-
Notice: S4ME will have a short interruption of service on May 30. More information here.
Antivirals as ME/CFS or Long Covid treatments (e.g. valacyclovir, valgancyclovir, amantadine)
- Thread starter Lidia Thompson
- Start date
I will provide one as soon as possible.
But she's basically saying the same as I from her personal experience. Acyclovir suppresses flares fully or if not acute causes a dissolution of exertion intolerance.
She's saying something along the lines of: No matter how much I go over my exertion threshold (she's been a mild/moderate patient for 25 years and knows pacing very well) I don't have PEM.
I switched from aciclovir to valaciclovir ten days ago. I am experiencing it just as I could expect it from the information available on the differences between the two drugs. Valaciclovir is more effective and it lasts longer in the body.
It was a bit tricky to find the right dosage and I experimented a bit. I started with 500mg twice daily. I experienced two very strong peaks where I felt really drugged and after ten hours I felt sober again which I thought might be ok with shingles or HSV prevention but not with ME/CFS.
If the theory is true that ME of the flu-like lead symptom group who respond to aciclovir represents a smoldering abortive type of herpes reactivation that the immune system can't control anymore (Maria Ariza, Ohio State) I think you don't want to be sober. Not even for a couple of hours.
I chatted with a friend who is a researcher and a pharmacolcogist and knows (val)aciclovir well because they use it at the children's hospital where he works to prepare the kids against CMV reactivation before immune therapy. He looked it up for me and yes, at the hospital valaciclovir is given every eight hours.
I have decided on a regime of 4x250. I am taking two doses within three hours in the morning to push the drug mirror higher up during the day while I am active and take the third dose in the late afternoon. I don't exert myself in the evening and I take the last dose when I go to bed.
I have been pretty active when at the same time I continue to rest for one or two hours during the day. I feel that if I wanted to do more I needed to take a higher dose of the drug and that's not feasible for me at the moment.
I will go off the drug in a couple of days – I prefer to do it in a cold turkey fashion because I really don't want to be active while not on a high enough dose of the drug and risk the building of resistancies. And it is only when I'm sober that I can return to listen to my body to find out about my exertion threshold.
I hope I find a good specialist soon who will help me to find out what's sensible for me to do. Is it to go continually on the drug and start work rehabilitation like some patients do it. Is it to continue to just take valacyclovir in emergency situation and from time to time to give the nurse and super pacer part of me a holiday as I have been doing it for the first year of experimenting with the drug?
I am really curious what time will bring!
It was a bit tricky to find the right dosage and I experimented a bit. I started with 500mg twice daily. I experienced two very strong peaks where I felt really drugged and after ten hours I felt sober again which I thought might be ok with shingles or HSV prevention but not with ME/CFS.
If the theory is true that ME of the flu-like lead symptom group who respond to aciclovir represents a smoldering abortive type of herpes reactivation that the immune system can't control anymore (Maria Ariza, Ohio State) I think you don't want to be sober. Not even for a couple of hours.
I chatted with a friend who is a researcher and a pharmacolcogist and knows (val)aciclovir well because they use it at the children's hospital where he works to prepare the kids against CMV reactivation before immune therapy. He looked it up for me and yes, at the hospital valaciclovir is given every eight hours.
I have decided on a regime of 4x250. I am taking two doses within three hours in the morning to push the drug mirror higher up during the day while I am active and take the third dose in the late afternoon. I don't exert myself in the evening and I take the last dose when I go to bed.
I have been pretty active when at the same time I continue to rest for one or two hours during the day. I feel that if I wanted to do more I needed to take a higher dose of the drug and that's not feasible for me at the moment.
I will go off the drug in a couple of days – I prefer to do it in a cold turkey fashion because I really don't want to be active while not on a high enough dose of the drug and risk the building of resistancies. And it is only when I'm sober that I can return to listen to my body to find out about my exertion threshold.
I hope I find a good specialist soon who will help me to find out what's sensible for me to do. Is it to go continually on the drug and start work rehabilitation like some patients do it. Is it to continue to just take valacyclovir in emergency situation and from time to time to give the nurse and super pacer part of me a holiday as I have been doing it for the first year of experimenting with the drug?
I am really curious what time will bring!
Last edited:
Evergreen
Senior Member (Voting Rights)
Here's a summary:
The slides start with some research. She says some specialists prescribe (val)acylovir based on a hypotheses that persistent or reactivated herpes infections contribute to symptoms for a subset of ME/CFS patients. She summarises this study - placebo-controlled - which concluded:
She then talks about Lerner's studies, with reported good response and lasting recovery.
Then on to her experience:
She was doing better - in what she calls a remission - and then got chicken pox, covid and staph aureus infections, one after the other. She had a big crash. That was two years ago.
Since then she has been trying to support her immune system, first with herbal tinctures which weren't effective enough. She asked her doctor for acyclovir and got it, but the next day saw an immunologist who independently prescribed acyclovir, presumably on the basis of lab results for herpes simplex I (shown on slide but unclear where those results are from, and no column labels, nor what they mean, but the immunologist clearly picked out herpes simplex as warranting treatment).
