Tenofovir (Viread) / Raltegravir (Isentress) Cures ME/CFS Patient Sick for 20 Yrs + Tenofovir Poll

[patient.journey]

I've been on tenofovir daily since 2008. I developed ME in 2014, so I have been on tenofovir throughout the whole of my ME. It has not made any difference (good or bad) for my ME symptoms, and I have no side effects from it.

Saw your story ! U mostly had an auto immune reaction that caused this because of the vaccine u mentioned and here is the other group which won't be infectious caused

 

[Stretched]

I've been on tenofovir daily since 2008. I developed ME in 2014, so I have been on tenofovir throughout the whole of my ME. It has not made any difference (good or bad) for my ME symptoms, and I have no side effects from it.

Your post can be puzzling and it begs the ? - obviously, you take it for viral loads? So, does this imply at least one case where MECFS is not a viral disease; bigger implication involves PWCs superfluous use of at least this one ARV, of many?

Any thoughts re this, given the discussion further back in this thread?

 

[heapsreal]

I've been on tenofovir daily since 2008. I developed ME in 2014, so I have been on tenofovir throughout the whole of my ME. It has not made any difference (good or bad) for my ME symptoms, and I have no side effects from it.

How did you develop me/cfs? Did it dtart with mono/ebv or similar?

 

[patient.journey]

How did you develop me/cfs? Did it dtart with mono/ebv or similar?

It's started after hepatitis b vaccine ! I went through his post .

It looks like autoimmune cause

 

[fingers2022]

I've been on tenofovir daily since 2008. I developed ME in 2014, so I have been on tenofovir throughout the whole of my ME. It has not made any difference (good or bad) for my ME symptoms, and I have no side effects from it.

Hi Max, presumably you were on Tenofovir for something other than ME...not exactly a recreational drug unless used prophylactically I guess.
Like all of us, you'd be a study with n=1, but your experience suggests that Tenofovir doesn't prevent ME, which might scotch any RV theory.
As this is interesting, I wonder if you would share some more details with us - either on the thread or via PM - like how your ME started, its nature (does it seem 'viral'?), symptoms, level of function etc. How confident are you of your ME diagnosis? Are you happy that other possibilities have been satisfactorily ruled out via tests etc.?

 

[Hip]

It seems that Dr Chia has the most ME/CFS patients on tenofovir, and although it's early days, so far he is finding that less than 1 in 3 patients respond to tenofovir, but that the ones who do respond to this drug get significant benefits. Dr Weir also found tenofovir helps some patients but not others. So like all the other ME/CFS treatments, tenofovir seems to work only for a certain subset of patients.

 

[fingers2022]

It seems that Dr Chia has the most ME/CFS patients on tenofovir, and although it's early days, so far he is finding that less than 1 in 3 patients respond to tenofovir, but that the ones who do respond to this drug get significant benefits. Dr Weir also found tenofovir helps some patients but not others. So like all the other ME/CFS treatments, tenofovir seems to work only for a certain subset of patients.

The obvious conclusion is that we need to know what folk are suffering from

 

[Hip]

The obvious conclusion is that we need to know what folk are suffering from

Indeed, but nobody invests enough money into ME/CFS research. Dr John Chia's findings of non-cytolytic enteroviruses in the tissues of ME/CFS patients in 2007 has still not been replicated, even 10 years later.

I find it infuriating that many labs around the world immediately attempted to replicate the XMRV findings (and of course they all came out negative). Whereas nobody has bothered to replicate DR Chia's findings, even though non-cytolytic enteroviruses are an obvious potential cause of ME/CFS.

It's the same with Dr Martin Lerner's ideas on abortive herpesvirus infections in non-permissive cells being a cause of ME/CFS; great idea, and some evidence to support it. But nobody has taken the idea of abortive herpesvirus infections in ME/CFS any further forward since Dr Lerner proposed it over a decade ago.

 

[ScottTriGuy]

...but your experience suggests that Tenofovir doesn't prevent ME, which might scotch any RV theory...

I've been on arvs since 2002, but got sick with ME in 2012, so find it very unlikely ME is RV, I think enterovirus is much more likely and some arvs are also anti enteroviral.

 

[fingers2022]

Indeed, but nobody invests enough money into ME/CFS research.

There is some money going into research now. Sadly, in UK much of it squandered on stuff like Esther Crawley's (cough, spit) projects. Wouldn't it be great if a group of researchers, medics & sufferers (don't forget the sufferers!) got together to workshop what should be priority for research? The input could include research history, medic and patient experience. As above, diagnosis and participant selection would be critical. One of the principles would be open minds and objectivity...except that anyone with a psychological bias would be at least excluded and possibly hung drawn and quartered at the door...not that I have any strong subjective feelings about psychologists

 

[fingers2022]

I've been on arvs since 2002, but got sick with ME in 2012, so find it very unlikely ME is RV, I think enterovirus is much more likely and some arvs are also anti enteroviral.

