Antivirals as ME/CFS or Long Covid treatments (e.g. valacyclovir, valgancyclovir, amantadine)

Holinger said:
That sounds truely fascinating and frustrating at the same time.
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It`s bizarre. Even the MECFS clinic was like, we have never heard anything like it, and they must have had thousands of patients at this point.

The reason why they wanted to try it was because I described my MECFS fluctuating so wildly throughout all my time with MECFS. Just random fluctuations out of nowhere with flu like feeling, which was always accompanied by lots of phlegm when I was mild. So the guy at the clinic had some kind of herpes re-activation theory from birth (which I thought sounded very unserious). Definitely sounded like he wasn't even expecting any massive positive effect at all when he proscribed the drug.

Hope I can live long enough to get an answer!!
 
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Posts moved from Plasma cell targeting with the anti-CD38 antibody daratumumab in ME/CFS -a clinical pilot study, 2025, Fluge et al

Jonathan Edwards said:
We are all very aware that ME/CFS is a placeholder term that we think points to some common aspect of pathomechanism and that criteria are simply a best shot at capturing that and largely irrelevant other than as a way of standardising research questions.
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I think that there is one group of patients that fulfill the CCC – to which I belong – who have chronic HHV-6B reactivation and whose symptoms can fully be explained by this single pathomechansim. And then there's probably a rest of patients who fulfill the criteria too but who have a different illness alltogether where chronic herpes reactivation is not the driver.

That's the reason why I am advocating for putting more resources into determining the role of chronic HHV-6B reactivation in ME/CFS. As soon as we know how to seperate these two groups objectively the criteria can be adjusted to fit the different groups more adequately.

From my perspective – with aciclovir in reserve that helps me to fight flares – I think that this way of going forward in research is much more reasonable than advocating for research that tries to find some random drug that already exists and hoping to incidentally find a miracle cure. Going after herpes directly with full force will bring concrete and crucial results about pathomechanim fast whereas the latter approach – that is discussed here – strikes me as a desperate attempt at trying to win the lottery.
 
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PageofME said:
I think that there is one group of patients that fulfill the CCC – to which I belong – who have chronic HHV-6B reactivation and whose symptoms can fully be explained by this single pathomechansim.
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OK, but why pick HHV-6B reactivation? There may be some data on increased levels in saliva but how does HHV-6 explain things any better than anything else? And why is it reactivated (which would be the real question) and how would explain delayed PEM?

You seem to be starting from the assumption that HHV6 has the edge on other things but I suspect other members here haven't heard a reason for it.
 
PageofME said:
I watched the Norwegian documentary about Fluge's work. This is exactly what he's doing in my view.
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Well, you have yourself admitted that you are unfamiliar with immunology. I know Oystein and Olav and I can assure you that there was nothing random about their choices. It has all been very logically argued. They may be off track but they do have a rationale. What is the rationale for 'randomly' picking HHV6?!!
 
What worries me about the idea of HHV6 is that it was originally proposed on the basis that there might be immunodeficiency in ME/CFS but that has not been confirmed (if there was we would expect other opportunistic problems and those are not reported). If there is no immunocompromise then the symptoms of ME/CFS do not seem to fit with recognised accounts of HHV6 infection in adults.
 
PageofME said:
But I am.

I watched the Norwegian documentary about Fluge's work. This is exactly what he's doing in my view.
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Okay then you have seriously misunderstood. F&M observed massive improvements in cancer patients with ME/CFS following treatment for cancer. So significant they were asking for more chemotherapy. They have followed this clinical observation through several drug trials, including a positive phase 2 of cyclophosphamine, and are now using daratumumab in order to try and get that effect in a safer drug.

There is also evidence from a study that ME/CFS B cells express more CD38 when stimulated than the B cells of healthy controls. Daratumumab is an anti CD38 drug. That is not in any way trying random drugs in an attempt to find a miracle cure. It is following the clinical and scientific evidence where it leads you.
 
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V.R.T. said:
Okay then you have seriously misunderstood. F&M observed massive improvements in cancer patients with ME/CFS following treatment for cancer. So significant they were asking for more chemotherapy. They have followed this clinical observation through several drug trials, including a positive phase 2 of cyclophosphamine, and are now using daratumumab in order to try and get that effect in a safer drug.

There is also evidence from a study that ME/CFS B cells express more CD38 that stimulated than other cells. Daratumumab is an anti CD38 drug. That is not in any way trying random drugs in an attempt to find a miracle cure. It is following the clinical and scientific evidence where it leads you.
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I think there is a case for saying that F&M might be making a few leaps of faith, and that we’re cutting them a bit of slack because they have demonstrated that 1) they are very good at doing trials, 2) they are willing to accept negative data, and 3) we want treatments as soon as possible.

