Differences between HIV/AIDS symptoms and CFS symptoms

[sorin]

This is more a question for the moderator of this website - can we post pictures with our dermatological conditions on legs, for example rashes or hot spots to exemplify some question or we should not attach pictures?

 

[Daffodil]

@ScottTriGuy it is my understanding that endogenous retroviruses do not develop resistance to 1 drug.

it's really looking to me that HERV's might play a part in this illness...it it were another retrovirus, you would think someone would have found it by now.

there is even a very old article about someone with autism responding to AZT

anyway, maybe the people who respond to antiretrovirals have a different illness...who the heck knows...

 

[sorin]

@ScottTriGuy

it's really looking to me that HERV's might play a part in this illness...it it were another retrovirus, you would think someone would have found it by now.

anyway, maybe the people who respond to antiretrovirals have a different illness...who the heck knows...

I agree with @Daffodil that CFS seems to be caused by a retrovirus. Then, again the question I kept asking since long time ago, why antiretrovirals are not given as treatment for CFS and people with CFS are sent to psychotherapy?

 

[Daffodil]

i think EBV or something else activates HERVs so maybe earlier on the illness, HIV meds might work but later on, the HERV's cause inflammation and all kinds of other problems so we need other meds for the downstream affects....?

 

[waiting]

I am not sure what you mean by tissue-specific pathology, but demeirleir/Lombardi did find HERV activity when they tested gut tissue samples from CFS patients....albeit only 8 samples......

there is evidence of HIV patients having less likelihood of developing diseases such as MS....and there are trials of antiretrovirals going on with MS right now.....and even lupus

so the idea of antiretrovirals helping autoimmunity isn't new...right?
thanks

I'm off-topic re: ME vs HIV/AIDS -- but of course, Dr. Chia *has* shown tissue pathology in stomach biopsy staining for enterovirus.

Very frustrating that no other researcher appears to have attempted to replicate his findings. I thought I read here somewhere he had sent his samples to the CDC to see if they could replicate? I can't recall the results...?

 

[Hip]

Very frustrating that no other researcher appears to have attempted to replicate his findings.

In fact, numerous studies performed in the 1980s and 1990s found enteroviruses in the blood and muscle tissues biopsies of ME/CFS patients. Dr Chia's work replicated these original findings. So there is a lot of evidence linking enterovirus to ME/CFS.

I thought I read here somewhere he had sent his samples to the CDC to see if they could replicate?

Unfortunately, the CDC was unable to detect the presence of enteroviruses in the samples. If I understood him correctly, Dr. C seemed to think that the CDC's failure to find evidence of enteroviruses in these samples was due to their age. He asked them to search again using a different, more sensitive technique and they declined.
Source: 1

 

[waiting]

In fact, numerous studies performed in the 1980s and 1990s found enteroviruses in the blood and muscle tissues biopsies of ME/CFS patients. Dr Chia's work replicated these original findings. So there is a lot of evidence linking enterovirus to ME/CFS.

Thank you, @Hip -- excellent!

Do you think the reason for the failure to continue research on this promising avenue is the same reason for all the other research not pursued -- lack of funding? Or do you think it's not pursued for other reasons?

Also, I'd be interested to learn if you think enteroviral infection as a cause of ME fits into the Dubbo study findings -- where (to paraphrase, perhaps incorrectly), any infection, given high severity (& perhaps the individual's genetics, I might add) could lead to ME (in about 10%) of people?

I wonder if, even though the triggering infections were different, ending in the same common pathway -- ME -- that it is still useful to identify & treat the original trigger?

I understand that there is not a proper, targeted tx yet for enterovirus, but I think I read that Dr. Chia was hopeful that new Hep C treatments might also work on enterovirus. Plus -- and this is really "blue-skying" it, if the ME stigma is reduced & ME research universally taken seriously, a pharmaceutical company might develop a targeted tx for enterovirus.

 

[u&iraok]

In fact, numerous studies performed in the 1980s and 1990s found enteroviruses in the blood and muscle tissues biopsies of ME/CFS patients. Dr Chia's work replicated these original findings. So there is a lot of evidence linking enterovirus to ME/CFS.

Is there a way to tell if viruses are causing ME/CFS or if they are activated/reactivated/easily 'caught' (can't think of the right word) due to a disregulated immune system? This is one of my biggest questions.

 

[Hip]

Do you think the reason for the failure to continue research on this promising avenue is the same reason for all the other research not pursued -- lack of funding? Or do you think it's not pursued for other reasons?

Probably lack of interest is the main factor. There aren't any other researchers out there at the moment with much interest in enterovirus and ME/CFS — even though I think there are more studies linking enterovirus to ME/CFS than any other virus.