Good one. I'm being lazy with my own research, but do you know whether something like Tenofovir would be the drug of choice for enteroviruses?
Again, we might come back to a subset (a different illness even) of sufferers having a RV connection.

 

[Hip]

I've been on arvs since 2002, but got sick with ME in 2012, so find it very unlikely ME is RV

Although it has to be said that only tenofovir, raltegravir and elvitegravir have been shown to inhibit gamma-retroviruses, so if there were a gamma-retrovirus in ME/CFS, I am not sure if antiretrovirals other than those three would be able to inhibit it.


By the way, I've been learning a bit about pharmacokinetics recently (the study of how drugs are absorbed and distributed in the body), and from what I can work out, the in vivo anti-cytomegalovirus effect of raltegravir when you take this drug orally is very weak, almost non-existent (even though raltegravir has potent anti-cytomegalovirus effects in vitro).

So I don't think raltegravir would help combat any chronic cytomegalovirus infections a ME/CFS patient might have (even though I suggested earlier in this thread that raltegravir may inhibit herpesviruses).

There is not any data for the in vitro potency of raltegravir against EBV and HHV-6, so I cannot give any estimates on those; but if these two viruses are similar to cytomegalovirus, then we might assume that raltegravir may not have any in vivo potency against them either. So this suggests that the benefits raltegravir may have for ME/CFS are probably not a result of its anti-herpesvirus effects.

Pharmacokinetics is a useful thing to learn about, as it allows your to convert in vitro antiviral study data into estimates for the in vivo potency of that antiviral in the body.

 

[Stretched]

I’m trialing Atripla (Viraday, ARV) for high CMV readings (= 10), sporadic since 1991. I don’t know if it cycles or other, as readings weren’t followed the whole time since initial MD ID, Harvard, said then not much helps... .

Later, Valcyte, Oxymatrine,and other Dr Chia’s standard rx’s didn’t help the ME malaise feeling (in recent years)... . ‘Gave them the boot.

It seems that since CMV = HHV5, close to HHV6, either AV or ARV should help since we know they are viral???

‘ Feeling a little better now but too soon to know if combo pill (multi ARV) is the cause?

 

[Hip]

I’m trialing Atripla (Viraday, ARV) for high CMV readings

Atripla = efavirenz + emtricitabine + tenofovir, but I don't think any of those drugs have any direct antiviral activity against cytomegalovirus. Though it's possible that the immunomodulatory action of tenofovir might boost the general immune attack against viruses.

 

[fingers2022]

It seems that since CMV = HHV5, close to HHV6, either AV or ARV should help since we know they are viral???

My basic understanding is that there are different classes of ARV's, each class disrupting/regulating a different part of the replication cycle by inhibiting certain enzymes. I haven't looked into how AV's work...and here (ref. Hip! ) I am being specific and using ARV to mean anti-retroviral and AV to mean antiviral where the virus is NOT a retrovirus...but I can't see that the pathways can be the same otherwise we wouldn't have specific classes of ARV's. Sure, ARV's seem to be affecting cytokine levels, but via a different pathway to the way they regulate RV replication. So...I don't think we can just assume that any old RV or ARV will do the job. But I'm just a layman and there are well-funded expert scientists out there like ...Lipkin...Coffin...Crawley...White...Wessely.
I'm sure we are in safe hands, so sleep easy folks

 

[heapsreal]

Although it has to be said that only tenofovir, raltegravir and elvitegravir have been shown to inhibit gamma-retroviruses, so if there were a gamma-retrovirus in ME/CFS, I am not sure if antiretrovirals other than those three would be able to inhibit it.


By the way, I've been learning a bit about pharmacokinetics recently (the study of how drugs are absorbed and distributed in the body), and from what I can work out, the in vivo anti-cytomegalovirus effect of raltegravir when you take this drug orally is very weak, almost non-existent (even though raltegravir has potent anti-cytomegalovirus effects in vitro).

So I don't think raltegravir would help combat any chronic cytomegalovirus infections a ME/CFS patient might have (even though I suggested earlier in this thread that raltegravir may inhibit herpesviruses).

There is not any data for the in vitro potency of raltegravir against EBV and HHV-6, so I cannot give any estimates on those; but if these two viruses are similar to cytomegalovirus, then we might assume that raltegravir may not have any in vivo potency against them either. So this suggests that the benefits raltegravir may have for ME/CFS are probably not a result of its anti-herpesvirus effects.

Pharmacokinetics is a useful thing to learn about, as it allows your to convert in vitro antiviral study data into estimates for the in vivo potency of that antiviral in the body.

Tenofovir hasnt stop shingles/varicella virus from reactivating but then neither has famvir but without famvir its much worse of a reactivation.

It seems blood tests are quite poor at testing for chronic infections and its possible these infections arent in the blood but instead in other tissue eg EV in stomach biopsies and herpes viruses in nervous tissues.

