Why is nobody talking about this Enterovirus study?

[bread.]

@Janet Dafoe (Rose49)

 

[Hip]

Hip, do you know of any research which tries to answer why the 1% get symptomatic polio, is there any difference in genetics or whatever?

I have not seen any research. And since since poliomyelitis is generally not a problem anymore in the West (and since poliovirus should soon be fully eliminated from the whole world as a result of the work of the Bill & Melinda Gates Foundation), you probably will not see any new research into it.

I would imagine, though, that the crucial factor which determines whether poliovirus causes no harm at all, or causes serious injury, is whether this virus is able to enter the central nervous system during the acute infection.

This I think might also explain why coxsackievirus B infection usually causes no serious harm, but in a few cases leads to ME/CFS: it may simply be whether this virus is able to enter the brain during the acute infection stage.

During an acute viral infection, there's always the mother of all battles going on between the virus and the immune system, with the immune system desperately trying to find the right antibody that can neutralize the virus. But finding the right antibody takes time, and for the first few days of the infection, the immune system does not have the appropriate antibody, thus the virus can run riot in the body during this period.

So if during this acute infection the virus is able to breach into the brain, then you might expect a worse outcome. Normally the brain is protected from infection by its blood-brain barrier, which isolates the brain from the bloodstream and the pathogens in the blood.

But there are backdoors into the brain that viruses can use. In the case of enterovirus, the entry route into the brain is most likely the vagus nerve, which runs from the stomach to the brain. Dr Chia in one of his presentations points out that enterovirus can travel along the vagus, from stomach to brain, in only 3 days.


So to answer you question: yes, genetics may be a factor, but perhaps more importantly, whether or not you are run down at the time you caught the acute infection may be crucial. If you are run down and your immunity is weaker than normal, this may give the virus an opportunity to enter the brain.

I don't believe in the psychological theories of ME/CFS, but there are several studies showing lots of ME/CFS patients experienced major chronic stress (eg from events like divorce) in the year before they developed ME/CFS. Now we know that chronic stress reduces immunity, so if you were unlucky enough to catch a potentially nasty pathogen like coxsackievirus B or poliovirus during a time of chronic stress, perhaps this might allow the pathogen to do a lot more harm than normal.

 

[Pyrrhus]

I would imagine, though, that the crucial factor which determines whether poliovirus causes no harm at all, or causes serious injury, is whether this virus is able to enter the central nervous system during the acute infection.

This is my understanding as well, and it is certainly an under-appreciated point.

But there are backdoors into the brain that viruses can use. In the case of enterovirus, the entry route into the brain is most likely the vagus nerve, which runs from the stomach to the brain. Dr Chia in one of his presentations points out that enterovirus can travel along the vagus, from stomach to brain, in only 3 days.

There was an experiment in the 1970's where primates were injected with poliovirus directly into the muscles, and they were able to observe symptoms that suggested the virus travelled from the muscles, through peripheral nerves to the spinal cord, and from the spinal cord into the brain. Then they repeated the experiment but they first severed the spinal cord. In this second experiment, the animal subjects did not develop any symptoms above the location of the severed spinal cord, suggesting that the virus required an intact nervous route to the brain in order to infect the brain.

 

[gbells]

I don't believe in the psychological theories of ME/CFS, but there are several studies showing lots of ME/CFS patients experienced major chronic stress (eg from events like divorce) in the year before they developed ME/CFS. Now we know that chronic stress reduces immunity, so if you were unlucky enough to catch a potentially nasty pathogen like coxsackievirus B or poliovirus during a time of chronic stress, perhaps this might allow the pathogen to do a lot more harm than normal.

I don't buy this. If the virus is a new pathogen then there is a lag time of a few weeks for the body to generate an effective antibody defense so any stress wouldn't matter because there is no real defense to inhibit. However, if a person already has antibodies and it is a repeat exposure then exposure to stress would inhibit antibody based defense so under that condition there would be increased virulence.

 

[Daisymay]

Thanks Hip, yes that makes a lot of sense. I first got Epstein Barr infection, never got over it and six months later came down with another severe viral infection which turned out to be Coxsackie B3. I was teaching infants at the time and many of the children had a mild viral infection which they got over easily, whereas I was off work for months and never recovered. The hospital doctor I saw said that I was in the worst sort of job for someone whose immune system did n't seem to work properly as I was exposed to many viruses.