Also, I'd be interested to learn if you think enteroviral infection as a cause of ME fits into the Dubbo study findings -- where (to paraphrase, perhaps incorrectly), any infection, given high severity (& perhaps the individual's genetics, I might add) could lead to ME (in about 10%) of people?

It did occur to me that one possibility might be that an EBV infections allows a latent, past enterovirus infection to reactivate, and then cause ME/CFS. It would be interesting to test for reactivated enteroviruses in patients who have their ME/CFS triggered by mononucleosis. Mono is caused by EBV in 90% of cases. After mononucleosis, ME/CFS is found as a sequelae in 9% of cases. Ref: 1

But I think it is perhaps more likely that EBV just by itself is a trigger / ongoing cause of ME/CFS.

Is there a way to tell if viruses are causing ME/CFS or if they are activated/reactivated/easily 'caught' (can't think of the right word) due to a disregulated immune system? This is one of my biggest questions.

I guess one way is using drugs which fight off the virus: if that leads to remission of symptoms, it is suggestive that the active viral infection was the cause, rather than the consequence of ME/CFS.

Dr Chia did this using IV interferon, which fought off the enterovirus infection in ME/CFS patients (as evidenced by reduced enterovirus infection in stomach tissues), and led to a full remission of ME/CFS symptoms (unfortunately the enterovirus infection and the ME/CFS symptom slowly returned after several months to a year).

Although I guess it could be argued that the interferon may have modulated the immune system in such as way as to for example ameliorate autoimmunity, and it was that which led to ME/CFS remission, not the viral clearance. Though I think the viral explanation is more likely.


You also find in parvovirus B19-induced ME/CFS that the symptoms go into full remission after the virus is treated and cleared with IV immunoglobulin. In this case, though, I believe the remission is permanent.

 

[u&iraok]

I guess one way is using drugs which fight off the virus: if that leads to remission of symptoms, it is suggestive that the active viral infection was the cause, rather than the consequence of ME/CFS.

Dr Chia did this using IV interferon, which fought off the enterovirus infection in ME/CFS patients (as evidenced by reduced enterovirus infection in stomach tissues), and led to a full remission of ME/CFS symptoms (unfortunately the enterovirus infection and the ME/CFS symptom slowly returned after several months to a year).

Although I guess it could be argued that the interferon may have modulated the immune system in such as way as to for example ameliorate autoimmunity, and it was that which led to ME/CFS remission, not the viral clearance. Though I think the viral explanation is more likely.

Why do you think the enterovirus and the ME/CFS came back?

 

[Hip]

Why do you think the enterovirus and the ME/CFS came back?

I think it is simply because the antiviral effects of IV interferon, although powerful, did not fully eradicate the virus, but just reduced the areas of infection. So once interferon was discontinued, the viral infection expanded again, and all the ME/CFS symptoms then came back.

The same would be the case in HIV: antiretrovirals will greatly lower viral load, but do not eradicate HIV, so if you stop taking the antiretrovirals, the HIV viral loads will go up again.


However, it does not aways work that way, because when you look at IV immunoglobulin to treat parvovirus B19 infection, this does greatly lower viral load, but my understanding is that when you then stop giving the immunoglobulin, the viral load remains low, with the immune system then keeping the virus under control.

Just why in one case you get a permanent eradication of the high viral load, but in another it is only a temporary eradication I don't know.

 

[halcyon]

Just why in one case you get a permanent eradication of the high viral load, but in another it is only a temporary eradication I don't know.

My guess is that is has to do with the presence of dsRNA in the enterovirus infections. Apparently dsRNA is quite durable and resistant to enzymatic degradation. As Chia has shown with his immunoperoxidase testing on tissue samples, there will be the odd cell here or there with dsRNA in it, surrounded by many cells that don't have dsRNA but do have viral protein in them and are infected. Interferon is probable able to knock down the virus in most of the infected cells but probably is not able to fully eradicate the dsRNA. Once the interferon is stopped the infection probably grows back from the dsRNA left behind. It's Chia's weeds and seeds analogy. You can pull all the weeds but if you don't get the seeds the weeds will just grow back.

 

[Hip]

My guess is that is has to do with the presence of dsRNA in the enterovirus infections.

That is a very plausible hypothesis.

I think that is the mechanism that Tam and Messner proposed in their paper on coxsackievirus persistence: they found that coxsackievirus B can persist in stable dsRNA forms within cells, and what's more, they found these dsRNA forms possess the full viral genome, and having this complete genetic package, these dsRNA forms can later spring back to their original viral particle form, thereby rekindling the viral infection again.

