Does Valtrex block mitochondrial reproduction?

[ukxmrv]

@ukxmrv,

Do you find Immunovir to work better than inosine?

@Ema,

I can't remember if I tried Inosine in the end. There was a "recipe" on one of the old CFS groups and a long discussion on making your own "Immunovir" and also taking separate components. We tried different things to see how they worked.

I'll have to look through my box of " tried supplements" with labels and empty bottles and notes when I can. I keep a boxes of empties and also saved documents of records. My brain can't keep up now with all the things I have tried. Also the dust.

Sorry about that.

 

[JalapenoLuv]

@Ema,

I can't remember if I tried Inosine in the end. There was a "recipe" on one of the old CFS groups and a long discussion on making your own "Immunovir" and also taking separate components. We tried different things to see how they worked.

I'll have to look through my box of " tried supplements" with labels and empty bottles and notes when I can. I keep a boxes of empties and also saved documents of records. My brain can't keep up now with all the things I have tried. Also the dust.

Sorry about that.

This is why you should keep a treatment diary.

 

[heapsreal]

Further, if your goal is to find a cure, you can't take things that poison mitochondria.

If it did poison mitochondria, people wouldnt feel better on antivirals??

 

[heapsreal]

@ukxmrv,

Do you find Immunovir to work better than inosine?

Labs i did showed immunovir increased my nk numbers.

Inosine i didnt feel alot better on it so i think there might be a difference but i guess its a cost thing.

Cycloferon increased nk nk function considerably.

Arbidol i used for about 6 weeks, it cleared up my sinus infections while on it, but i didnt get any testing while using it. I would like to try it again and see what response i get from it?

 

[JalapenoLuv]

If it did poison mitochondria, people wouldnt feel better on antivirals??

Depends. There are a few factors in play. The improvements take a very long time. So maybe the process is that the viral counts go down, followed by decreased autoantibodies which allows the mitochondria to recover. However the patients aren't recovered enough to exercise so something is keeping the mitochondria from increasing. In vitro research indicates that valtrex type drugs do this so it is logical to think that the drug that causes the improvement could be the limiting factor. The only two things I've seen that can increase mitrochondria are high intensity strength training and PQQ supplement.

 

[Ema]

Microbiology
Mechanism of Action
Valacyclovir is a nucleoside analogue DNA polymerase inhibitor. Valacyclovir hydrochloride is rapidly converted to acyclovir which has demonstrated antiviral activity against HSV types 1 (HSV-1) and 2 (HSV-2) and VZV both in cell culture and in vivo.

The inhibitory activity of acyclovir is highly selective due to its affinity for the enzyme thymidine kinase (TK) encoded by HSV and VZV. This viral enzyme converts acyclovir into acyclovir monophosphate, a nucleotide analogue.

So here is the deal for anyone who is still reading this thread and wants the real story in terms of Valtrex.

Acyclovir and it's prodrug Valtrex (valacyclovir) are nucleoside analogues, but they are not thymidine analogues, they are guanosine analogues.

http://en.wikipedia.org/wiki/Nucleoside_analogue

These antiviral drugs are very safe because they do not work in healthy cells, they only work in virally infected cells.

The drugs work by inhibiting a viral enzyme called thymidine kinase.

Now to make matters more complicated, there is also a cellular thymidine kinase present in healthy cells. But the cellular thymidine kinase are not able to phosphorylate the drugs which is a fancy way to say that the drugs have no effect in healthy cells.

However, in virally infected cells, the drug is able to effect cessation of viral replication.

A nice explanation is here:

Acyclovir undergoes monophosphorylation (adds one phosphate group) catalyzed by a virus-encoded enzyme thymidine kinase. The formation of the monophosphate can only take place in the presence of the virus, thus the drug accumulates as the monophosphate only in infected cells. It is then converted to a diphosphate and triphosphate by “normal” host enzymes in the cell. ACV-triphosphate inhibits the viral DNA polymerase from incorporating guanosine triphosphate and is itself incorporated. The DNA cannot grow further, add more groups and the chain terminates.

The mechanism of action is thus twofold: inhibition of viral DNA polymerase and chain termination of DNA once it has been incorporated into the nucleic acid.

http://www.emedexpert.com/classes/herpes-medications.shtml

So (besides the fact that the article itself states that no conclusions can be drawn as to in vivo mitochondrial toxicity), Valtrex does not even fall into the class of drugs that are discussed as even *potentially* toxic to the mitochondria.

I actually think it would be interesting to study the antivirals and the mitochondria. But at this point, there is no reason at all to discontinue antivirals based on concerns over toxicity to the mitochondria. There is no evidence to support this position.

 

[JalapenoLuv]

These antiviral drugs are very safe because they do not work in healthy cells, they only work in virally infected cells.

According to Xiong this is false because acyclovir has a significant bystander effect in vivo.