Day by day she felt better and steps went up. No matter how much she went over her baseline, no PENE.
However, other things she measures look worse "Body Battery", resting heart rate (higher), heart rate variability (lower).
Then she tried another drug and it seems that didn't end well - her next update will be about that.
Last edited:
Thanks for this summary. I would like to add what Molly is saying about dosage:
Because Molly and her immunologist believe that there is an ordinary problem with herpes as a comorbidity to ME/CFS and the doctor is not prescribing it in the fashion of Dr. Lerner against ME/CFS directly dosage seems to be inspired by fighting ordinary herpes flares.
It's interesting what you @Evergreen write about the idea of the doctor that she's tackling HSV with the drug. Because the dosage of acyclovir is rather similar to fighting a shingles episode where the drug is prescribed in a higher dose and over a longer time.
To fight an ordinary HSV reactivation acyclovir is prescribed for five days at 200mg every three hours. Molly had instead the double amount of 400 mg daily for two weeks. She does write something about the rationale behind this. She says that in Germany there is the idea evolving that some (ME/CFS?) patients can't control herpes well and should therefore be put on an aciclovir for several weeks and that that was on off-label use. It's quite confusing, actually.
Because it is on the contrary a standard practice that low dose aciclovir or rather valaciclovir because of its longer endurance is used when people have regular HSV or shingles outbreaks in a preventative way.
What I think is maybe the most important point of Molly's account is that instructed by her doctor after two weeks she went down on a "preventative" dosage of 2x400mg of acyclovir and that now she's experiencing that she's becoming acute again, in the language of most ME/CFS patients she develops PEM again.
And this is so important: Why, because we acyclovir responders do not get a little bit or a lot better in certain symptoms like fatigue or cognitive issues but we don't relapse anymore at all. Similarly when we go off thr drug we're not just a little bit less well again but we simply experience ME/CFS coming back again. I feel that this is difficult for people to understand because from what I've seen the efficacy of a drug for ME/CFS is always discussed as a matter of a bettering/worsening of certain symptoms.
But what acyclovir responders all have in common is something different: We don't have "crashes", PEM, or how I like to call it flares or episodes anymore. And when we go off the drug we're relapsing again and have to pace again to stay stable. While we don't have to pace on the drug – but are in my case instead tired because of the side effects.
I am not surprised to hear that Molly states that she's relapsing on that low "preventative* dose of acyclovir because from my experience and from what other acyclovir responders write on Reddit and elsewhere 2x400mg of acyclovir is not a high enough dose for moderate ME/CFS. I needed 1600-2400mg of acyclovir a day to prevent relapsing continually and are now without flares on 1000mg of valacyclovir a day. I don't think that I could go down on 500mg of valacyclovir and certainly not on 800mg of acylovir – because it's metabolized really fast.
In Switzerland I know that aciclovir is not even used for prevention but only valacyclovir because of its slower metabolisation.
What Molly's doctor is doing is pretty stupid in my view because the dosage that she's prescribing might be just the perfect regime to allow the hypothesised atypically reactivated virus or viruses (EBV? VZV? HHV6b?) at the root of ME/CFS flares to develop resistances against herpes antivirals.
Exactly for this reason I have tried several times to find out what valacyclovir treatment regime our @Rick Sanchez was on, because in his account he was a responder for three months and then experienced the power of the drug fading over the next six. He could also just have been on a standard herpes prevantative regime that Molly is now on and that's critically not strong enough to fight ME/CFS flares. But up to now he's decided not to share this informations with us, unfortunately.
Thinking this all through I think that I am going to write to my ME/CFS specialist that other ME/CFS specialists prescribe acyclovir to ME/CFS patients in this risky fashion because they think of herpes as a comorbidity and don't know that it is hypothesised in an atypical reactivation pattern as a possible root cause of ME/CFS.
Last edited:
Evergreen
Senior Member (Voting Rights)
The immunologist put her on 400mg every 3 hours, 5 times a day. Molly was to feed back after a week, which she did, and she was told to continue the same for another week. Then from week 3, she was to take 400mg twice a day.
There is no indication that the immunologist was trying to treat her ME/CFS. My understanding is that the dose of 400mg every 3 hours is used for immunocompromised people.
Last edited:
On the third to last sheet Molly writes: Seit drei Tagen sollte ich die Dosis auf zweimal täglich reduzieren, und ich merke, wie die Erschöpfung wieder zunimmt.
It is formulated a bit sloppy but I think that she means: Seit drei Tagen habe ich wie verordnet die Dosis auf zweimal täglich reduziert, und ich merke wie die Erschöpfung...
In English: For the past three days, I have reduced the dose to twice a day as prescribed, and I am noticing the increasing exhaustion again. (Google)
I belive that when speaking of exhaustion she's pointing to her experience of becoming mildly acute with an ME/CFS flare (PEM) again. What do you think that this means?
