Valcyte, Valtrex, and Famvir experiences -- Let's talk

[Who Me?]

You have good stuff to say but I can't read it. I Know I'm not alone.

After the 2nd it 3rd paragraph I check out.

And multiquotes? They just make it even worse.

 

[IrisRV]

thanks for screwing with my brain even more.

I apologize. I am taking out all the quotations now.

 

[IrisRV]

You have good stuff to say but I can't read it. I Know I'm not alone.

After the 2nd it 3rd paragraph I check out.

And multiquotes? They just make it even worse.

Sorry. I don't mean to offend you or the other people with my long posts. It's the way I write, and while I'm trying to change, it's not easy. I will attempt to refrain from posting overmuch until I get it under control.

I fixed the post above so it won't disturb people with visual issues.

 

[fdotx]

Edit:
I answered @fdotx here, but my post was overlong and detailed and contained too many quotations making it upsetting for some members.

@Who Me? answered much, much more succinctly. Therefore, I have removed my post so it wouldn't bother people with visual issues.

IrisRV, I saw that you wrote and was so looking forward to reading it and now it's gone. It wasn't too long for me - darn I wish I'd read it when I had the chance - at a glance it looked like it had some great info. ;-(

 

[IrisRV]

IrisRV, I saw that you wrote and couldn't read it at that time but was so looking forward to it and now it's gone. It wasn't too long for me - darn I wish I'd read it when I had the chance - at a glance it looked like it had some great info. ;-(

I saved it. PM me if you want it. You could probably copy it into a Word document, break it up into smaller chunks, and read it by the littles.

Sorry, I'm not up to working through it and editing it down to a couple of paragraphs and no quotations. I'm afraid that if you want it, you'll have to take it as it is and do the best you can with it.

 

[fdotx]

I saved it. PM me if you want it. You could probably copy it into a Word document, break it up into smaller chunks, and read it by the littles.

Sorry, I'm not up to working through it and editing it down to a couple of paragraphs and no quotations. I'm afraid that if you want it, you'll have to take it as it is and do the best you can with it.

IrisRV it showed up - I guess since I'd opened it once my computer still had it. Read it all - thanks so much for all the info! I copied to a draft so will have it.

 

[IrisRV]

IrisRV it showed up - I guess since I'd opened it once my computer still had it. Read it all - thanks so much for all the info! I copied to a draft so will have it.

Terrific! I hope it helps.

 

[fdotx]

Here is what I think it is, dumbed down, since I can't read anything @IrisRV. Too long, too many quotes for my brain.

Most docs say everyone has been exposed to these viruses so not a big deal that you show IgG. Some don't even care if you are IgM. They don't take that into account when looking at the total health of the patient.

But docs who treat ME/CFS feel that even positive IgG is significant for us and why many use antivirals. They say, well yes people were exposed but have those other people been sick for 20 years?

http://news.yahoo.com/long-term-ant...ctive-persistent-lyme-symptoms-212028938.html

Even though the above article is about chronic Lyme it mentions CFIDS and the idea is the same - he says you can treat the inciting agent until the cows come home and it won't help. I read that a virus has to be replicating in order for an anti viral to work and my PCP said even with the flu if you don't get tamiflu going in the first day or 2 it won't work. I do have high titers and my early antigen for EBV is very high ( tested at Stanford) but she doesn't even test for it anymore because she saw no correlation between results and how a person felt. I am trying acyclovir based on anecdotal evidence but don't understand scientifically how it can work....

 

[Cort]

Thanks

I was a patient of Dr Lerner early on. He taught me most of what I know about AVs, although what I know is from a layperson/patient perspective.

One thing I learned was that antiherpetics (Valcyte, Valtrex, Famvir, acylovir) are not entirely interchangeable. Some work better on some herpesviruses, while others are more effective for different herpesviruses. While they all have some effect on all herpesviruses, often a person needs the most effective one to get the infection down sufficiently. Then a different AV might be sufficient to keep the virus suppressed long term.

Valcyte is the most effective for CMV and HHV6, the beta-herpesviruses. Valtrex is good for the alpha- and gamma-herpesviruses (HSV, chicken pox, EBV). Famvir seems to be more effective than Valtrex for CMV and HHV6, but not as effective as Valcyte. Since they are all effective to some extent, if you can't tolerate (or afford) the most effective one for your virus, you might still get some help from one of the others.

Lerner has, in some cases, used fairly high doses of antivirals, but he monitored very carefully for side effects -- labs every 4 weeks. If you didn't get the labs, he wouldn't give you a new script for the med. If your labs show things heading in the wrong direction, he'd immediately reduce the dose, change the AV, or take you off AVs altogether. In all the decades he treated ME patients with AVs, he never had a single case of one of the rare, but potentially dangerous side effects of the AVs -- neutropenia, liver damage, etc. He believed that was because he watched so carefully and changed course as soon as the labs showed the slightest sign of those side effects. I remember him frequently cautioning me, "Those side effects are completely reversible, if you catch them in time. So you must always do your labs on time."

IIRC, he said many people have chronic or recurring herpesviruses because the virus has moved into tissues that are not easy to get to with meds. Higher doses raise the blood level of the med so more (even though it's only a fraction of what's in the blood) gets into the tissues. Once you get the tissue levels down, lower doses or a less effective AV might be sufficient to keep the virus suppressed.

I am in a similar boat to your friend, @Cort, in that I relapse if I stay off Valcyte too long. I had a big improvement on Valcyte, but I'm nowhere near hiking in the hills yet. Other family members (who were never as sick as I was) became fully functional with Valcyte and in some cases, other symptomatic treatments.

Thanks for the insights.

I compared Lerner's dose of valtrex with what Dr. Peterson prescribed for a patient. I adjusted for the patients weight. Dr. Lerner was prescribing much more valtrex than Dr. Peterson - something like 3-4x's more if memory serves. I was surprised there would be such a difference.

Here's a recovery/recoverying story from one of Dr. Lerner's patients - http://www.cortjohnson.org/forums/threads/valcyte-and-valtrex-return-alan-to-work.2278/

Do you have any insights into Dr. Lerner's Vistide regimen's? I think he turned pretty strongly towards Vistide in the end. We were going to do a blog on it and get the word about his approach and then he died

 

[IrisRV]

Do you have any insights into Dr. Lerner's Vistide regimen's? I think he turned pretty strongly towards Vistide in the end.

I'm sorry, I don't. I hadn't seen Dr Lerner for several years. I'm not surprised he was looking at Vistide, though. He tried to stay on top of new treatments. Do you know if he left some notes or more complete writings that might give us a clue as to his approach and how successful he thought it was?

 

[Remy]

Do you have any insights into Dr. Lerner's Vistide regimen's? I think he turned pretty strongly towards Vistide in the end. We were going to do a blog on it and get the word about his approach and then he died

I did cidofovir with Lerner for about a year in 2013. It did not cure me unfortunately but it didn't make me worse either. I now wonder if the IV saline and the Probenecid were as helpful as the cidofovir.

 

[fdotx]

I'm sorry, I don't. I hadn't seen Dr Lerner for several years. I'm not surprised he was looking at Vistide, though. He tried to stay on top of new treatments. Do you know if he left some notes or more complete writings that might give us a clue as to his approach and how successful he thought it was?

If he left behind a spouse or children I would think they would be more than happy to help someone who remembered and admired their husband/father. Perhaps they have some of his papers - just a thought....

 

[Justin]

Here is a question for more experienced members with AVs:

I have almost all Neuro, POTS, GI, PEM and sensory issues and went down hill quite quickly.

Do AVs work for these symtoms or do they rend to help those with Flu-like malaise, swollen glands, headaches, muscle and joint pains, etc.

Looking to here some feed back. I have seen a top sepcialist but is more intoimmune stuff.

 

[Remy]

Here is a question for more experienced members with AVs:

I have almost all Neuro, POTS, GI, PEM and sensory issues and went down hill quite quickly.

Do AVs work for these symtoms or do they rend to help those with Flu-like malaise, swollen glands, headaches, muscle and joint pains, etc.

Looking to here some feed back. I have seen a top sepcialist but is more intoimmune stuff.

I was having a return of my OI symptoms when Lerner put me on Valcyte. They cleared up again within a week.

 

[Justin]

@Remy did you have diagnose POTS?

How were your other symptoms and what kind of other symptoms did you have?

 

[IrisRV]

Here is a question for more experienced members with AVs:

I have almost all Neuro, POTS, GI, PEM and sensory issues and went down hill quite quickly.

Do AVs work for these symtoms or do they rend to help those with Flu-like malaise, swollen glands, headaches, muscle and joint pains, etc.

Looking to here some feed back. I have seen a top sepcialist but is more intoimmune stuff.

Bottom line is that AVs help with viruses. If you're fighting a virus, it pays to take something to help your body in that fight, whatever your symptoms are. The damage being done may not show up in obvious symptoms right away, but the viruses could be doing long-term damage.

Some AVs may act as microglial inhibitors, and so might help with related symptoms even if you're not fighting a virus. It might not be easy to get them prescribed for that, though.

In my case, AVs helped with cognitive dysfunction and brain fog, and all the flu-like symptoms including extreme exhaustion. I think they helped a bit with sensory issues, but I never had them as severely as many PWME.

I would say it didn't help with OI, although it may have helped a bit, but nowhere near enough. Florinef and verapamil worked for that.

I'm fortunate not to have GI symptoms, so I can't speak to that. I don't remember hearing other patients saying AVs help with GI issues, though.

Off the top of my head, I can't think of a top ME specialist into immune stuff who doesn't use AVs when they are needed. I'd go with a top specialist on this one. If they think you needs AVs, you probably do. If they're not suggesting AVs, then AVs are likely not going to help.

 

[Mavis and Max]

Chiming in on this thread based on Ron Davis and Bob Naviaux's statement today on Antivirals, quoted in full here:
Viruses and CFS: Statements by Ron Davis and Bob Naviaux

• Posted on:September 9, 2016
  

Ron Davis:

There is a great deal of evidence that a variety of viruses can initiate ME/CFS, but it is less clear that a virus is involved in sustaining the disease. However, some patients may have a continuous problem with viruses, especially those viruses we always carry like EBV and HHV6.
These viruses are usually kept in check by the immune system. Any suppression of the immune system can cause reactivation of these viruses (e.g., shingles). It is possible (we have new supporting data on this) that the immune system is somewhat impaired in ME/CFS, which will make it difficult to keep these viruses suppressed. If we can find the cause of this disease and cure it, this virus problem should go away.

Also, there is a common misunderstanding about viral infection among some patients and even some doctors. Most viral assays used by doctors test for the presence of antibodies to viruses, not the viruses themselves. The presence of antibodies shows that the person had a viral infection in the past, but does not constitute evidence that it is still present.

A direct assay for a virus is needed in order to find out if any virus is present. The current state-of-the-art assay is a PCR test for DNA or RNA from a virus. (Serology tests are tests for antibodies, not viruses.)

We are conducting these direct PCR assays in the Severely Ill Patient Study, as well as extensive DNA sequencing for any as-yet-undiscovered viruses. We need to keep an open mind and have all ideas on the table and follow the data.

Our goal is to find an accurate biomarker, find the cause, find a treatment for the cause, find a cure and then prevent the disease.
Bob Naviaux:

Question- Many ME/CFS experts have improved the symptoms in some patients by treating with antivirals and Ampligen (polyIC double stranded RNA). I think this proves that ongoing viral infections are causing our symptoms. It is not merely “tired patients” who are stuck in a lowered metabolic state because of a past trigger (which now is gone).

First of all, it is important that people actually read our paper first before drawing conclusions from news reports and blogs and criticizing something that we never said. I have seen a number of generalizations starting to appear in blogs and reports by journalists in even good newspapers and magazines that are starting to drift too far afield from the actual science in our paper.

We devoted a section of the paper to this and related questions about infections. The section title was, “A Homogeneous Metabolic Response to Heterogeneous Triggers”. It concluded with the sentence, “Despite the heterogeneity of triggers, the cellular response to these environmental stressors in patients who developed CFS was homogeneous and statistically robust.” As background for this conclusion, I recommend reading our paper on this topic entitled, “Metabolic features of the cell danger response” (PMID 23981537).

Second, many people do not understand that the first response our body mounts against a viral, bacterial, or any kind of infection is metabolic. Yes, our chemistry is our first line of defense. Our chemistry reflects our instantaneous state of health. Innate immunity is coordinated by mitochondria and is an essential first step in developing adaptive immunity to any infectious agent. Without innate immunity there can be no antibodies and no NK cell activation, no mast cell activation, and no T cell mediated immunity.

In addition, all antivirals have metabolic effects that have nothing to do with inhibiting viral DNA or RNA synthesis directly. Many antiviral drugs inhibit the key metabolic enzyme SAdenosylhomocysteine Hydrolase (SAHH). Inhibition of SAHH causes an increase in intracellular SAH levels. SAH is a potent inhibitor of DNA, RNA, protein, and small molecule methylation. This affects both viral and host cell epigenetics, gene expression, mRNA translation, and protein stability.

The inhibition of methylation reactions in the cell also affects neurotransmitter (dopamine, norepinephrine, and serotonin) and phosphatidylcholine membrane lipid synthesis, folate and B12 metabolism, and many other reactions. So by giving antivirals, doctors are not just inhibiting viruses, they are also inhibiting many host cell metabolic functions.
Sometimes the inhibition of host cell functions can attenuate ME/CFS symptoms for a time, but in other cases, using potent antiviral drugs inhibits mitochondrial and methylation reactions and can delay a full recovery from ME/CFS.

Ampligen is a form of double stranded RNA called poly(IC), for poly inosinic:cytosinic acid. We have studied the action of polyIC extensively and have published this in our studies of autism and virology. It acts by binding to an innate immune receptor called TLR3, creating a simulated viral infection. If you expose a pregnant animal to a single dose of polyIC at the beginning of the second trimester, she develops a 24-hour flu-like illness then completely recovers. However, her pups have social and cognitive abnormalities similar to autism for life. If you look at their brains, you find that they have activated microglia and brain inflammation for life.

In adults, Ampligen also binds the TLR3 receptor, and activates an incomplete antiviral response characterized by a non-MyD88 dependent activation of interferon and other cytokines. Long-term use of polyIC carries a risk for toxicity because of chronic innate immune stimulation. In certain clinical situations like cancer or Ebola virus infection the toxicity is actually part of the therapeutic effect.

Chronic interferon release causes flu-like symptoms, and the inhibition of mitochondrial protein translation. This can lead to secondary mitochondrial dysfunction. As I noted in an earlier Q&A response, sometimes the inhibition of mitochondrial function can make some people with ME/CFS feel better temporarily because some symptoms can come from unbalanced overactivity of some of the hundreds of functions mitochondria perform. However, in the long term, any pharmacologic inhibition of mitochondrial function will delay a full recovery.

Third, latent and reactivated viral and bacterial infections can occur, but in the case of ME/CFS that has lasted for more than 6 months, this may be the exception rather than the rule. Some doctors and scientists have not done a good job at educating patients and other scientists about the difference between serological evidence of infection in the form of antibodies like IgM and IgG, and physical evidence of viral replication like PCR amplification of viral RNA or DNA, or bacterial DNA.