 

[gbells]

I think the effect of stress on acute viral infection would be to delay and possibly inhibit antibody defense. However the herpes viruses (EBV, HHV6) disable antibody response by stopping T-cell triggering of apoptosis so it really wouldn't matter. The only good thing about having multiple virus infections is that they can trigger latency and stop the viruses from reproducing further. However, you're still stuck with the cells are are already infected and those will increase through cell division growth.

 

[gbells]

By antibody defense I mean the creation of antibodies to new viruses. Wish I could edit these posts!

 

[Gemini]

It would be useful to compare the ME/CFS findings from both groups-- they were similar in their AFM studies, 70% and 80% respectively.

Full-page article in today's New York Times "Scientists Find Clues to Mysterious Paralysis in Children" compares the two AFM studies, Nature Medicine's to Lipkin's, with quotes from Avi Nath at NINDS.

Excerpts[my bold]:

"The research published Monday in the journal Nature Medicine, points to a long-suspected culprit: enteroviruses, a group of common viruses that usually produce mild effects, but can sometimes cause neurological symptoms.

"The findings support another recent study in which Columbia University researchers, using a different technique with fewer patients, also found enterovirus antibodies in spinal fluid."

"This takes us a lot further than we have been, said Dr. Avi Nath, a senior investigator for the National Institute of Neurological Disorders and Stroke, who was not involved in either study. Coming from two different laboratories with two entirely different techniques, we are now at the point where we can say we have a candidate virus to study."

"The Columbia study, published in the journal mBio, found a clearer EV-D68 signal."[versus EV-A71]

"We think that D68 is where the action is, said the senior author, Dr. W. Ian Lipkin, director of the Center for Infection and Immunity at Columbia's Mailman School of Public Health. We're saying it looks like a duck and it quacks, and it's a duck."

"Dr. Nath, also a member of the A.F.M task force, said that to confirm the finding, similar studies should be run during future A.F.M. bursts, next expected in August to October 2020."

@Hip though Lipkin's next step is to test ME/CFS samples, AFM investigators use of different labs & techniques emphasizes the importance of your reaching out to the VirScan researchers, fingers crossed they respond.

@Uknmy besides a crowdfund, perhaps we should ask Dr. Nath & NIH to fund an ME/CFS VirScan study?

 

[Gemini]

These so-called experts obviously did not pay much attention in class when learning about enterovirus: those who know about enterovirus will tell you that you usually do not find enterovirus in the cerebrospinal fluid during an enterovirus brain infection.

@Hip to your point perhaps these experts would benefit from reading today's NYTimes AFM article :

"And while enteroviruses have been detected in stool and respiratory mucus of some AFM patients, substantiating a role in neurological disease requires evidence involving cerebrospinal fluid, which circulates in the brain and spinal cord.

But enteroviruses dissipate quickly from this fluid. The CDC has found enteroviruses (EV-D68, EV-A71, or Coxsackie virus), in cerebrospinal fluid in only four of the 590 cases since 2014."

 

[Gemini]

Speaking of Avi Nath, wonder if he's testing his ME/CFS Clinical Study participants with VirScan, VirCapSeq-VERT, and/or SeroChip microarrays?

@Cort did he mention any of them during your interview by any chance?

 

[Gemini]

Speaking of Avi Nath, wonder if he's testing his ME/CFS Clinical Study participants with VirScan, VirCapSeq-VERT, and/or SeroChip microarrays?

Hot off the press, Avi Nath just published a VirScan study re: dengue encephalitis which describes his experience using the tool (Ann Neurology, Nov 2019):

www.ncbi.nlm.nih.gov/pubmed/31461177

@Hip VirScan was also involved in a measles virus breakthrough just published in Science and reported in today's New York Times: "Measles Can Kill Memory Used in Immune System."

These applications highlight all the more the importance of your reaching out to researchers to use it in ME/CFS.

In 2015 Ian Lipkin said: "The approach is clever and a technological tour de force...This is a powerful new research tool."

https://sparkonit.com/06/06/what-is-virscan-and-how-does-it-work/

 

[Hufsamor]

do you know of any research which tries to answer why the 1% get symptomatic polio, is there any difference in genetics or whatever?

I found this article yesterday.
It's about who gets the post polio syndrome.

My mother have been struggling with post polio, and as we are two children with me/ cfs and the third one isn't to healthy either, I've always wondered if it lays in the genes. (I am mostly wondering if the polio alters the genes, as other family conditions is found everywhere in the family, uncles, grandparents, cousin, but this me/cfs seems to be only us)

This article is a bit too complicated for me to read in English, but I believe it says that genes do play a role.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5116905/

 

[Pyrrhus]

Thanks for that interesting article! Yes, it does talk about a genetic role in the susceptibility to a more serious form of enteroviral infection.