It's only on the second to last slide that she begins discussing this other drug. After she's finished discussing aciclovir.
I was also wondering whether she's discussing ME/CFS patients with herpes comorbidities or problems with herpes in general. And actually I conclude that she's discussing that there's this emerging idea in Germany that ME/CFS patients have often comorbid problems with herpes and yes, as you say, they might think that because of an immune defect ME/CFS patients then need higher dosage and to be put on longer therapies to fight herpes flares.
And it makes so much sense because in the new German Konsenus Statement and also in the older Long Covid and ME/CFS guide for clinicians that was created by Carmen Scheibenbogen there are everytime explicitly mentioned that in a group of patients there are herpes reactivations that should then be treated with herpes drugs to help patients stabilise their ME/CFS and not getting worse because of additional chronic infections.
I think what makes Molly's account difficult to understand is that she's not well read into herpes reactivation causative theories of ME/CFS and thus hasn't fully grasped the difference of these two understandings of the role of herpes in ME/CFS. On the one hand she's summarizing Lerner's ideas – full recovery on herpes drugs because herpes is at the root of ME/CFS – and then again the emerging German leading clinicians' idea of the role of herpes in ME/CFS as a comorbitiy that is a important and more difficult to treat compared to non-ME/CFS patients because of immunity issues.
I will end again by stating that I think this is really stupid, and it's so good to realise what's going on. Even though top researchers from the US who are researching Long Covid cohorts with ME/CFS are saying that herpes reactivation is one of the most important hypotheses for explainig ME/CFS pathomechanism in Germany everyone seems to follow Prof. Scheibenbogen and autoimmunity theory. And this is now leading them to treat patients with these potentially risky herpes drug therapies.
Last edited:
Evergreen
Senior Member (Voting Rights)
You are right that she says that 3 days after reducing her dose, she started feeling exhausted again, @PageofME, I missed that line when flicking through. I'll go back and fix my post.
I don't think the immunologist necessarily thinks that ME/CFS patients in general are immunodeficient. But it sounds reasonable to consider Molly immunodeficient, given that she was having one infection after another and had lab results that (presumably) showed she had an active infection.
I'm not sure I follow. Are you saying you think that the immunologist treating Molly's herpes simplex infection as she did was stupid and risky, and instead should have treated her with an untested regimen based on a hypothesis? If so, I do not agree at all.
I am saying that given that we have all this anecdotal evidence of patients mostly self-medicating with aciclovir who write that they have to be on high doses continually in order not to relapse and that we have all the research and theories pointing to herpes playing a central role as the cause of ME7CFS doctors should be careful with prescribing herpes drugs to ME/CFS patients.
I especially think that the regimes that are aimed at preventing standard herpes reactivation with low doses are maybe the perfect conditions to foster the building of resistances of herpes against the standard herpes drugs in ME/CFS.
I didn't say that doctors of ME/CFS patients shouldn't fight their herpes flares with herpes drugs but they should urgently be trained on the current evidence and hypotheses including anecdotal experiences of ME/CFS patients who are aciclovir responders to become aware that standard preventative herpes regimes are potentially not suitable in the aciclovir responder group of ME/CFS patients because this dosage might be directly messing with what's going on in patients.
I am not a doctor but I find it weird that they are – as you suggest – fighting herpes flares that are not presenting with the typical outer symptoms of HSV or VZV reactivation but with a rationale that is based on fuzzy lab results (acute lytic herpes reactivation can't be determined via antibodies in blood tests but only via PCR).
Last edited:
Evergreen
Senior Member (Voting Rights)
I disagree. I have not seen any evidence yet that would warrant clinicians changing their practice. What evidence have you seen that suggests pwME and herpes infections deteriorate more than the wider population of people with herpes infections following standard treatment for those herpes infections?
I'm frustrated with the lack of science in this discussion, so I've tried to find placebo-controlled trials of anti-virals.
Richman et al. 2019 (including Klimas) discuss 3 papers that look at either acyclovir, valacyclovir or valgancyclovir:
1. Straus et al. 1988 - negative trial of acyclovir
2. Lerner AM, Beqaj SH, Deeter RG, Fitzgerald JT. Valacyclovir Treatment in Epstein-Barr Virus Subset Chronic Fatigue Syndrome: Thirty-six Months Follow-up. In Vivo. 2007;21(5):707–713.
3. Montoya et al. 2013
In Straus et al. 1988's trial of acyclovir, 87.5% (21/24) of those who completed the trial were "responders". The problem is that the responders were evenly split between those who got the drug and those who got the placebo. While many people improved, no-one was responding to acyclovir. It's unlikely that the dose was too low, since 3 of the 27 who started the trial had to withdraw due to nephrotoxicity from acylovir. @PageofME, why do you think Straus et al. 1988 found that acyclovir was not effective if acyclovir is, indeed, effective for some?
I've started a thread for Lerner et al. 2007's trial of valacylovir and a thread for Montoya et al. 2013's trial of valgancyclovir.
Last edited: