NZ team reactivate research into DRACO (renamed VTose), the universal antiviral that could cure ME/CFS

[godlovesatrier]

Hang on. Surely POTS would have multiple causials? One being low cardiac function. Another being viral infection. I guess there would be lots of reasons. Maybe even low mito function simply causing the blood and body to feel so letharic that this induces pots. Also some on the forum don't have POTS.

Then again Cort did post an article the other day on his site saying that Even if you don't have symptoms you probably still have POTS. So maybe it's a symptom picture issue. Even so if we all have it surely there are multiple causes?

I have to agree that in some patients the damage will be repaired/go away. Probably based on how long they've been sick etc etc. Whereas in others thry will get a bit of life back but not much. I'm rapidly realising how every treatment I try just boosts my energy or immune function or lowers my viral load. But my point is I'm not convinced a root cause treatment will be any better. Not because it's not possivle bit because this is 2020 not 2120.

In 100 years nutrition, medicine and medical science will have moved on so much thst many products exist and hopefully!! God willing. Start to work universally to help the body.

As with covid19 we have a world preoccupied with quick fixes that are specific and have a finite timer. There's a real lack of innovation and new ideas. In terms of drugs and the like. It just bothers me that universal vaccines of ant kind even for coronaviruses are not being government funded worldwide.

 

[Learner1]

there is not much evidence to suggest ME/CFS itself is autoimmune at present, even though it sometimes comes with autoimmune comorbidities.

Really? Maybe in the UK, but everywhere else, it is recognized that there's a not insignificant subgroup with autoimmunity.

https://www.researchgate.net/public...or_Autoantibodies_in_Chronic_Fatigue_Syndrome

https://www.researchgate.net/public...cephalomyelitisChronic_Fatigue_Syndrome_MECFS

https://solvecfs.org/recent-autoimm...amsay-2016-2017-grantee-carmen-scheibenbogen/

http://simmaronresearch.com/2020/05...gue-syndrome-herpesviruses-regulatory-t-cell/

https://www.frontiersin.org/articles/10.3389/fimmu.2018.00229/full

 

[Learner1]

POTS often gets triggered by a viral infection and then sometimes goes away in younger patients. This is exactly what happened to me, after a bad episode in my early 20's I was POTS free for several years until things took a downturn a couple of years ago. There are some anecdotal reports on resolution of MCAS and POTS following treatment protocols, here is one. If I had access to all these treatments I'd be fairly optimistic about my POTS at least improving.

This is exactly the treatment protocol I've been pursuing, with Rituximab. It has been helpful.

 

[Hip]

Really? Maybe in the UK, but everywhere else, it is recognized that there's a not insignificant subgroup with autoimmunity.

Like I said, there's not much evidence to suggest ME/CFS is autoimmune. The few primary studies you linked to does not constitute much scientific evidence. It's not until you get multiple secondary studies can you say that the evidence has accumulated for a particular hypothesis/theory.

And note that just because a doctor looks at some primary studies and tries out a speculative experimental treatment based on those studies, it does not imply the findings of the studies have been proven and have become generally accepted.



Phase III clinical trials proved rituximab a dismal failure as a treatment for ME/CFS. The Phoenix Rising forum's own experience with rituximab was equally bad: with only 1 pure ME/CFS patient out of 30 who tried rituximab getting some improvements. The rest either had no benefits, or actually experienced serious adverse events, like lung infections requiring chest surgery to dig out the infections from the lung.

So that was a blow for the autoimmune theory of ME/CFS.

Of course, there are 4 or 5 different types of autoimmunity under the Coombs and Gell classification, so it's possible that ME/CFS might involve some other form of autoimmunity not directly linked to B-cells. So we might remain open-minded about autoimmunity as a causal factor in ME/CFS.

 

[Learner1]

Here's the problem. It is now well recognized that ME/CFS is not one single entity that one can do a simple random double blind placebo study on. It is recognized that there are subsets of patients who have a number of different etiologies, symptoms, and drivers of their disease. This is why no one has solved this problem yet.

There are doctors that are treating this as an autoimmune disease at least in some patients that they have carefully identified. My doctor has treated several patients successfully with Rituximab, and others who've had Rituximab who are not so successful, but who are not at all sorry that they gave it a try. He thought it was worth a try in me, and as my cytokines showed a clear autoimmune tendency and I had two autoimmune conditions that he believed were triggered by Epstein-Barr and or one of my other herpes family viruses like I was a good candidate for Rituximab. I am now 16 months out from my initial treatment, and it seems to have been successful and my symptoms are much improved from where I started.

