Discussion in 'General ME/CFS News' started by Ember, Jan 31, 2013.
The more I look into enteroviruses, the more likely they look to be either causal or triggering, though I don't think anyone can prove they are not just opportunistic. These enteroviruses can replicate very slowly, disrupt cell metabolism, and even infect nearby cells without destroying the cell they come from or entering the blood stream. Once infected they will spread very slowly through all muscle tissue and perhaps other tissues (I do not know the range of tissues they can infect). Most blood vessels are wrapped in a thin layer of muscle. If that muscle becomes infected the ability for the blood vessels to adapt could be compromised, and this could explain OI.
Given that over 80% of us are positive by stomach biopsy, and that this will miss a percentage of patients, its entirely possible that this family of viruses explains ME.
I am positive for Coxsackie B3, diagnosed via blood test in about 1989. To find this virus now would probably require biopsy.
The question that has been intriguing me for several months now is what turns a latent and pervasive enteroviral infection into ME? I am blogging some ideas on this, but let me say that I am not proposing its a new enteroviral infection, I think its a reactivation of an already pervasive enteroviral infection in the gut wall. This allows lipopolysaccharide to enter the blood stream, and ME begins.
What enables the reactivation varies - new infections (even herpes viruses or bacterial) or anything that suppresses the immune system such as toxins, prolonged stress, poor diet or physical injury will do it. Connective tissue disorders increase the risk that LPS will cross into the blood stream, and methylation disorders increase the risk that the liver will be overwhelmed by the LPS and it will enter general circulation. Finally the type of gut bacteria present may matter. LPS is a family of different molecules, and different bacteria make different forms of it.
Some of you make have noted that I have been talking about phosphodiesterases. I think they got overactivated in ME, though its just an hypothesis (I can only show mild elevation and sporadic acute activation from the literature). This ties into the LPS problem.
I have much more to say on this but I may not be ready to blog this for months.
Hello Alex, I liked your post it is interesting you have evidence of this class of virus in yourself and have more ideas to share. One idea might be that perhaps patients around the globe having to wait 6 months before a diagnosis of CFS could allow for this class of virus to be masked in resulting negative blood samples? What do you think?
However, I was considering a few other problems with this idea linking it to explaining ME outright, in my view.
1# To my knowledge, Dr Chia's cohort of this study with positive tissue biopsies had a CFS (Fukuda) cohort and didn't require signs of abnormal neurological signs, such as universal dysautonomia.
On this basis, research evidence would be limited in showing that people with unexplained chronic fatigue and four symptoms (CFS Fukuda) have high rates of enterovirus demonstrated with biopsies and not neurological disease, ME. Conversely, they could all have ME, because they weren't given the tests to allow for this being likely.
Basically if you compare what ME does to people vs Fukuda CFS then we are talking two different conditions. Did the Fukuda CFS enterovirus groups have classic ME symptoms and disabilities, where they severely affected? We don't know. This is a problem. Fukuda CFS criteria creates this problem.
2# Having a high percentage of enterovirus in biopsies could simply prove that PWME or CFS have an underlying immune suppression that makes them susceptible to enteroviruses and/or other chronic infections. Meaning enterovirus might not be the cause, but an effect of the disease process.
That being said Alex, one positive aspect is the UK felt the need to respond to Chia's research by making a webpage on it on the NHS public disinformation service that usually prefers 'childhood trauma'. Which might imply, you are onto something!
Hi Research 1st, I think that this class of virus still has evidence at six months most of the time, even if only antibodies to the virus. However, its a ubiquitous virus family. It was dismissed for the same reason as EBV - everyone gets it, but not everyone gets ME, so it can't be a cause. This ignores the possibility of different viral infection progression in patients of course, and with the discovery of mechanisms of latency in herpes viruses and enteroviruses these need to be looked at again. Its not about if you have the virus, its about what the virus is doing. Latent viral infection from enteroviruses is very uncommon - except in Chia's biopsy data.
Chia I think did use Fukuda, but I am not sure about now. Neurological signs can easily arise due to multiple factors with this class of virus. If the muscle in the blood vessel lining is infected, then the capacity to regulate blood flow, including to the brain, will be decreased. Lost blood flow can induce many of our cognitive issues. I am in the process of trying to figure out mechanisms that show excessive degradation of cyclic AMP and will then cause failure to properly form memory as well as other issues. I will have to update my understanding of neurology to get into this, so it will not be quick for me to finish investigating.
There is always going to be cohort issues though until we have a diagnostic test. Also Chia finds enterovirus in over 80% but not everyone. While some will be false negatives, some might simply be misdiagnosed or a different subset.
I do agree though that these viruses, as is the case with herpes family viruses and other pathogens, might only be present as opportunistic infections due to underlying immune deficits. However I am slowly working on a model to show how LPS might induce these changes. What the enteroviruses do (as do connective tissue disorders and methylation disorders) is show a path how LPS might get into the blood.
Don't thank me though, thank Chia and the virologists who have been looking into enteroviruses for decades. Its the slow accumulation of data on mechanisms that make these explanations possible. I have posted this link before, read the article on page 23:
http://www.investinme.org/Documents/Journals/Journal of IiME Vol 3 Issue 1 Screen.pdf
The only other disease I am aware of in which viruses such as Coxsackie B3 are typically present is heart failure.
I have come to agree with you. I have taken Valcyte that helped me a great deal, but did little for the fatigue.
I have been taking Oxymatrine for about five years now. I started on the White Tiger brand, and switched to Equilibrant after it became available. I am taking a variety of other immune shifting supplements, including LDN, Rich's methylation supplements, and Artesunate.
So far, the results have been good, but not great. I do feel that my immune system is shifting, since I have had four colds in the last year, after going over 20 years without one. After watching Lewyllen Kings interview with Dr, Chia, I am upping my dose of Equilibrant. I had been taking three a day, but I am going to see if I can work my way to 9. In the interview, Dr. Chia mentioned that his son Andrew had taken 9 a day. I have met Andrew, and he certainly seems to have recovered.
I had Dr. Chia test a stomach sample and he found a greater than 50% prevalence of EV's. Testing at ARUP verified that I have three different EV's present. It is my belief that it is going to take some amount of time for my immune system to clear that many cells, so I am prepared to stick with the Equilibrant for the long haul.
I don't believe that we will have the full story until we can determine what is causing our immune systems to stay stuck in TH2 mode. It is my belief that the immune shift the we seem to suffer from allows the EV's to proliferate and do their damage.
I have noticed that if I stop the Oxy for any length of time, I start feeling considerably worse. I have had stomach problems for many years, and have taken a lot of Zantac. As I have upped my dose of Equilibrant, the need for Zantac has all but disappeared. I can eat almost anything without the problems that I had before.
I am taking a daily dose of Manuka honey that is very helpful for my GI tract. Interesting product from your area of the world ( New Zealand).
In 2005, I was spending almost all day in bed. My blood pressure had dropped to 80/50 with a pulse of 50. Today, my BP runs about 115/70, and I am able to watch my grandson two days a week. Keeping up with a two and a half year old is a challenge, but I am able to do it. I need to spend a day resting up afterward, but the PEM is tolerable.
It is winter here in North America, which is always my worst time, but this year is not nearly as bad as last year.
There are quite a lot of factors that can drive Th2 present in ME. I hope to blog about a few of them when I write my blogs on LPS, gamma delta T cells and how this might all fit together. However I will not be posting any of those for some months: many of my pending blogs now use hundreds of references and sources, they are not easily typed out in an afternoon.
I have never tried oxymatrine, but I am definitely considering it.
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