Antivirals as an ME/CFS treatment (e.g. valacyclovir, valgancyclovir, amantadine)

[Jonathan Edwards]

This effect is consistent with what infectiologists know about aciclovir. It works within one hour – against herpes, of course.

It may have an effect on viral replication in one hour but that is a very long way from it having noticeable clinical effects. And in a situation of latency one would not expect much to happen at all. The situation is completely different from something like evolving shingles.

In the ME world I have seen that doctors try herpes drugs with their patients for weeks and months and claim that sometimes it begins to work after many weeks. That's another question and I have no idea why they believe that. But maybe you do?

I think it unlikely that it makes any difference to ME/CFS at all.

 

[PageofME]

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

I understand. It's interesting to hear what's going on in Basel. My specialist is in Chur. Sorry, you lost yours! Do you know that Jonas from the Schweiz. Gesellschaft für ME und CFS has a list of Swiss doctors who know ME?

 

[PageofME]

It may have an effect on viral replication in one hour but that is a very long way from it having noticeable clinical effects. And in a situation of latency one would not expect much to happen at all. The situation is completely different from something like evolving shingles.



I think it unlikely that it makes any difference to ME/CFS at all.

Yes, viral replication stops in one hour and it's not only me personally who feels the effect but it's what that infectious disease clinician claims can be observed in the patients as well.

Latency: I have tried it for one week when I felt I needed a break from pacing. It of course does make a huge difference. I was able to lead a completely normal live for one week because there was't a flare after a couple of hours/days of not staying under my pathological limit of exertion.

The first aciclovir study into ME was done in 1988 because there is anecdotal evidence of it having a good effect in ME since back then. It is also recommended in the contemporary literature that herpes drugs should be investigated further.

Pharmaceutical Interventions in Chronic Fatigue Syndrome: A Literature-based Commentary - PubMed

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating disorder characterized by prolonged periods of fatigue, chronic pain, depression, and a complex constellation of other symptoms. Currently, ME/CFS has no known cause, nor are the mechanisms of illness well understood...

pubmed.ncbi.nlm.nih.gov

I'll post the literature on the usage of aciclovir when I come across it again.

 

[jnmaciuch]

Yes, viral replication stops in one hour and it's not only me personally who feels the effect but it's what that infectious disease clinician claims can be observed in the patients as well

I think the point Jonathan is making is: if a herpesvirus reactivation was making people feel awful, the “feeling awful” would be mediated by the immune response to the virus, as in pretty much all other infections. In which case, the immune system would still be responding to virus and still causing symptoms for much longer than an hour, regardless of whether viral replication has decreased in that hour.

That’s why, for example, it may take several days for symptoms to improve with paxlovid, but something that targets the immune response directly (like an NSAID) would make people feel better within an hour. And why the awful bitter taste from paxlovid may appear much quicker than any benefits—because that’s an off-target affect on your cells rather than viruses.

Yes, viral replication stops in one hour and it's not only me personally who feels the effect but it's what that infectious disease clinician claims can be observed in the patients as well.

The clinician would not be able to differentiate between immediate off target effects and effects of reduced viral replication either.

Acyclovir is known for affecting other cellular pathways besides its effect on viral replication.

 

[ryanc97]

Antivirals are cheap and easy to get. If it worked we would know by now.

 

[Rick Sanchez]

Antivirals are cheap and easy to get. If it worked we would know by now.

Not to mention a large amount of pwME would have been on antivirals for herpes. It's an extremely common treatment.

 

[PageofME]

That’s why, for example, it may take several days for symptoms to improve with paxlovid, but something that targets the immune response directly (like an NSAID) would make people feel better within an hour.

I can only tell you what I've read in that paper. Infectiologists believe that the activity of aciclovir can be observed very fast because that's how they find out how much to give the patients. And they believe that this overlaps with aciclovir's pharmacology.

What you are saying is very interesting, very sophisticated but I can't see how it is relevant to the discussion on how fast ME patients who respond to aciclovir have an alleviation of symptoms.

 

[PageofME]

Antivirals are cheap and easy to get. If it worked we would know by now.

Well, at least I know that they work.

Sorry, that aciclovir doesn't work for you.

However, your ideas are wrong. There is ample anecdotal evidence that aciclovir has activity in a group of ME/CFS patients and in the drug research overview on aciclovir research in ME/CFS from 2019 that I posted above researchers concluded that there should be more studies into aciclovir and other herpes anti-virals, preferrably by seperating subgroups. Because it could be shown in several small studies that a part of the participants had an improvement.

 

[jnmaciuch]

What you are saying is very interesting, very sophisticated but I can't see how it is relevant to the discussion on how fast ME patients who respond to aciclovir have an alleviation of symptoms.

The timelines are a pretty good indication that any positive effect of aciclovir is from an off-target effect, not its action on herpesvirus replication

 

[Jonathan Edwards]

There is ample anecdotal evidence that aciclovir has activity in a group of ME/CFS patients

And since anecdotal evidence in ME/CFS is worthless, where does that get us?
If there was even a small subgroup that had useful responses, trials should pick up a signal.
I am also not very impressed by the 'clinical seat of the pants' of 'infectiologists' to be honest. That sounds way outside the sphere of reliable evidence.