Autopsies on mecfsers would seem to be more appropriate until technology improves, looking for infections in different tissue. Sophia Mirza who died of ME and is on her death certificate, pathologists who studied her spinal cord said it had herpes type lesions on it similar to varicella virus and a couple of similar rare autopsies to this.

A very similar condition or maybe even another subgroup of cfsme is mollarets meningitis. Generally caused by hsv 1 or 2 or varicella virus and is detected in a spinal tap but even this test isnt accurate as i have read where many of these patients have had several attacks or reactivations and its taken several spinal taps before they detect the viral cause. Its possible that any virus could cause mollarets which is described as a low grade chronic reoccurring form of meningitis.

After all that, does taking antivirals or antiretrovirals actually get to where we need it or do they only really get a the few pieces of virus that might make the blood stream, so its containing it but not fully getting at these infections.

Are we better off with trying to strengthen our nk cells and t cells. A treatment that seems to be more effective than chemo with cancers so it seems. These new cancer drugs are targeted at increasing the innate immune system to fight cancer. Maybe an option for cfsme although cost is very significant.

 

[Max80]

Hi Max, presumably you were on Tenofovir for something other than ME...not exactly a recreational drug unless used prophylactically I guess.
Like all of us, you'd be a study with n=1, but your experience suggests that Tenofovir doesn't prevent ME, which might scotch any RV theory.
As this is interesting, I wonder if you would share some more details with us - either on the thread or via PM - like how your ME started, its nature (does it seem 'viral'?), symptoms, level of function etc. How confident are you of your ME diagnosis? Are you happy that other possibilities have been satisfactorily ruled out via tests etc.?

I developed ME after Hepatitis B vaccines. I was diagnosed with ME by a doctor at a clinic specialising in ME.

Following the ME diagnosis I had a muscle biopsy last year, which confirmed Macrophagic Myofasciitis (MMF). This is caused by aluminium hydroxide in the vaccine. Research in France has concluded that patients with MMF develop ME. So I'm 100% sure in my diagnosis.

My understanding from research papers is that some people with MMF develop autoimmunity, but not all. MMF results in a constant activation of the immune system due to the persistence of the vaccine adjuvant, and I think this leads to the ME and resulting symptoms in patients with MMF.

My symptoms are chronic fatigue, muscle pain & weakness, cognitive impairment. My symptoms worsen with physical and mental exertion (PEM), with a delayed worsening.
I have to rest for about 20-22 hours a day to minimise pain and fatigue. Simple tasks can hit me hard later. I use a wheelchair frequently when out of the house.

 

[fingers2022]

Tenofovir hasnt stop shingles/varicella virus from reactivating but then neither has famvir but without famvir its much worse of a reactivation.

It seems blood tests are quite poor at testing for chronic infections and its possible these infections arent in the blood but instead in other tissue eg EV in stomach biopsies and herpes viruses in nervous tissues.

Autopsies on mecfsers would seem to be more appropriate until technology improves, looking for infections in different tissue. Sophia Mirza who died of ME and is on her death certificate, pathologists who studied her spinal cord said it had herpes type lesions on it similar to varicella virus and a couple of similar rare autopsies to this.

A very similar condition or maybe even another subgroup of cfsme is mollarets meningitis. Generally caused by hsv 1 or 2 or varicella virus and is detected in a spinal tap but even this test isnt accurate as i have read where many of these patients have had several attacks or reactivations and its taken several spinal taps before they detect the viral cause. Its possible that any virus could cause mollarets which is described as a low grade chronic reoccurring form of meningitis.

After all that, does taking antivirals or antiretrovirals actually get to where we need it or do they only really get a the few pieces of virus that might make the blood stream, so its containing it but not fully getting at these infections.

Are we better off with trying to strengthen our nk cells and t cells. A treatment that seems to be more effective than chemo with cancers so it seems. These new cancer drugs are targeted at increasing the innate immune system to fight cancer. Maybe an option for cfsme although cost is very significant.

Thanks for this HR.
This does make me come back to more natural approaches, which has been my life's philosophy.
I hate taking ARV's, fuck knows what else they may be doing.
Taking them blind too - limited evidence, no personal tests.
I've set myself 6 months on Tenofovir - if no significant improvement, I think I should back off.
What a debacle, huh?
Or maybe I'm just a basket case....cheers Si, you were right all along...and you are seriously dead

 

[Stretched]

Atripla = efavirenz + emtricitabine + tenofovir, but I don't think any of those drugs have any direct antiviral activity against cytomegalovirus. Though it's possible that the immunomodulatory action of tenofovir might boost the general immune attack against viruses.

I’m curious why you hold back on the other two rx’s? The NRTI and N-NRTI mehanisms for HHV6, for which they were designed ought to have efficacy in one HHV lower subset on the
same class of virus, CMV, I presume, though I’m only self studied and not versed in the nuances or commonalities of each virus class.
There are many ARV’s and variations aimed
to work where others missed.

 

[Hip]

@Stretched, are you saying that these antiretroviral drugs have efficacy against HHV-6?