The coxsackievirus B dsRNA studied by Tam and Messner is slightly different to the dsRNA studied by Tracy and Chapman, as the latter cannot spring back to their original viral particle form, and can no longer produce viral particles, because as you know, an essential part of their genome needed to manufacture viral particles has been deleted and lost. So this latter type of dsRNA does not contain the full viral genome, but rather a partially deleted viral genome.


I am not clear, though, on the relationship between the full viral genome dsRNA found by Tam and Messner, and the partially deleted viral genome dsRNA found by Tracy and Chapman. I'd like to know: do these two slightly different forms of dsRNA co-exist in the same virally infected cell? And if so, under what circumstances is the full genome dsRNA produced in the cell, and under what circumstances is the partially deleted genome dsRNA produced?

If it is only full genome dsRNA that can act as the "seeds" that allow the coxsackievirus B infection to rekindle and grow back (which would make sense), then perhaps one way to permanently eradicate coxsackievirus B might be to devise a treatment that promotes the formation of the partially deleted genome dsRNA rather than the full genome dsRNA.

That way the dsRNA "seeds" would not contain the full genome needed to rekindle the infection of viral particles, so then once all the viral particles were wiped out by say interferon treatment, they could never grow back again.

 

[Johannawj]

https://www.linkedin.com/pulse/mecfs-new-herv-k102-afp-immunosenescence-paradigm-laderoute

 

[sorin]

https://www.linkedin.com/pulse/mecfs-new-herv-k102-afp-immunosenescence-paradigm-laderoute

So, following this new reseaerch, is there any treatment (or even cure) discovered for CFS?

 

[sorin]

This thread I have started I named it initially, "Differences between HIV/AIDS symptoms and CFS symptoms" but now I think maybe is more appropriate to ask what is different between HIV symptoms and CFS symptoms? Is something that appears in one disease and is not in the other?

 

[msf]

No ME has been around for a long time...there have been many outbreaks worldwide way before that. Australia had 3 outbreaks of it in the 1950s. http://www.hfme.org/meoutbreakscause.htm

(the outbreaks may of started around time of nuclear testing?)
.........

https://en.wikipedia.org/wiki/History_of_chronic_fatigue_syndrome

I have no way to prove the validity or non-validity of this theory, but the idea of people with ME as some kind of Godzilla appeals to me.

 

[barbc56]

I have no idea about the validity of this persons theory. But hopefully he is using an n=1 as a case study that only indicates that this theory may be true.Does he have other citations that explain this in more detail or at a level my addled mind can understand?

What is the medicinal property in St. Johns Wort that he uses to justify using it as a treatment for me/cfs? It looks like the only scientic indication is for mild depression. Is there something different in SJW than in an AD?

This is more a reflection of my lack of understanding what the author is saying. I do get the part about the cortisol levles. Beyond that I'm lost. Any citations to help understand this would be appreciated. I'll check his other work to see if that helps.

http://www.mayoclinic.org/drugs-supplements/st-johns-wort/evidence/hrb-20060053

Edit. Retrovirus?
Edit. Now that I've read the entire thread, I think I understand this better.

 

[Johannawj]

Marian Laderoute

https://touch.www.linkedin.com/?ses...n.com/in/hervk102#profile/463134295/name:2_di

 

[Johannawj]

"The virus is called HERV-K, and it incorporated itself — permanently — into the human genome between 2 and 5 million years ago. It's a human endogenous retrovirus — an example of nature's own genetic engineering.

Retroviruses — like the human immune deficiency virus (HIV) that causes AIDS — inject their own genetic material into cells. Sometimes, they stay there forever.

Because they're part of the DNA, they are passed down from generation to generation in the same way as genes for eye color or height. Experts estimate that these viruses make up as much as 8 percent of the human genome.

Usually they just sit there doing nothing. But some have been blamed for causing some types of cancer and autoimmune diseases such as multiple sclerosis. HERV-K is suspected of playing a part in the development of breast cancer, for instance.

Dr. Avindra Nath, originally an AIDS researcher, knew that some patients with HIV have a syndrome that resembles ALS — which gradually paralyzes and kill patients as their nerve cells die.

"When you treat them with anti-HIV drugs, they get better," Nath, now at the National Institute for Neurological Disorders and Stroke, told NBC News."

http://www.nbcnews.com/health/healt...use-crippling-disease-als-study-finds-n436911

(HERV-K Suppression Using Antiretroviral Therapy in Volunteers With Amyotrophic Lateral Sclerosis (ALS), Nath Avindra NINDS

https://clinicaltrials.gov/ct2/show/NCT02437110)