Do I think it's a cure for ME/CFS? No, as we typically have a number of other drivers of our disease, which must also be addressed, in addition to fixing the damage done by the originating infections and autoimmunity. Do I think it has the potential to help a number of other ME/CFS patients? Absolutely. And it is a shame that certain patients decide to deride it every chance they get, When it is a very useful tool for treatment, under certain conditions. The studies that were done on Rituximab did not select patients carefully, the patients fit a broad definition of ME/CFS, and are not specifically chosen because they had identified autoimmunity.

Be patients who are saying it's not autoimmune and the autoimmune treatments don't work seem to be the ones who have not had the antibody testing, not done IVIG, and not tried these treatments. It would be extremely helpful if other patients weren't discouraged by patients who do not have the experience with these tools to be able to judge appropriately.

The studies do show that many of us do have autoimmunity, and there are studies showing that tools like IVIG and Rituximab can be used to battle the antibodies that we have. Rituximab is only one tool in the arsenal and it only goes after one type of B cells. There are other types of B cells and T cell driven immunity that it would not help. There are other tools for that, and they have not been adequately tried. Again having people who have not tried these nay saying before anyone has a chance to see if they're successful is very sad, and may discourage people who, selected carefully, might stand to benefit and have great relief from some very significant symptoms.

 

[Hip]

Here's the problem. It is now well recognized that ME/CFS is not one single entity that one can do a simple random double blind placebo study on. It is recognized that there are subsets of patients who have a number of different etiologies, symptoms, and drivers of their disease. This is why no one has solved this problem yet.

It's been assumed that ME/CFS might involve subtypes, and it seems likely to be the case; but as yet we have not really got much of a handle on what the subtypes might be.

My doctor has treated several patients successfully with Rituximab, and others who've had Rituximab who are not so successful, but who are not at all sorry that they gave it a try.

Well ideally that doctor would run a ME/CFS subtype clinical trial on his rituximab treatment, stating what blood test criteria (cytokines, autoantibodies, etc) he uses to judge whether a patient is a suitable candidate for rituximab, and then publishing his results. Then if the results were good, we would know that rituximab can be useful for a clearly defined ME/CFS subtype. So it's down to these doctors to publish.

I would want to make sure that those ME/CFS patients in the trial did not have comorbid autoimmune diseases, otherwise the rituximab may be treating those, rather than the ME/CFS. And you would have to make sure the ME/CFS patients in the trial were not misdiagnosed, with for example lupus, which has similar symptoms to ME/CFS, and is known to respond to rituximab.

I am now 16 months out from my initial treatment, and it seems to have been successful and my symptoms are much improved from where I started.

But aren't you always trying dozens of different treatments at the same time? How can you work out your improvements specifically came from rituximab?

 

[Learner1]

Clinicians don't typically publish. My doctor is pretty busy, helping people. He treats patients as individuals, and customizes treatments to the individual and has a pretty good track record of doing so.

Finding treatments that work is not an armchair hobby of reading a bunch of double blind placebo studies. Rather, the best doctors test patients, figure out their unique characteristics and idiosyncrasies, and treat them.

In 2015, the IOM Report said that an integrated approach, using systems biology, might be used. Last year, Ron Tomkins stated that personalized medicine was one of the 4 main things they were going to be pursuing. My doctors are doing this today. Each individual is unique and gets unique treatment.

I course, I have been doing other treatments. The body is an integrated system of systems with treatments working synergistically to help the health of the patient . I am not convinced that my hormones (thyroid adrenals, sex hormones, vitamin D) helped my POTS and MCAS, nor did hyperbaric oxygen therapy, mitochondrial cocktail nutrients, or the supplements I take for sleep. I take drugs and supplements for MCAS and POTS but they did nothing for the root cause, and I started them in 2017. IVIG helped some, as it goes after the autoimmunity to a degree, but it was only after wiping out my B cells with Rituximab that I was able to greatly cut back on the other treatments for my autoimmune symptoms as most of my symptoms are greatly reduced. I still have high blood pressure, but I suspect there are multiple factors driving it.

 

[Hip]

Clinicians don't typically publish. My doctor is pretty busy, helping people. He treats patients as individuals, and customizes treatments to the individual and has a pretty good track record of doing so.

Maybe you can encourage your doctor to publish. That way they would be helping far more people, as once thousands clinicians around the world see a positive result (assuming it's positive) for certain ME/CFS subtypes, they may follow suit with the same treatment.

Quite a few busy ME/CFS clinicians take the time to conduct studies and publish: Chia, Lerner, Peterson, Klimas, Lapp, Kaufman, Kogelnik, De Meirleir, Brewer, Myhill, Gottfries, Fluge and Mella, Ramsay, Behan, Chaudhuri, Richardson. In fact it seems most of the top clinicians do publish studies.