We have learned in our autism studies with Dr. Judy Van de Water that supertiters of antibodies do not mean new or reactivated viral replication. Supertiters of IgG antibodies mean that the balancing T-cell and NK cell mediated immune activity is decreased. This is a functional kind of immune deficiency that causes an unbalanced increase in antibodies.

This is like the famous figure-and-ground illusion that shows the silhouette of two faces that also create the form of a vase. Both things happen. But which is cause and which is effect? Increased IgG antibodies to CMV, EBV, HHV6, Coxsackie, etc. are not good evidence of a reactivated viral infection. This can be proven in most cases by trying to measure viral DNA or RNA by PCR in the blood or swollen lymph nodes. In most cases, supertiters of IgG are PCRnegative. There are exceptions to this generalization.

Chronic PCR surveillance studies in healthy humans are showing that little waves of viral replication happen periodically throughout our lives. We have been, and are regularly infected by hundreds of viruses over a lifetime.

Sometimes this is obvious and causes a symptom like blisters or an ulcer around the mouth. However, most of the time these waves of viral replication are silent and produce no symptoms at all because they are handled in the background by the innate and cell-mediated immune system.

Even the deadly poliovirus infected 150 to 1800 people, producing only mild or unnoticed infections, for every one person who developed paralytic disease. In most of the cases of ME/CFS that I have seen where IgG antibody titers have been measured before, during, and after antiviral therapy, the antibody titers remain high after treatment, even though the patient may report symptomatic improvement.

I believe the symptomatic improvement after antiviral treatment may have more to do with the metabolic effects of antivirals in ME/CFS than their action on viral replication. The good news is that this hypothesis can be studied scientifically and put to the test easily using the tools of PCR and metabolomics.

Good science needs to remain open, ask the questions without bias, design good experiments, take careful measurements, then have the courage to follow the data wherever they may lead.

 

[Strike me lucky]

Chiming in on this thread based on Ron Davis and Bob Naviaux's statement today on Antivirals, quoted in full here:
Viruses and CFS: Statements by Ron Davis and Bob Naviaux

• Posted on:September 9, 2016

Ron Davis:

There is a great deal of evidence that a variety of viruses can initiate ME/CFS, but it is less clear that a virus is involved in sustaining the disease. However, some patients may have a continuous problem with viruses, especially those viruses we always carry like EBV and HHV6.
These viruses are usually kept in check by the immune system. Any suppression of the immune system can cause reactivation of these viruses (e.g., shingles). It is possible (we have new supporting data on this) that the immune system is somewhat impaired in ME/CFS, which will make it difficult to keep these viruses suppressed. If we can find the cause of this disease and cure it, this virus problem should go away.

Also, there is a common misunderstanding about viral infection among some patients and even some doctors. Most viral assays used by doctors test for the presence of antibodies to viruses, not the viruses themselves. The presence of antibodies shows that the person had a viral infection in the past, but does not constitute evidence that it is still present.

A direct assay for a virus is needed in order to find out if any virus is present. The current state-of-the-art assay is a PCR test for DNA or RNA from a virus. (Serology tests are tests for antibodies, not viruses.)

We are conducting these direct PCR assays in the Severely Ill Patient Study, as well as extensive DNA sequencing for any as-yet-undiscovered viruses. We need to keep an open mind and have all ideas on the table and follow the data.

Our goal is to find an accurate biomarker, find the cause, find a treatment for the cause, find a cure and then prevent the disease.
Bob Naviaux:

Question- Many ME/CFS experts have improved the symptoms in some patients by treating with antivirals and Ampligen (polyIC double stranded RNA). I think this proves that ongoing viral infections are causing our symptoms. It is not merely “tired patients” who are stuck in a lowered metabolic state because of a past trigger (which now is gone).

First of all, it is important that people actually read our paper first before drawing conclusions from news reports and blogs and criticizing something that we never said. I have seen a number of generalizations starting to appear in blogs and reports by journalists in even good newspapers and magazines that are starting to drift too far afield from the actual science in our paper.

