some threads on this topic, for example this one.

My own interest in post-concussion syndrome is not that it may be a trigger for ME/CFS or that the long term effects of mild traumatic brain injury may be misdiagnosed as 'CFS', more that they may share underlying mechanisms.

After all concussion is unambiguously neuroinflammation and it's suspected that what happens in post-concussion syndrome is that low level microglial activation continues after the gross brain injury appears to have healed.

Interesting also that apart from the shared common symptoms like fatigue and cognitive problems, post-concussion syndrome symtoms also include alcohol intolerance and what looks very much like PEM to me - both of which we thought were rare and possibly unique to ME/CFS.

There's also quite a literature on exercise and rehabilitation after concussion as many concussions are suffered by professional athletes and of course there's an onus on getting them back to their day job.

To date standard medical advice has been to avoid all exercise until completely symptom free but one researcher claims success using GET as early as possible to prevent concussion developing into post-concussion syndrome (which occurs only in a minority of concussion cases).

Where this GET differs is that it is very carefully individually tailored and monitored with the aim to cease exercise immmediately that any adverse symptoms are experienced (no push on through or love your pain here).

If I remember correctly their theory is that post concussion, the various brain regions are out of sync and that gradually introducing exercise, while not exacerbating symptoms, may help to reintegrate them. If caught early enough presumably.

Not that I'm suggesting this as useful for ME/CFS but it's an interesting theory that neuroinflammation could result in asynchrony between brain regions.

Anyway, back to the topic!

 

[Mij]

I wonder what has happened to that organisation? The latest news seems to be from 2008 - when it was set up!

They are on Facebook now.

 

[MeSci]

They are on Facebook now.

Do you have a link?

 

[Mij]

@MeSci click on "contact us" on their website and they provide the link to Facebook.

https://www.facebook.com/EVForg/

 

[Hip]

It's just that the TBI cases get told they have post-concussive syndrome so they don't flock to CFS doctors. The usual rehabilitation attempts do not help or make things worse.

Seems that those with post-concussion syndrome (PCS) even get PEM from physical exertion:

Doctors will frequently consider symptoms following the concussion and when exactly they occur. If, for example, the symptoms started right after the head trauma and tend to worsen with physical activity, but get better with rest, then they will usually determine that the concussion caused the symptoms.

Source: Post-Concussion Syndrome | MD-Health.com

That really does make me think that PCS is very similar, if not the same, as ME/CFS.

It would be interesting to treat PCS patients with rituximab and see if there are any responders.

We need ways to increase nk function .

The supplement Biobran MGN-3 significantly increases natural killer cell activity (by 300% according to the manufacturer). However, in studies the benefits for Biobran MGN-3 on ME/CFS turned out to be minimal. In the words of Biobran themselves:

Biobran has had very limited success with Chronic Fatigue Syndrome, indicating that this condition is likely to be much more complex than a straightforward viral infection. Ref: 1

 

[heapsreal]

@Hip i looked into biobran a couple years back. It was rediculusly expensive . I used ahcc which is what they use to make biobran. After 3 months at 3 grams a day i didnt feel any improvement and no increase in nk cells. Not able to get nk function tested now.

I've mentioned it in other past threads where cycloferon increased my nk function and numbers , also felt better but i think we need to cycle off and on for them to keep working. Continual use like many things, it loses its stimulating effects on the immune system .

 

[Hip]

@heapsreal
I have tried some NK cell function booster supplements myself, and perhaps saw some mild improvements in ME/CFS symptoms, but not significant enough to make me want to continue taking the supplements.