I don't think you are going to convince anyone, and saying that people's 'ideas are wrong' alongside anecdotes is likely to ensure it.

 

[ryanc97]

Well, at least I know that they work.

Sorry, that aciclovir doesn't work for you.

However, your ideas are wrong. There is ample anecdotal evidence that aciclovir has activity in a group of ME/CFS patients and in the drug research overview on aciclovir research in ME/CFS from 2019 that I posted above researchers concluded that there should be more studies into aciclovir and other herpes anti-virals, preferrably by seperating subgroups. Because it could be shown in several small studies that a part of the participants had an improvement.

Is that so?

So why hasn't it worked for everyone then?

 

[ryanc97]

Lets be real. This stuff is cheap from indiamart. Why isnt ME CFS cured then?

 

[ChronicallyOverIt]

Let’s be real. This stuff is cheap from indiamart. Why isnt ME CFS cured then?

Also 67% of the global population has HSV1 orally. You can easily get these prescribed by a doctor for cold sores, you don’t need to go the sketchy way. Antivirals for HSV are possibly at this point the most tired and tested “treatment”.

 

[ChronicallyOverIt]

Anecdotal evidence and “subgrouping” are perfect signs of P-hacking. Sub grouping to “responders” is just grabbing more people with placebo response and making it significant

 

[PageofME]

Also 67% of the global population has HSV1 orally. You can easily get these prescribed by a doctor for cold sores, you don’t need to go the sketchy way. Antivirals for HSV are possibly at this point the most tired and tested “treatment”.

That's all wrong. The lip cream for cold sores can be bought without a prescription. However, the amount of aciclovir they contain is too small to effectively fight an ME flare. Also no one claims that HSV-1 or -2 play a role in ME.

The most interesting research focuses on HHV-6 or HHV-6b more precisely.

Have you read about it at all?

Aciclovir is not used against the known full and lethal flares of HHV-6 in the immunocompromised because there are other drugs that have "very good" activity. But aciclovir has "good activity" against HHV-6b too according to a medical school text book that I read.

As I said above not only the anecdotal evidence but also the literature demands that the research into aciclovir and other herpes drugs for ME is promising and should be continued.

 

[PageofME]

Anecdotal evidence and “subgrouping” are perfect signs of P-hacking. Sub grouping to “responders” is just grabbing more people with placebo response and making it significant

The researchers in the paper above of course do not suggest to supgroup by placebo response. They suggest to subgroup by PCR, for example for HHV-6.

It's all not so complicated. And contrary to what you believe this research has not been done.

Sometime when I read comments of ME patients (being one myself) why herpes and herpes drugs shouldn't be researched my impression is that many believe that scientific evidence into simple questions grows on trees or falls from the sky and then could just be picked up.

 

[Utsikt]

The most interesting research focuses on HHV-6 or HHV-6b more precisely.

Have you read about it at all?

Perhaps you could share which papers you think are the most interesting? There might be some threads already.

 

[ChronicallyOverIt]

I have read about HSV-1 and HSV-2 quite a bit. I was talking about getting prescribed
acyclovir orally in pill form. If you have a positive igg, and are worried about passing on to partner etc. you can get it prescribed even for oral hsv-1.

But aciclovir has "good activity" against HHV-6b too according to a medical school text book that I read.

You may need to get a new textbook, or perhaps there is a new mechanism you can elaborate? HHV-6b does not have the same kinase as HSV-1 & HSV-2. Acyclovir only targets this specific kinase to HSV-1 and HSV-2. It is ineffective for HHV-6. An hour response time is quite interesting as people with full HSV-1 & HSV-2 outbreaks the acyclovir takes many days to clear their outbreaks and fully stop viral replication. This is in the perfect kinase match scenario too.

You say it’s unexplored but it’s one of the most beat to death avenues, it was probably one of the first things I heard of and many patients do. So many patients have tried antivirals with null results.

Theres even a more recent study occurring:

UK ME/CFS Biobank HHV-6 Study: Recruitment in its Final Phase - The ME Association

The HHV6 study, which is looking at the association between symptom exacerbation […]

meassociation.org.uk

 

[Rick Sanchez]

MECFS clinics who do antivirals already start off with a high dosis right away, and for long enough that IF it actually worked we would know by now. If I had to venture a guess I would say at least thousands of MECFS patients would have tried vala / acy by now (at the hypothetically required dosis)

The fact that more ppl say they had a positive effect from LDN or whatever supplement, than from antivirals says everything there is to say rly.

 

[PageofME]

The timelines are a pretty good indication that any positive effect of aciclovir is from an off-target effect, not its action on herpesvirus replication

When I fight my ME flares with aciclovir I have just the same timeline as the infectiologists see in their patients fighting their HSV-1 or two brain inflammations.

Do you want to claim that aciclovir does not work as pharmacologists have figured out by directly stopping the virus to replicate but fights reactivation by side effects. You have funny ideas!