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Coxsackievirus B vaccine appears feasible, and may drastically reduce ME/CFS incidence in future

Hip

Senior Member
Messages
17,852
Dr John Chia, the late Dr John Richardson and others maintain the view that enteroviruses such as coxsackievirus B are responsible for most cases of ME/CFS.

Thus if there were an effective vaccine for coxsackievirus B, this may well drastically reduce the incidence of ME/CFS in future.

Looking around on PubMed for evidence of any success in developing a coxsackievirus B vaccine, it seems that there have been a some effective attempts. Thus a coxsackievirus B vaccine appears feasible.

The question is, why hasn't such a vaccine been introduced, when it could help prevent one of the worst diseases known to man (in terms of reduced quality of life)?



Here are the details of some successful experimental attempts in developing and testing a coxsackievirus B vaccine:

In this study: A Vaccine to Coxsackievirus Prepared by High Pressure, it says:
"using different murine model systems it has been demonstrated that classic as well as newly developed vaccination procedures are quite successful in preventing Coxsackievirus B3 infections."​

In this study: High yield production of an inactivated coxsackie B3 adjuvant vaccine with protective effect against experimental myocarditis, it says:
"we have shown that vaccine can be made against Coxsackie B3 virus with good protective effect and significant neutralisation antibody titre."​

In this study: Vaccination with coxsackievirus B3 virus-like particles elicits humoral immune response and protects mice against myocarditis, it says:
"These results demonstrate that CVB3 capsid proteins expressed in insect cells have the intrinsic capacity to assemble into non-infectious VLP, which afforded protection from CVB3 infection to mice when used as a vaccine."​

In this study: Vaccination procedures against Coxsackievirus-induced heart disease, it says:
"using different murine model systems it has been demonstrated that classic as well as newly developed vaccination procedures are quite successful in preventing Coxsackievirus B3 infections. In particular, the application of an interferon-gamma-expressing recombinant Coxsackievirus variant against Coxsackievirus B3-induced myocarditis has been effective."​

This study: Characterization of attenuated coxsackievirus B3 strains and prospects of their application as live-attenuated vaccines discusses the problems to be overcome in the development of live-attenuated vaccines. (But I don't have access to the full paper).
 
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Waverunner

Senior Member
Messages
1,079
Very interesting, thanks. The reason why no vaccine has been introduced in my eyes, is the fact, that it is too expensive to get it approved, like most inventions in the medical field are. In a free market, when there is demand, there is supply. In a regulated market, there is supply only, if the cost of regulation is smaller, than the discounted future cash-flows.
 

heapsreal

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i wonder if a vaccine would only help prevent the infection, where if one has it then its too late, they would probably have antibodies to the infection which arent working anyway, so im not sure how a vaccine that helps our antibody response would be affective. I dont really know but just thinking off the top of my head??

Maybe our best best is an antiviral for enteroviruses??
 

adreno

PR activist
Messages
4,841
Maybe a vaccine would not help us personally, but preventing further outbreaks would certainly be desirable. Anyway, if a vaccine could be shown to prevent ME, we would know the mechanism of our disease, and how to treat it.

But is coxsackie infection really enough to develop ME? If we infect animals with cocksuckie virus, do they develop ME?
 

Hip

Senior Member
Messages
17,852
The reason why no vaccine has been introduced in my eyes, is the fact, that it is too expensive to get it approved

If the associations between coxsackievirus B and the serious diseases this virus is suspected of causing — diseases such as ME/CFS, diabetes type 1, autoimmune diseases, fatal myocarditis and fatal heart attack — could be definitely proven, then I suspect there would be a far greater effort to develop and introduce a coxsackievirus B vaccine. (Remember that association alone does not prove causation.)

This 2007 study found that 40% of people who died suddenly of a heart attack (myocardial infarction) had evidence of an enterovirus infection in their heart tissues, and in 16%, the specific enterovirus detected was coxsackievirus B.

Given that there are about 225,000 fatal heart attacks per year in the US, if enterovirus / coxsackievirus B can be proven to be the actual cause of these heart attacks, that would mean that enterovirus is killing 90,000 people per year in the US, and out of these, coxsackievirus B is killing 36,000 people per year.


And this 1977 study showed that during a two-month period at King Edward VII Hospital, Sussex, UK, 10 out of 38 patients admitted to the hospital due to suffering acute heart attack had serological evidence of a very recent coxsackievirus B infection. That is to say, around 25% of heart attack patients during this period suffered from a flu-like illness caused by coxsackievirus B seven days prior to admission.

Other studies which have linked enterovirus to heart attacks include this one, this one and this one.


Dr John Chia is doing sterling work in trying prove a causal relationship between coxsackievirus B / enterovirus infections like and ME/CFS. Chia has already demonstrated a strong association of enterovirus to ME/CFS (he found enterovirus in the guts of 82% of ME/CFS patients, but in just 20% of healthy controls ). More convincingly, Chia in now trying to definitely prove that enterovirus infection causes ME/CFS, with his more recent study focusing on showing that a percentage of patients will develop ME/CFS soon after contracting an acute enterovirus infection. This type of study adds much weight to demonstrating a causal relationship.
 
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Hip

Senior Member
Messages
17,852
i wonder if a vaccine would only help prevent the infection, where if one has it then its too late, they would probably have antibodies to the infection which arent working anyway, so im not sure how a vaccine that helps our antibody response would be affective.

A coxsackievirus B vaccine could certainly help prevent further cases of ME/CFS, but I am not sure if this vaccine would be of any benefit to patients that already have ME/CFS linked to coxsackievirus B.

Having said that, it is strange that antibody levels are very low in ME/CFS patients others with chronic coxsackievirus B and echovirus infection. Indeed, these levels are so low, that only ARUP Lab, with its super-sensitive antibody tests can detect the coxsackievirus B and echovirus antibodies in ME/CFS patients.

I am not sure why there are so few antibodies in chronic coxsackievirus B and echovirus infections. This is not the case with other viruses (eg, HHV-6, EBV, and parvovirus B19), which even in chronic infections, generally precipitate a strong antibody response that can easily be detected.

Might part of the reason that chronic coxsackievirus B and echovirus infections seem to cause diseases like ME/CFS be due to the lack of antibody response in chronic infections? I don't know; I am just speculating here.

If so, perhaps a coxsackievirus B vaccine (which should stimulate the production of antibodies) might be of benefit to ME/CFS patients also.
 

Hip

Senior Member
Messages
17,852
is coxsackie infection really enough to develop ME? If we infect animals with cocksuckie virus, do they develop ME?

The above mentioned study by Dr Chia, which found that ME/CFS does get triggered in a small number of people after an acute enterovirus infection, certainly seems to strongly suggest that enterovirus can cause ME/CFS.

So for these enterovirus-triggered ME/CFS patients, enterovirus can be considered a necessary condition for developing ME/CFS; but since the study found the majority of people do not develop ME/CFS after an acute enterovirus infection, enterovirus is clearly not a sufficient condition for developing ME/CFS.

In other words, there must be other factors at play determining who develops ME/CFS from enterovirus infection and who does not — factors such as genetics, the presence of other co-infections in the body, and the presence of other disease conditions (for example, diseases like irritable bowel syndrome, which statistically many people with ME/CFS have, and often had even before they caught their ME/CFS-triggering virus).
 

adreno

PR activist
Messages
4,841
In other words, there must be other factors at play determining who develops ME/CFS from enterovirus infection and who does not — factors such as genetics, the presence of other co-infections in the body, and the presence of other disease conditions (for example, diseases like irritable bowel syndrome, which statistically many people with ME/CFS have, and often had even before they caught their ME/CFS-triggering virus).
This makes sense. But if coxsackie is a necessary condition, a vaccine would still prevent ME, regardless of other factors. But this presupposes that other pathogens do not trigger ME, or we would only prevent some forms of the outbreaks.
 

Hip

Senior Member
Messages
17,852
definately common, are you coming across any research treatments for EV

As is well known, Dr Chia has used oxymatrine and interferon infusion treatments against enteroviruses in general, with some success. I did collect a list of drugs and supplements (in studies found on PubMed) that were shown to have antiviral effects against echovirus; these include: amantadine, ribavirin, Epimedium (horny goat weed), betulin, betulinic acid, Ficus carica, and Spatholobus suberectus.
 

Hip

Senior Member
Messages
17,852
This makes sense. But if coxsackie is a necessary condition, a vaccine would still prevent ME, regardless of other factors. But this presupposes that other pathogens do not trigger ME, or we would only prevent some forms of the outbreaks.

I personally think it is most unlikely that the other major ME/CFS-associated pathogens, namely HHV-6 and EBV, are the triggering cause of ME/CFS. This is simple because nearly all adults (90 to 95%) already have these viruses in their bodies, and if you have them already, HHV-6 and EBV could not possibly be candidates for the new, acute viral infection you catch which triggers ME/CFS.

By contrast, the various serotypes of coxsackievirus B and echovirus are relatively rare, and so that makes these viruses much more likely candidates for the ME/CFS-triggering viral infection you catch out of the blue as an adult.


Sure, there are other known infectious causes of ME/CFS, such as Chlamydia pneumoniae, Coxiella burnetii and parvovirus B19, but these are easily tested for (and usually successfully treated with antibiotics or IV immunoglobulin). So sure, you don't have to have coxsackievirus B and echovirus as your ME/CFS-triggering infection.

And ME/CFS occasionally has non-infectious triggers, such as physical trauma (particularly car accidents involving head or neck injury).

But outside of these known causes, and non-infectious causes, for the reasons explained, my money is on enterovirus being the main culprit responsible for virally-triggered ME/CFS of unknown etiology.

More evidence for an enterovirus etiology for triggering ME/CFS comes from the fact that ME/CFS often appears in epidemic infectious outbreaks. So this must be due to a virus capable of actually causing an epidemic. Not all viruses can cause epidemics. There are never epidemic outbreaks of HHV-6 and EBV, as we know these two viruses just do not behave like that. However, enteroviruses very often appear in epidemic outbreaks, so again this supports enterovirus as a candidate for the virus that triggers ME/CFS.


Though HHV-6 and EBV pre-existing the body may well play a causal role in ME/CFS after catching a triggering enterovirus: enteroviruses are known to be immunosuppressive, and thus may allow HHV-6 and EBV to reactivate; in other words, having an enterovirus infection as the primary triggering cause of ME/CFS may be the very reason we see HHV-6 and EBV reactivation in ME/CFS.
 

Hip

Senior Member
Messages
17,852
I should mention in this discussion that my own ME/CFS-triggering virus (which Dr Chia told me was almost certainly an enterovirus), which I observed spreading from person to person in my circle of friends and family, actually caused three heart attacks (one fatal) in three people. Prior to contracting the enterovirus infection, these three were all healthy, with no heart problems at all; but as soon as they contracted it: wham! So I have had first hand experience of how enteroviruses can cause heart attacks.

If coxsackievirus B is really causing around 36,000 deaths by heart attack each year in the US alone, we should be really be raising awareness of these human calamities that are due to coxsackievirus B.

How can something that (likely) kills 36,000 individuals a year not be at the very top of scientific and political agendas and policy making?
 
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adreno

PR activist
Messages
4,841
How can something that (likely) kills 73,000 individuals a year not be at the very top of scientific and political agendas and policy making?
You can't ascribe all heart attacks to coxsackie.
 

Hip

Senior Member
Messages
17,852
You can't ascribe all heart attacks to coxsackie.

True, not all. There are around 225,000 fatal heart attacks per year in the US, with 40% of these (90,000 deaths) linked to enterovirus in general, and 16% (36,000 deaths) linked to the enterovirus coxsackievirus B in particular.

Though other infectious agents have also been linked to fatal heart attacks: Cytomegalovirus and Chlamydia pneumoniae.
 
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heapsreal

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I personally think it is most unlikely that the other major ME/CFS-associated pathogens, namely HHV-6 and EBV, are the triggering cause of ME/CFS. This is simple because nearly all adults (90 to 95%) already have these viruses in their bodies, and if you have them already, HHV-6 and EBV could not possibly be candidates for the new, acute viral infection you catch which triggers ME/CFS.

By contrast, the various serotypes of coxsackievirus B and echovirus are relatively rare, and so that makes these viruses much more likely candidates for the ME/CFS-triggering viral infection you catch out of the blue as an adult.


Sure, there are other known infectious causes of ME/CFS, such as Chlamydia pneumoniae, Coxiella burnetii and parvovirus B19, but these are easily tested for (and usually successfully treated with antibiotics or IV immunoglobulin). So sure, you don't have to have coxsackievirus B and echovirus as your ME/CFS-triggering infection.

And ME/CFS occasionally has non-infectious triggers, such as physical trauma (particularly car accidents involving head or neck injury).

But outside of these known causes, and non-infectious causes, for the reasons explained, my money is on enterovirus being the main culprit responsible for virally-triggered ME/CFS of unknown etiology.

More evidence for an enterovirus etiology for triggering ME/CFS comes from the fact that ME/CFS often appears in epidemic infectious outbreaks. So this must be due to a virus capable of actually causing an epidemic. Not all viruses can cause epidemics. There are never epidemic outbreaks of HHV-6 and EBV, as we know these two viruses just do not behave like that. However, enteroviruses very often appear in epidemic outbreaks, so again this supports enterovirus as a candidate for the virus that triggers ME/CFS.


Though HHV-6 and EBV pre-existing the body may well play a causal role in ME/CFS after catching a triggering enterovirus: enteroviruses are known to be immunosuppressive, and thus may allow HHV-6 and EBV to reactivate; in other words, having an enterovirus infection as the primary triggering cause of ME/CFS may be the very reason we see HHV-6 and EBV reactivation in ME/CFS.

Its the horse or the cart thing, and theres no way to know unless someone had an nk function test prior to get cfs/me. Maybe we have had poor nk function all along and this has let all these other infections in.
Or enterovirus has lowered our nk function and those other infections then reactivate and go along for the ride.
I suppose we treat what we find for now and try to improve our immune system.
 

adreno

PR activist
Messages
4,841
Its the horse or the cart thing, and theres no way to know unless someone had an nk function test prior to get cfs/me. Maybe we have had poor nk function all along and this has let all these other infections in.
Or enterovirus has lowered our nk function and those other infections then reactivate and go along for the ride.
I suppose we treat what we find for now and try to improve our immune system.
I like your practical, no-nonsense approach to treating this crap. No messin' around. Go get 'em, lol :ninja:
 

Hip

Senior Member
Messages
17,852
Its the horse or the cart thing, and theres no way to know unless someone had an nk function test prior to get cfs/me. Maybe we have had poor nk function all along and this has let all these other infections in.
Or enterovirus has lowered our nk function and those other infections then reactivate and go along for the ride.
I suppose we treat what we find for now and try to improve our immune system.

I think there is a way to know that HHV-6 or EBV cannot be the trigger for ME/CFS, by the following logic:

If we had poor NK function all along, we would have got ME/CFS when we first contracted HHV-6, which typically occurs around the age of 3 years old (most people acquire HHV-6 very early in infancy). Or we would have got ME/CFS when we first contracted EBV, which typically happens in our teens. But no, we usually live our lives right through to adulthood in full health with both these herpes family viruses in our bodies, without getting ME/CFS

Then some time later in adult life, we catch some mystery respiratory virus, and wham, ME/CFS is then suddenly triggered. Ergo, it must be this mystery respiratory virus (which I suggest is an enterovirus) which is the triggering cause of ME/CFS, and not HHV-6 or EBV, which we already had in our bodies for many years without any manifesting health problems.

Do you follow the argument I am giving?

If it were HHV-6 triggering ME/CFS, then everyone would tend to get ME/CFS when they were around 3 years old — the typical age by which you will have acquired HHV-6. And if it were EBV triggering ME/CFS, then everyone would tend to get ME/CFS when they were a teenager — the typical age you acquire EBV.

But in fact CFS is rarely found in childhood and adolescence, but typically hits in the age range of 20 to 40 years old.

So in summary: we can use the fact that we know HHV-6 or EBV are generally acquired early in life, in infancy and adolescence respectively, to discount the possibility that they are the triggering virus of ME/CFS — a disease which usually first appears in adults between 20 and 40 years old
 

heapsreal

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I think there is a way to know that HHV-6 or EBV cannot be the trigger for ME/CFS, by the following logic:

If we had poor NK function all along, we would have got ME/CFS when we first contracted HHV-6, which typically occurs around the age of 3 years old (most people acquire HHV-6 very early in infancy). Or we would have got ME/CFS when we first contracted EBV, which typically happens in our teens. But no, we usually live our lives right through to adulthood in full health with both these herpes family viruses in our bodies, without getting ME/CFS

Then some time later in adult life, we catch some mystery respiratory virus, and wham, ME/CFS is then suddenly triggered. Ergo, it must be this mystery respiratory virus (which I suggest is an enterovirus) which is the triggering cause of ME/CFS, and not HHV-6 or EBV, which we already had in our bodies for many years without any manifesting health problems.

Do you follow the argument I am giving?

If it were HHV-6 triggering ME/CFS, then everyone would tend to get ME/CFS when they were around 3 years old — the typical age by which you will have acquired HHV-6. And if it were EBV triggering ME/CFS, then everyone would tend to get ME/CFS when they were a teenager — the typical age you acquire EBV.

But in fact CFS is rarely found in childhood and adolescence, but typically hits in the age range of 20 to 40 years old.

So in summary: we can use the fact that we know HHV-6 or EBV are generally acquired early in life, in infancy and adolescence respectively, to discount the possibility that they are the triggering virus of ME/CFS — a disease which usually first appears in adults between 20 and 40 years old

true, or what ever the initial trigger damages the immune system somehow.

In my case i got cmv mono at 31 and while in a post viral state/low immunity i got chickenpox for the second time in my life as i first had it as a child, so then i was in a double post viral state when i then got ebv mono, this was all within 6 months. So i suppose while i was down i kept getting kicked. I suppose prior to this i did have alot of stress prior to this with lots of sleep deprivation due to work as well as young babies ( i am a dad who got up at all hours of the morning feeding and changing bums etc)etc. but im sure others have been through the same thing without getting cfs/me??

For me i think i am really in this herpes/antiviral sub group, mostly because of how it started and because of my response to antivirals.

I know they say most people aquire ebv/cmv/hhv6 etc early in life but there are alot of us cfsers who dont have some of these infections, i have never had hhv6, so i suppose if i got a hhv6 mono now it would make me very ill, there are a few i have also come across who have never had cmv and are neg to igg. So i dont think its that rare for adults 30+ to get mono for the first time, maybe its this group that get really sick, just like how adult chickenpox is alot more viscious then child chickenpox. I also have never had myco or cpn and they are suppose to have been aquired by most adults as well?

I think its really individual to work these out, so many variables, maybe there is a herpes sub group as well as an EV sub group who can also have herpes viruses reactivate, maybe these are people who dont really respond to antivirals for herpes infection because they still have an underlying EV infection which is left untreated.

Personally i dont discount any cause as i believe in sub groups, immune defiencies and auto immune possibilities. It would be good if there were actually specialists who could work this out, without us having to go through all the trial and error stuff.

cheers!!!
 

adreno

PR activist
Messages
4,841
So in summary: we can use the fact that we know HHV-6 or EBV are generally acquired early in life, in infancy and adolescence respectively, to discount the possibility that they are the triggering virus of ME/CFS — a disease which usually first appears in adults between 20 and 40 years old
We might not have weak immune systems to begin with, but that doesn't necessarily mean that a new pathogen is needed to trigger ME/CFS. Stress, toxins, meds, vaccines, aging, gut dysbiosis, any kind of strong environmental insult that shift the balance of the immune system, could trigger a reactivation of prior infections.