We devoted a section of the paper to this and related questions about infections. The section title was, “A Homogeneous Metabolic Response to Heterogeneous Triggers”. It concluded with the sentence, “Despite the heterogeneity of triggers, the cellular response to these environmental stressors in patients who developed CFS was homogeneous and statistically robust.” As background for this conclusion, I recommend reading our paper on this topic entitled, “Metabolic features of the cell danger response” (PMID 23981537).

Second, many people do not understand that the first response our body mounts against a viral, bacterial, or any kind of infection is metabolic. Yes, our chemistry is our first line of defense. Our chemistry reflects our instantaneous state of health. Innate immunity is coordinated by mitochondria and is an essential first step in developing adaptive immunity to any infectious agent. Without innate immunity there can be no antibodies and no NK cell activation, no mast cell activation, and no T cell mediated immunity.

In addition, all antivirals have metabolic effects that have nothing to do with inhibiting viral DNA or RNA synthesis directly. Many antiviral drugs inhibit the key metabolic enzyme SAdenosylhomocysteine Hydrolase (SAHH). Inhibition of SAHH causes an increase in intracellular SAH levels. SAH is a potent inhibitor of DNA, RNA, protein, and small molecule methylation. This affects both viral and host cell epigenetics, gene expression, mRNA translation, and protein stability.

The inhibition of methylation reactions in the cell also affects neurotransmitter (dopamine, norepinephrine, and serotonin) and phosphatidylcholine membrane lipid synthesis, folate and B12 metabolism, and many other reactions. So by giving antivirals, doctors are not just inhibiting viruses, they are also inhibiting many host cell metabolic functions.
Sometimes the inhibition of host cell functions can attenuate ME/CFS symptoms for a time, but in other cases, using potent antiviral drugs inhibits mitochondrial and methylation reactions and can delay a full recovery from ME/CFS.

Ampligen is a form of double stranded RNA called poly(IC), for poly inosinic:cytosinic acid. We have studied the action of polyIC extensively and have published this in our studies of autism and virology. It acts by binding to an innate immune receptor called TLR3, creating a simulated viral infection. If you expose a pregnant animal to a single dose of polyIC at the beginning of the second trimester, she develops a 24-hour flu-like illness then completely recovers. However, her pups have social and cognitive abnormalities similar to autism for life. If you look at their brains, you find that they have activated microglia and brain inflammation for life.

In adults, Ampligen also binds the TLR3 receptor, and activates an incomplete antiviral response characterized by a non-MyD88 dependent activation of interferon and other cytokines. Long-term use of polyIC carries a risk for toxicity because of chronic innate immune stimulation. In certain clinical situations like cancer or Ebola virus infection the toxicity is actually part of the therapeutic effect.

Chronic interferon release causes flu-like symptoms, and the inhibition of mitochondrial protein translation. This can lead to secondary mitochondrial dysfunction. As I noted in an earlier Q&A response, sometimes the inhibition of mitochondrial function can make some people with ME/CFS feel better temporarily because some symptoms can come from unbalanced overactivity of some of the hundreds of functions mitochondria perform. However, in the long term, any pharmacologic inhibition of mitochondrial function will delay a full recovery.

Third, latent and reactivated viral and bacterial infections can occur, but in the case of ME/CFS that has lasted for more than 6 months, this may be the exception rather than the rule. Some doctors and scientists have not done a good job at educating patients and other scientists about the difference between serological evidence of infection in the form of antibodies like IgM and IgG, and physical evidence of viral replication like PCR amplification of viral RNA or DNA, or bacterial DNA.

We have learned in our autism studies with Dr. Judy Van de Water that supertiters of antibodies do not mean new or reactivated viral replication. Supertiters of IgG antibodies mean that the balancing T-cell and NK cell mediated immune activity is decreased. This is a functional kind of immune deficiency that causes an unbalanced increase in antibodies.