My mother have been struggling with post polio, and as we are two children with me/ cfs

That's interesting- how would you describe the similarities or differences between post-polio syndrome and ME/CFS? Did your mother have paralytic or non-paralytic polio? When did her post-polio symptoms start?

 

[Hufsamor]

would you describe the similarities or differences between post-polio syndrome and ME/CFS?

Im not really sure there are any differences ? Except from the muscle weakness and eventually pain form the affected area, the damage the polio did to a particular nerve. I've read a lot of places, that postpolio and me/cfs is the syndromes closest to each other. After watching our mum, my brother and I consider it to be the same thing, only with known trigger and unknown trigger.
(I believe we are even more exhausted than her, but it's hard to know, we have different lives. And my mother have never had brain fog , my brother and I are suffering a lot from that. But brainfog is considered as a symptom of postpolio, so I guess she's just been lucky.)

What separates the postpolio and me/ cfs diagnosis, is that a postpolio patient usually have a damage that can be confirmed at a hospital.( I'm not completely sure what they measure, but I believe it's some nerve -signals? )

I do know people with postpolio with a lot of pain, sharp pain, from the damaged nerves. This pain will come from the foot or whatever where the damage is done, But you don't need to have that. My mother have more what I would call 'normal ' me/cfs-fibromyalgia pain.

My mother was 3 years old when she got polio. She doesn't know if she was completely paralysed for a short while, but she was very, very weak in both her feet and had to train a lot to get her strength back.
As a child I remember us walking down the pavement and her wrist all the sudden gave in.

She, herself, consider her postpolio-the exhaustion, this me/cfs -look -alike, to have started in her 50 s. (I however, believe she has been affected from her 30 s. But she wasn't working, and she's not a very social type, so she adjusted her life. A lot)

In my life, I've known 2 women suffering from post polio, who's had children. Two of them (my mother and another) have children with me/ cfs. I knew a third woman with damage, limping, after polio, but lots of energy, and she was talking to me years ago, about her worrying for one of her children, collapsing on her bed after school. (I don't think this girl ever developed me/ cfs, but something didnt work quite right with her energy delivering)

So: except from the damage nerves, it's said from doctors, and I believe from my own observations, that postpolio and me/cfs is as close as can be. Maybe the same sickness.
From observation, but with very, very few participants, I believe one might inherit this weakness from a polio parent.
For some reason, I believe you inherit mother, but perhaps not father.

(I know only one post polio man with children. He was not paralysed as a child, but very sick. And struggling a lot as an adult with his postpolio. But even though most of his 5 children have their issues, non of them have me/cfs. One man only is, of course, hardly enough to base a theory on. But it makes me wonder)

 

[Hufsamor]

Parallels Between Post-Polio Fatigue and Chronic Fatigue Syndrome: A Common Pathophysiology?

http://www.postpolioinfo.com/library/parallels.pdf

These data suggest that the polioviruses may be the prototypes for chronic fatigue-producing agents, since they routinely and often preferentially damage neurons responsible for brain activation and the BFG. Post-polio fatigue may provide a complete model for a post-viral fatigue syndrome, since the causative agent is know, the damage done by the agent to the brain has been demonstrated histopathologically, and the signs of that damage -- neuroanatomic, neuropsychologic, neuroendocrinologic and electroencephalographic -- have been documented and correlated with the symptoms of fatigue.

However, polioviruses are not the only agents for which the brain's activating system is the "favourite location." Lesions in the reticular formation, putamen, thalamus, hypothalamus and white matter have been associated with a variety of viral encephalitides whose symptoms include markedly impaired cortical activation and fatigue

 

[Hufsamor]

https://www.em-consulte.com/en/article/897941
The comparison of SF36 showed significant lower role physical, bodily pain, general health, vitality, social functioning and mental health in patients with ME/CFS as compared to PPS

 

[Pyrrhus]

So: except from the damage nerves, it's said from doctors, and I believe from my own observations, that postpolio and me/cfs is as close as can be. Maybe the same sickness.
From observation, but with very, very few participants, I believe one might inherit this weakness from a polio parent.
For some reason, I believe you inherit mother, but perhaps not father.

Thank you so much for your in-depth response! Very interesting. Yes, there could certainly be genetic factors that would influence susceptibility to ME/PPS. If there is an ongoing infection, the infection could also be transferred from mother to child during pregnancy.

You may have seen this recent paper:
https://www.tandfonline.com/doi/abs/10.1080/21641846.2019.1687117

Thanks!