I trust @Jonathan Edwards if he says that their rationale is well reasoned, and that that might mean that they have crossed the threshold of where it might be warranted to do treatment trials even if they are based on some unverified assumptions.

From a layperson perspective, one of the main differences between F&M and the other treatment researchers is that F&M’s ideas can’t be easily picked apart with existing negative findings. Most proposed treatments seem like they are based on memes or hype about what someone thinks is wrong, regardless of what the data says.
 
The problem with all these viral reactivation tests is that there is no healthy controls done to interpret them against because no HC people get these tests.

So ME people panic and start taking all kinds of tests in a bid to find something wrong and once you see the high viral scores (which we have no HC population to compare to) they zoom in on that and assume it is a “latent virus” causing their symptoms. Then they start loading on antivirals for the cure.


I’ve been there and done that.
 
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ryanc97 said:
The problem with all these viral reactivation tests is that there is no healthy controls done to interpret them against because no HC people get these tests.

So ME people panic and start taking all kinds of tests in a bid to find something wrong and once you see the high viral scores (which we have no HC population to compare to) they zoom in on that and assume it is a “latent virus” causing their symptoms. Then they start loading on antivirals for the cure.


I’ve been there and done that.
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Expect that there have been several large scale studies looking at different viruses in ME/CFS and HC and finding largely no differences. So any explanation will have to be different to the standard explanation seen online.
 
Jonathan Edwards said:
OK, but why pick HHV-6B reactivation? There may be some data on increased levels in saliva but how does HHV-6 explain things any better than anything else? And why is it reactivated (which would be the real question) and how would explain delayed PEM?

You seem to be starting from the assumption that HHV6 has the edge on other things but I suspect other members here haven't heard a reason for it.
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I'll write an answer to that in the upcoming weeks. I believe that I can give you very good arguments on all of the questions you raise that do make HHV-6b reactivation hypothesis the most plausible of all the ideas on causative mechanism that were brought forward.
 
PageofME said:
I think that there is one group of patients that fulfill the CCC – to which I belong – who have chronic HHV-6B reactivation and whose symptoms can fully be explained by this single pathomechansim. And then there's probably a rest of patients who fulfill the criteria too but who have a different illness alltogether where chronic herpes reactivation is not the driver.

That's the reason why I am advocating for putting more resources into determining the role of chronic HHV-6B reactivation in ME/CFS. As soon as we know how to seperate these two groups objectively the criteria can be adjusted to fit the different groups more adequately.

From my perspective – with aciclovir in reserve that helps me to fight flares – I think that this way of going forward in research is much more reasonable than advocating for research that tries to find some random drug that already exists and hoping to incidentally find a miracle cure. Going after herpes directly with full force will bring concrete and crucial results about pathomechanim fast whereas the latter approach – that is discussed here – strikes me as a desperate attempt at trying to win the lottery.
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Did you test by IgM or by PCR?
 
Venicequeenf said:
Did you test by IgM or by PCR?
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I could try aciclovir on speck with a prescription by my throat-ear-nose doctor. She had no idea what I could have at that time. I hadn't heard of ME either. I thought I had Mollaret meningitis, a self-ending "benign" form of HHV-1 brain inflammation and managed to get her to write me a prescription. Aciclovir worked within one hour – and has ever since.

I use it mainly in emergency situations now. I am pretty stable with pacing.

Now, together with my family doctor we're looking for a specialist who has the interest to do sputum PCR in the style of Jacqueline Cliff's research. My specialist is quite far away and overloaded with work.

I saw you're from Basel. Are you a patient too? Do you have a good ME specialist there?
 
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PageofME said:
I could try aciclovir on speck with a prescription by my throat-ear-nose doctor. She had no idea what I could have at that time. I hadn't heard of ME either. I thought I had Mollaret meningitis, a self-ending "benign" form of HHV-1 brain inflammation and managed to get her to write me a prescription. Aciclovir worked within one hour – and has ever since.

I use it mainly in emergency situations now. I am pretty stable with pacing.

Now, together with my family doctor we're looking for a specialist who has the interest to do sputum PCR in the style of Jacqueline Cliff's research. My specialist is quite far away and overloaded with work.

I saw you're from Basel. Are you a patient too? Do you have a good ME specialist there?
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That is interesting. Is it not possible to test active viral persistance/corculation by PcR in EDta blood?

I had a good specialist (rehab) bit she stopped working there and her patients incl me got sent back to the Hausarzt or in other words: they are left to fight alone now which is hard because no one there now to make special blood tests or try new medications
 
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