This is like the famous figure-and-ground illusion that shows the silhouette of two faces that also create the form of a vase. Both things happen. But which is cause and which is effect? Increased IgG antibodies to CMV, EBV, HHV6, Coxsackie, etc. are not good evidence of a reactivated viral infection. This can be proven in most cases by trying to measure viral DNA or RNA by PCR in the blood or swollen lymph nodes. In most cases, supertiters of IgG are PCRnegative. There are exceptions to this generalization.

Chronic PCR surveillance studies in healthy humans are showing that little waves of viral replication happen periodically throughout our lives. We have been, and are regularly infected by hundreds of viruses over a lifetime.

Sometimes this is obvious and causes a symptom like blisters or an ulcer around the mouth. However, most of the time these waves of viral replication are silent and produce no symptoms at all because they are handled in the background by the innate and cell-mediated immune system.

Even the deadly poliovirus infected 150 to 1800 people, producing only mild or unnoticed infections, for every one person who developed paralytic disease. In most of the cases of ME/CFS that I have seen where IgG antibody titers have been measured before, during, and after antiviral therapy, the antibody titers remain high after treatment, even though the patient may report symptomatic improvement.

I believe the symptomatic improvement after antiviral treatment may have more to do with the metabolic effects of antivirals in ME/CFS than their action on viral replication. The good news is that this hypothesis can be studied scientifically and put to the test easily using the tools of PCR and metabolomics.

Good science needs to remain open, ask the questions without bias, design good experiments, take careful measurements, then have the courage to follow the data wherever they may lead.

Basically saying what i have said for a long time. Drs cant tell if a chronic infection is active or not. I think a better guide as any for chronic infections is high or low lymphocytes and neutrophils or high cd8 t lymphocytes which are commonly high in herpes viruses. But none of these tests can tell us which infection is going on, only that there looks like an infection going on.

The low nk numbers and or function makes it possible to also have a chronic infection or susceptible to infections.

Not sure i agree that avs and abx have metabolic effects, time will tell. I think its possible the metabolic issues may come from the initial infection damaging the hypothalamus and possibly pituitary gland. This gives many of us sub optimal thyroid, adrenal hormones and sex hormones, all which can negatively effect energy, cause orthostatic dysfunctions, sleep dysfunction and other neuro symptoms.

 

[ShyestofFlies]

Has anyone experienced blood test levels for HHV6 to go up (they were high before, now they've tripled) while you're on treatment?

I'm on valcyte (generic) 450 mg twice a day.

Gonna ask my doc at my next appointment, she doesn't seem concerned- but that's a few months off.

 

[Carolineelizabeth]

I'm about to start Valcyte and am curious to know how well people handled it in terms of side effects. I am fairly sensitive to medications and for this reason my doctor wants me to start on a pediatric formulation so I can increase the dose slowly, but sadly it is not covered by insurance. I would love to hear how people handled a starting dose of 450 mg (which is covered, thankfully). I have had GI problems for years from extensive and aggressive abx treatment and am concerned about the impacts of this drug on my appetite in particular (I am at an all-time low BMI).

I am IgM and IgG positive for Mycoplasma and have high IgG titres for HSV-1 and of course EBV. I am never positive for any PCR tests and am NOT positive for the usual suspects such as HHV-6 and CMV.

I will be layering in Valcyte with Famvir and adding LDN. The Famvir has been OK, apart from some initial sorting out, which involved low-grade fever, swollen lymph nodes, and a big drop in appetite. I started to see some gains in my endurance and energy (mild, but I'll take what I can get). Adding doxy 100 mg bid seemed to really help (!) and I was able to make it through a 2-hr lecture (I am teaching part-time until I can start disability in the spring). I am under no illusion that my Mycoplasma infection has been dealt with once and for all, but I am placing my trust in my doctor for the time being on this one.

I am a newish Stanford patient. It it still early days and I would welcome feedback on what to expect with the Valcyte wrt to GI issues and other side effects. I've been sick for 10+ years. Thanks!!