Cytotoxic gene therapy mediated by gene transfer of the herpes simplex virus thymidine kinase (HSV-tk) gene followed by acyclovir (ACV) treatment has been reported to inhibit malignant tumor growth in a variety of studies. The magnitude of "bystander effect" is an essential factor for this anti-tumor approach in vivo....The apoptotic phenomena appeared in the CD3-expressing ACC-M cells. The results show that HSV-tk/ACV system killed ACC-M cells using its bystander effect. These results confirm that HSV-tk/ACV system is potential for cancer gene therapy.
-Xiong T, Li Y, Ni F, Zhang F. Monitoring of bystander effect of herpes simplex
virus thymidine kinase/acyclovir system using fluorescence resonance energy
transfer technique. J Biomed Nanotechnol. 2012 Feb;8(1):74-9.

So all of the tissue next to the infected tissue will be loaded with mitochondrial poison. This actually explains why people with longer histories of CFS before treatment don't get well, they have a higher infection load which translates into more bystander poisoning. Smaller loads would have less poisoning and more mytochondria.

I don't think the type of inhibitor that valtrex is matters since Martin's research determined that it has high in vitro toxicity to mitochondria.

 

[Ema]

According to Xiong this is false because acyclovir has a significant bystander effect in vivo.



So all of the tissue next to the infected tissue will be loaded with mitochondrial poison. This actually explains why people with longer histories of CFS before treatment don't get well, they have a higher infection load which translates into more bystander poisoning. Smaller loads would have less poisoning and more mytochondria.

I don't think the type of inhibitor that valtrex is matters since Martin's research determined that it has high in vitro toxicity to mitochondria.

Martin's research determined no such thing, actually.

So now because your first theory fell completely apart under closer examination, you're changing tacks entirely and going for the "bystander effect" dealing with malignant tumor cell lines and not anything to do with our population in the slightest? Do you just have some sort of vendetta against Valtrex? Because nothing else makes sense here.

And certainly not bystander poisoning...talk about a population difference! These are genetically modified cancer cells that are then treated with acyclovir. As far as I know, no ME/CFS patient has these and to draw any sort of conclusions regarding what healthy or virally infected cells would do from this extremely specific study is reaching of the very worst kind.

This study is not relevant at all to the topic at hand and provides no support to a hypothesis that Valtrex is toxic to mitochondria.

 

[JalapenoLuv]

Yes it is relevant and the ability to re-evaluate a position based on the evidence is a requirement for research.

Another issue I have is that Lerner comments that valtrex causes cells to be resistant to apoptosis. This could be due to the fact that they have a mitochondrial deficit (they are involved in the process). In the future researchers could develop a cure that requires the ability to apoptose. People who took valtrex might not be able to be cured.

http://www.hhs.gov/advcomcfs/meetings/presentations/presentation_10122010_martinlerner.pdf by M. Lerner, p.31.

 

[Ema]

So which is it, are they resistant to apoptosis or more likely to undergo apoptosis due to the bystander effect?!

 

[JalapenoLuv]

That question makes no sense. It is also against the forum rules to be argumentative.

 

[Valentijn]

That question makes no sense. It is also against the forum rules to be argumentative.

Ema's responses are not argumentative behavior - she's refuting your erroneous claims with solid scientific evidence and reasoning. And if you do think someone is in breach of the rules, you shouldn't be posting that, but rather reporting the "offending" post so the moderators can sort it out.

But it would be nice if you found support for your unusual claims before making them. It would really save us all a lot of grief.

 

[ukxmrv]

This is why you should keep a treatment diary.

I do JalapenovLuv,

But over 30 years technology changes, I move house and sometimes country, and paper records / computers deteriorate. Backups are lost.

I started with paper records in the 80s which disintegrated before scanners became available in the typical home. I think I have had computer records on every single type of media that has been used since the personal computer was invented.

My first computer records have been converted and transferred between many different software packages from the invention of the initial spreadsheets and word processors. I have boxes of medical tests, reports and records.

They are an archaeological dig. I'm too sick to catalogue the old stuff now or even to find where it all is. I'd need a proper document system and someone to scan/organise it all.

In 30 years time I wonder what my treatment diary will look like. We'll probably have a laugh on how primitive it all was.

 

[JalapenoLuv]

Ema's responses are not argumentative behavior - she's refuting your erroneous claims with solid scientific evidence and reasoning. And if you do think someone is in breach of the rules, you shouldn't be posting that, but rather reporting the "offending" post so the moderators can sort it out.

But it would be nice if you found support for your unusual claims before making them. It would really save us all a lot of grief.

Not at all. She is mocking the discussion and presenting no real rebuttle.

 

[CindyWillis]

@Ema,

I can't remember if I tried Inosine in the end. There was a "recipe" on one of the old CFS groups and a long discussion on making your own "Immunovir" and also taking separate components. We tried different things to see how they worked.

I'll have to look through my box of " tried supplements" with labels and empty bottles and notes when I can. I keep a boxes of empties and also saved documents of records. My brain can't keep up now with all the things I have tried. Also the dust.

Sorry about that.

I heard that Dr. Cheney is no longer using GCMAF? Is that true? If it is true, do you know what he is currently using to treat Chronic Fatigue? Thanks for the update. I had followed years ago but have not kept up to date currently.