 

[gbells]

The antivirals we have used so far have not been able to eradicate any of the ME/CFS viruses from the body, because present drugs are not powerful enough. If we could completely eradicate the virus, any downstream effects the virus has like autoimmunity might also disappear.

Chronic hepatitis C virus infection produces a fatiguing disease which has very similar symptoms to ME/CFS (similar enough that it is sometimes misdiagnosed as ME/CFS).

But nowadays the new and powerful antiviral Harvoni can totally eradicate the hepatitis C virus from the body, which then completely cures patients.

If we had an antiviral like DRACO or VTose which could totally eliminate enterovirus or herpesvirus, then we may well find ME/CFS patients are similarly completely cured.

HHV6 blocks caspase 3 and 8 and EBV blocks necroapotosis at RIPK 1 and 3 so DRACO/Vtose shouldn't work for anyone who has EBV (80% of ME patients).

Epstein–Barr virus (EBV) is a gamma herpesvirus that infects the majority of human adults. A recent report suggests that the latent membrane protein 1 (LMP1) of EBV interacts with RIPK1 and RIPK3, modulates their ubiquitination status, and inhibits TNF, Smac mimetic and caspase inhibitor-induced necroptosis

https://www.nature.com/articles/s41418-018-0172-x#:~:text=Facts,inhibitors competing for RHIM binding.

 

[Hip]

HHV6 blocks caspase 3 and 8 and EBV blocks necroapotosis at RIPK 1 and 3 so DRACO/Vtose shouldn't work for anyone who has EBV

I don't know much about it, but you might want to search Todd Rider's paper for the word "apoptosis", and see if the way that apoptosis is induced by DRACO can bypass the mechanisms that viruses use to block apoptosis.

It seems that viruses block early steps in the apoptotic pathway, whereas DRACO bypasses these early steps and targets the latter steps of the pathway:

The second natural process used by our approach is one of the last steps in the apoptosis pathway, in which complexes containing intracellular apoptosis signaling molecules, such as apoptotic protease activating factor 1 (Apaf-1) or FLICE-activated death domain (FADD), simultaneously bind multiple procaspases.

Virtually all viruses that inhibit apoptosis do so by targeting early steps in the pathway, for example by inhibiting p53, mimicking anti-apoptotic Bcl-2, or interfering with death receptor signaling.

 

[gbells]

Won't work. EBV still hangs on necroptosis and APAF hangs at caspase 3 for HHV6.

https://www.wikiwand.com/en/Death-

inducing_signaling_complex#:~:text=CAP4%20is%20also%20called%20FLICE,as%20FLICE%20must%20be%20activated.

https://www.wikiwand.com/en/APAF1

 

[Hip]

Won't work.

Can you explain why (with slightly more details)?

 

[Judee]

It's kind of a silly thought and I wouldn't know how to take it further than that but maybe Kimer Med could interest a venture capital firm in what they are doing. I think I read about one not too long ago that was investing in an Israeli vaccine company that was already working on Covid viruses. I'm sorry I don't remember more than that right now.

Anyway, it was just a thought.

Thanks for this update, @Hip. I think this sounds promising. I can see a domino effect happening. One doctor I had said everything is cumulative where the body is concerned and he's right. Take some of the load off and then the body can deal with the other things more effectively.

For instance, my mom's COPD was getting very bad however, we did not know her heart was also having issues. Now that we have doctors recognizing that and working with the heart as well, her COPD is very much improved. She gets only slightly winded when walking and catches her breath very quickly AND we've been able to lower her oxygen prescription and may be able to lower it more at some point. It's been a most pleasing turn around for her. Even some of her other issues have improved on their own.

She's still fragile but I'm seeing her have a lot more good days than bad.

 

[Hipsman]

Does Kimer Med know of this thread? Maybe they could clear up some things just like they did on LongeCity DRACO thread.

 

[gbells]

Can you explain why (with slightly more details)?

It's the downstream problem. DRACO isn't downstream enough of the apoptosis blocks for it to work. EBV blocks it downstream at the aforementioned checkpoint. You have to look hard at the apoptosis pathways that the viruses are affecting. I might be able to get it to work if I added more supplements but by itself it shouldn't work. Also, if I have to add more supplements why pay for an expensive drug as the supplements are cheaper? Doesn't make economic sense and it doesn't offer that much to simplify treatment. This may be a great drug for some viruses but not EBV so it won't be a silver bullet for ME.

Interestingly, medical immunotherapy hasn't developed any drugs which work either.

 

[Learner1]

It's the downstream problem. DRACO isn't downstream enough of the apoptosis blocks for it to work. EBV blocks it downstream at the aforementioned checkpoint. You have to look hard at the apoptosis pathways that the viruses are affecting. I might be able to get it to work if I added more supplements but by itself it shouldn't work. Also, if I have to add more supplements why pay for an expensive drug as the supplements are cheaper? Doesn't make economic sense and it doesn't offer that much to simplify treatment. This may be a great drug for some viruses but not EBV so it won't be a silver bullet for ME.

Which supplements are you using? I had no luck with artemisinin, which should work, an array of mushrooms, zinc, burbur and samento. Also resveratrol. It took Valcyte and IVIG to put a dent in it ..

 

[gbells]

Which supplements are you using? I had no luck with artemisinin, which should work, an array of mushrooms, zinc, burbur and samento. Also resveratrol. It took Valcyte and IVIG to put a dent in it ..

See my blog for some of them. I'm still testing so I'm not ready to go into all of them.
https://forums.phoenixrising.me/blog-articles/blog/self-experimenting-a-new-me-treatment.37056/

Interestingly, medical immunotherapy hasn't developed any drugs which work either.

It gets complicated because you have to hit the right checkpoints for the viruses you have. I have HHV6, EBV, Varicella Zoster and coxsackievirus so that's a lot of apoptosis blocking. The only one I don't have to deal with is cytomegalovirus thank goodness as that is a tough one. I didn't find any supplements that could touch it. I'll have to search more when I have less fatigue. Perhaps combined with drug therapy for CMV could be effective. Will have to research it.

There are a lot of herbs that are marketed for ME but are a waste of time. You have to really research them thoroughly or you can waste a lot of money. I've been working on my fast-slow apoptosis system for a decade trying different ones.

Immunoglobulins (antibodies) for EBV infected cells don't make sense because of multiple apotosis blocks, one is even right after the attachment site of the antibody. They aren't effective on latent EBV infected cells. The approach I took to generate my own antibodies was nagalase testing (3x normal blood level) and GcMAF however after 6 months of treatment this triggered systemic lupus erythematosus. If I were to do it again I would limit to 4 months. But after that you still have to deal with the EBV apoptosis blocks or, like the immunoglobulin, it won't work.

Avoid strong antioxidants (NAC, Vit E, resversatrol) as they are apoptosis inhibitors.

 

[Hip]

It's the downstream problem.

So even though the DRACO study says this drug targets "one of the last steps in the apoptosis pathway", and says that virtually all viruses inhibit apoptosis at the early steps in the apoptosis pathway, you are claiming that EBV blocks apoptosis right at the very end of the apoptosis pathway, beyond the point which DRACO targets?

Do you have a diagram of the EBV apoptosis pathway that backs up your claim?



And then you claim that by adding some supplements to DRACO, you can get it to work? And then you suggest that the supplements alone would work just as well as DRACO?!

I might be able to get it to work if I added more supplements but by itself it shouldn't work. Also, if I have to add more supplements why pay for an expensive drug as the supplements are cheaper?

 

[gbells]

So even though the DRACO study says this drug targets "one of the last steps in the apoptosis pathway", and says that virtually all viruses inhibit apoptosis at the early steps in the apoptosis pathway, you are claiming that EBV blocks apoptosis right at the very end of the apoptosis pathway, beyond the point which DRACO targets?

Do you have a diagram of the EBV apoptosis pathway that backs up your claim?



And then you claim that by adding some supplements to DRACO, you can get it to work?? And then you suggest that the supplements alone would work just as well as DRACO??!!!

Here's the best apoptosis summary I have. I'm pretty sure EBV blocks at TRIF, Nf-KB+, RIP and blocks macrophage antibody generation from nagalase inhibiting GcMAF at a high level of infection. The DRACO checkpoint is to assemble the RIP complex to trigger necroptosis which is blocked by EBV. There will be additional blocks if other viruses are present. If a chemical helps facilitate a blocked checkpoint it can be used to push it towards apoptosis. If you have enough activation it will apoptose. Just because the DRACO scientists claim something you can't accept it the data doesn't support it (it doesn't). EBV blocks necroptosis at the RIP complex so DRACO won't work alone if one is infected. Sorry to break it to you. However, you can really hammer that pathway if you know what you are doing since it is affected by other stimuli like shock proteins.

 

[godlovesatrier]

One issue with EBV that seems to be true is it's almost impossible to eradicate if your having an immune issue or disease. So maybe not surprising if Draco struggled with it in practice, but who knows. I know valtrex and valcyte are meant to eradicate at high doses over 2 or 3 years, but it's a powerful herx off that stuff, not sure how anyone could do that without taking 6 months off work to weather the herx.