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Author Topic: Valtrex acyclovir if you took in past please post your experiences valacyclovir  (Read 10563 times)

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Offline bimazek

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  • Posts: 781
from front page of this site today...

Valtrex (valacyclovir) has been found to lower HIV viral load 53% that is alot!! for a monotherapy

I had shingles and was taking Valtrex and i wrote in my diary, that i never felt better since being poz... i thought there must be something in the stuff, i even made a note to tell my Dr.

 anyway i did  a research on Valtrex     http://en.wikipedia.org/wiki/Valaciclovir

Valtrex   is a very potent inhibitor of viral DNA polymerase; it has approximately 100 times higher affinity to viral than cellular polymerase.

now we all know that this drug is very well tolerated so shouldn't i/we be on this if we are not below 350 yet and are not on HAART yet, seems like a good idea

esp. since there are 7 herpes viruses and the average person on planet has 5 of them all in their body

my long story short is

if you ever had shingles get on valtrex full time because it can only help

is anyone on HAART and Valtrex

please post

most everyone had chicken pox which is herpes virus

for me the fact that Valtrex   is a very potent inhibitor of viral DNA polymerase; it has approximately 100 times higher affinity to viral than cellular polymerase.   means that it will also stop hiv in this way because hiv has viral dna and i like something that is 100x worse for the bug than for my body

one of the issues with nukes, non nukes and protease (but not insertion inhibitors, not fuzeon and not maturation inhibitors, and such) is that body needs there enzymes and when you inhibit you stop a body process

to me this is a big of a break thru

to me it means as soon as you get hiv get on valtrex then when you get to below 500 or below 350 for absolute sure get on HAART

this is what it means to me, it may take 3 years for science to approve

but i had shingles and Dr. wanted me on valtrex full time anyway so why not

if it cuts VL in half that is half the damage to my body   half the  virus my body has to deal with

if you are on valtrex or acyclovir which is same thing either before haart or after haart or now or in past

please post your experiences


Aciclo-GTP is a very potent inhibitor of viral DNA polymerase; it has approximately 100 times higher affinity to viral than cellular polymerase. Its monophosphate form also incorporates into the viral DNA, resulting in chain termination. It has also been shown that the viral enzymes cannot remove aciclo-GMP from the chain, which results in inhibition of further activity of DNA polymerase. Aciclo-GTP is fairly rapidly metabolised within the cell, possibly by cellular phosphatases.

Aciclovir, the active metabolite of valaciclovir, is active against most species in the herpesvirus family. In descending order of activity:[1]

    * Herpes simplex virus type I (HSV-1)
    * Herpes simplex virus type II (HSV-2)
    * Varicella zoster virus (VZV)
    * Epstein-Barr virus (EBV)
    * Cytomegalovirus (CMV)











1. herpes simplex virus type 1 (cold sores and whitlows on fingers and hands, also half new cases of genital herpes)
2. herpes simplex virus type 2 (genital sores, also sometimes cold sores and whitlows)

The other viruses caught quite different illnesses. These are:

3. varicella-zoster virus (also called herpes varicella/chickenpox and herpes zoster/shingles)
4. Epstein Barr virus (often abbreviated to EBV)
5. cytomegalovirus (CMV)
6. human herpesvirus 6 (HHV6)
7. human herpesvirus 7 (HHV7)
8. human herpesvirus 8 (HHV8 or it can be called KSHV - see below)




1 - Herpes simplex virus type 1 (short version - see also cold sores):
How common? By age 15 around 25% of UK population, by age 30 around 50%. The rates are much higher in other countries.

2. Herpes simplex virus type 2 (short version - see also our Frequently asked questions):
How common? Around 25% of the sexually active UK population. Over the whole country between 3% and 10%. The rates are much higher in other countries.

3. Varicella-zoster virus (short version - see also our shingles and post-herpetic neuralgia pages):
How common? Almost 100% of UK population by adulthood.

4. Epstein Barr virus (EBV, also called glandular fever, mononucleosis, mono, kissing disease):
How common? Virtually everybody worldwide.

5. Cytomegalovirus (CMV)
How common? Half the population has CMV by a young age, with higher rates of infection in poorer areas.

6. Human herpesvirus 6 (roseola infantum/exanthem subitum)
How common? By the age of 2, almost all babies have type 6B virus.

7. Human herpesvirus 7:
How common? By the age of 3, almost all children have HHV-7.

8. Human herpesvirus 8 (also called Karposi's sarcoma herpes virus or KSHV) How common? This virus is quite common in some parts of the world. In Europe and the US it is not very common - under 10% have it.



from front page this site today

Herpes Drug Fights HIV Too

November 13, 2007

The anti-herpes drug Valtrex (valacyclovir) has been found to lower HIV viral load in the blood and genital secretions of men with underlying herpes simplex vius-2 (HSV-2) infection, according to a report on a study from AIDSmap. The study confirms earlier research and further suggests that herpes treatment, in the absence of HIV therapy, may have health benefits and help prevent ongoing transmission of HIV.

Richard Zuckerman, MD, MPH, of the section of infectious disease and international health at the Dartmouth-Hitchcock Medical Center in Lebanon, New Hampshire, and his colleagues studied valacyclovir treatment in 20 men infected with both HIV and HSV-2 in Lima, Peru. The men were randomized to receive either 500mg of valacyclovir twice a day or a placebo for eight weeks. Then after a two-week pause, the dosing groups were switched so that those who’d received placebo now received valacyclovir and those who’d received valacyclovir now received placebo for an additional eight weeks.

Treatment with valcyclovir was associated with a 31 percent decrease in HIV viral load from rectal samples compared with placebo, and a 53 percent decrease in HIV in the blood. The study’s authors conclude that suppressing HSV-2 production in people coinfected with HIV results in significant reductions in both HSV-2 and HIV
« Last Edit: November 13, 2007, 11:33:27 PM by bimazek »

Offline risred1

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Valtrex being an antiviral, it may have some broad capabilities.

But a reduced viral load is not a "non-detectable" viral load.

My concern is that the efficacy of Valtrex wouldn't pass muster as a anti-HIV medicine because of poor efficacy. Because it does exhibit some anti HIV efficacy, and Valtrex is so well tolerated, it is an understandable thought that if utilized to achieve some effectiveness as a interim tactic before applying the real anti HIV targetted meds.

But the obvious concern is, does Valtrex create mutations, and will those mutations take future medical treatments off the table?

From another point of view, If valtrex is dealing with other coinfections from Shingles and Herpes, perhaps some cross benefit to your immune system is available in fighting HIV.

I also can not find anything on the net that proports that Valtrex acts directly against HIV. So if Valtrex does not act against HIV, there may be no or little risk of resulting mutations.

I wish i could find some information on this.
risred1 - hiv +
02/07 CD4 404 - 27% - VL 15k
10/07 CD4 484 - 31% - VL 45k
05/08 CD4 414 - 26% - VL 70k
01/09 CD4 365 - 23% - VL 65k
05/09 CD4 291 - 23% - VL 115k - Started Meds - Reyataz/Truvada
06/09 CD4 394 - ?% - VL 1200 - Boosted Reyataz with Norvir and Truvada
07/09 CD4 441 - ?% - VL 118 - Boosted Reyataz with Norvir and Truvada
09/09 CD4 375 - ?% - VL Undetectable - Boosted Reyataz with Norvir and Truvada
12/09 CD4 595 - ?% - VL Undetectable - VIT D 34 - Reyataz/Truvada/Norvir

Offline Tim Horn

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  • Posts: 799
Risred:

My understanding is that Valtrex (or generic acyclovir) doesn't have any direct activity on HIV per se, but rather mediates its HIV viral load-reducing effects via its anti-HSV activity. By keeping HSV in check using either Valtrex or acyclovir, there may be less immune (and CD4+ cell) activity and, as a result, less HIV being churned out as a result. We've certainly seen this with other acute and chronic co-infections as well.

As Valtrex (and acylcovir) don't have any direct effects on HIV replication, it is unlikely that HIV has the capacity to develop mutations to resist the effects of these drugs (HIV really only has the ability to select for mutations that will reduce the sensitivity of drugs that impair its structure or behaviour). And I'm not aware of any data showing that HIV develops resistance mutations in the presence of Valtrex or acyclovir therapy.

Tim Horn

Offline fearless

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I read that study with interest. While not discounting their findings my experience while on Valtrex was the opposite. In early 2004 I had outbreaks of both butt herpes and shingles. I took Valtrex for a period of about 6 months. During this time my vl rose from about 30,000 to over 600,000.
Be forgiving, be grateful, be optimistic

Offline jack

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  • fomerly the loser known as Jake
I have never had shingles or herpes but my first HIV dr. had me on valtrex for a few years back in the day. That was back when they were just throwing anything up at the wall hoping for something to stick.

Offline J.R.E.

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  • Joined Dec-2003 Living positive, since 1985.
Hello,

I was only on Valtrex  once, and that was back around September /October of 2003. This was just prior to starting antiretrovirals, and just about the time of completing Prednisone. I was on the 1GM tablets, which were taken 3 times a day for 10 days.

All I can tell you, is the Valtrex worked very well, and very fast, in clearing up the mouth and lip lesions that I had back then.( which were very severe). My t-cells were at 16 back then. Can't comment on it's effect on viral load .


I was at the doctors about a week and a half ago, and asked for a prescription of Valtrex, because I felt something going on in my mouth. This prescription he gave me was also for the 1gm tablets taken 3 times a day for ten consecutive days. I filled the presription,  Ended up, the problems I was having in my mouth, are warts ( on the lower lip),... so I decided on not taking the Valtrex, as I didn't think the Valtrex would have any effect on the warts. A dermatologist appointment has already been made to handle that problem.


Ray
« Last Edit: November 14, 2007, 06:00:56 PM by J.R.E. »
Current Meds ; Viramune, Epzicom, 40mg of simvastatin, 12.5mg of Hydrochlorothiazide.
Metoprolol tartrate 25mg



http://forums.poz.com/index.php?topic=40802.0

http://forums.poz.com/index.php?topic=45159.0

http://forums.poz.com/index.php?topic=39722.msg495621;topicseen#msg495621

http://forums.poz.com/index.php?topic=46806.0

http://forums.poz.com/index.php?topic=39414.msg491701#msg491701


 In October of 2003, My t-cell count was 16, Viral load was over 500,000, Percentage at that time was 5%. I started my first  HAART regimen  on October 24th,03.

 As of 8/2514,  t-cells are at 402, Viral load <40

 Current % is at 11%

  
 62 years young.

Offline bobino

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  • Posts: 264

I have oral herpes (HSV-1), and my doctor has me on a maintenance dose of Valtrex, which is 500 mg once a day.  My doctor explained the rationale for taking it prophylactically in much the same way Tim did.  That is, it is suspected that an active HSV outbreak activates the immune system and leads to HIV replication.  By taking a maintenance dose, it is hoped that I will not only prevent herpes outbreaks but will also avoid any unnecessary stimulation of my immune system.

Since I've been on Valtrex, I haven't had a single outbreak of oral herpes, which is great.  Another benefit is that Valtrex can help prevent transmission of herpes.  This is important to me because my partner doesn't have HSV or HIV, and I'd very much like to keep it that way.

Suivons les rivières
Gardons les torrents
Restons en colère
Soyons vigilants

Offline bimazek

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  • Posts: 781
does this not mean that valtrex inhibits hiv viral DNA polymerase?


Aciclo-GTP is a very potent inhibitor of viral DNA polymerase; it has approximately 100 times higher affinity to viral than cellular polymerase. Its monophosphate form also incorporates into the viral DNA, resulting in chain termination.

It has also been shown that the viral enzymes cannot remove aciclo-GMP from the chain, which results in inhibition of further activity of DNA polymerase. Aciclo-GTP is fairly rapidly metabolised within the cell, possibly by cellular phosphatases.

when it says viral here does it mean all viral dna, all viral enzymes?

i think to get this big of a reduction 50% it cannot be just from reduction in the latent herpes

it has to have some suppression  via  incorporates into the viral DNA, resulting in chain termination. or
inhibition of further activity of DNA polymerase.

50% of hiv viral load could not be caused by a co infection of herpes this was ruled out wasnt 20 years ago

i am saying that since there are 8 of these and they all can and do infect most humans and since haart is toxic, would it not be a good idea before heart to damp down and suppress

this Valtrex inhibits  ALL DNA polymerase.  it is just that it does it 100x more with viral polymerase.
 how many viral polymerase are there?

all i am saying is i felt great when i was on it, like it was suppressing virialmia, viremia how do you spell it

there are 10 active infections in any human at any one time, skin infections, pimples, mouth, gut, lungs are constantly fighting things

there is no way that 50% of VL and hiv replication is from repressing ALL the 8 herpes family which are pretty well supressed before the valtrex

it must be the Valtrex inhibits  ALL DNA polymerase.

obviously it is not nearly as good as nuke, non nuke or protease

check out all these iRNA, microRNA, RNAi animations i posted

this chain termination is important




BobF

  • Guest
Hi.  I take 800mg of acyclovir daily as a preventative due to frequent cold sores previously.   I noticed it did bring my VL down from around 60,000 to 15,000 or so, but my CD4's kept dropping too, so I ended up starting HAART with Atripla in September.

Offline bimazek

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  • Posts: 781

I have now been on Valtrex, obstensibly to keep my shingles from coming back-- no symtoms for a year, for 3 days now and I definately feel an improvement in my HIV virimia, i feel less swelling and pain in my nodes under my chin and jaw line and  that full feeling in the nodes seems alot better, i am not yet on haart but i will definately go on haart when i get to 350, but i am scared as hell about haart, but anyway ... i cannot even read the forum about meds and side effects it makes me so upset so i stay here

ok

defiantely for me there is an effect on my hiv disease from the valtrex, my intestinal digestion is working better and as i said above the kind of viral swelling i feel in my nodes esp. near the neck and collar bone are much much less

i hope to stay on this until i go on hiv haart meds



please post esp. if you were on valtrex before starting hiv meds


Offline J.R.E.

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  • Posts: 7,215
  • Joined Dec-2003 Living positive, since 1985.


Some additional info regarding this topic :

http://www.medicalnewstoday.com/articles/89029.php


Ray
Current Meds ; Viramune, Epzicom, 40mg of simvastatin, 12.5mg of Hydrochlorothiazide.
Metoprolol tartrate 25mg



http://forums.poz.com/index.php?topic=40802.0

http://forums.poz.com/index.php?topic=45159.0

http://forums.poz.com/index.php?topic=39722.msg495621;topicseen#msg495621

http://forums.poz.com/index.php?topic=46806.0

http://forums.poz.com/index.php?topic=39414.msg491701#msg491701


 In October of 2003, My t-cell count was 16, Viral load was over 500,000, Percentage at that time was 5%. I started my first  HAART regimen  on October 24th,03.

 As of 8/2514,  t-cells are at 402, Viral load <40

 Current % is at 11%

  
 62 years young.

Offline bimazek

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tim- this goes into more detail on a cousin of valtrex and how and why it works
from wikipedia
Penciclovir is inactive in its initial form. Within a virally infected cell a viral thymidine kinase adds a phosphate group to the penciclovir molecule; this is the rate-limiting step in the activation of penciclovir. Cellular (human) kinases then add two more phosphate groups, producing the active penciclovir triphosphate. This activated form inhibits viral DNA polymerase, thus impairing the ability of the virus to replicate within the cell.

The selectivity of penciclovir may be attributed to two factors. Firstly, cellular thymidine kinases phosphorylate the parent form significantly less rapidly than does the viral thymidine kinase, so the active triphosphate is present at much higher concentrations in virally infected cells than in uninfected cells. Secondly, the activated drug binds to viral DNA polymerase with a much higher affinity than to human DNA polymerases. As a result penciclovir exhibits negligible cytotoxicity to healthy cells.

The structure and mode of action of penciclovir is very similar to that of other nucleoside analogues such as the more widely used aciclovir. A difference between aciclovir and penciclovir is that the active triphosphate form of penciclovir persists within the cell for a much longer time than the activated form of aciclovir, so the concentration within the cell of penciclovir will be relatively higher given equivalent cellular doses.

ok -- i found that there are 7 known families of   DNA_polymerase in humans, 5 in bacteria and  i cant find how many in different viruses... how many in herpes how many in hiv
http://en.wikipedia.org/wiki/DNA_polymerase

one of which is...

Family RT
the reverse transcriptase family contain examples both from retroviruses and eukaryotic polymerases. The eukaryotic polymerases are usually restricted to telomerases. These polymerases use a RNA template to synthesize the DNA strand.



Bacteria have 5 known DNA polymerases:

    * Pol I: implicated in DNA repair; has both 5'->3'(Nick translation) and 3'->5' (Proofreading) exonuclease activity.
    * Pol II: involved in replication of damaged DNA; has both 5'->3'chain extension ability and 3'->5' exonuclease activity.
    * Pol III: the main polymerase in bacteria (elongates in DNA replication); has 3'->5' exonuclease proofreading ability.
    * Pol IV: a Y-family DNA polymerase.
    * Pol V: a Y-family DNA polymerase; participates in bypassing DNA damage.




a related cousin compound is similar...     any time a drug causes  the dna of a virus to  "resulting in chain termination."  it has got to be a good thing  even if not completely

Aciclovir differs from previous nucleoside analogues in that it contains only a partial nucleoside structure: the sugar ring is replaced by an open-chain structure. It is selectively converted into acyclo-guanosine monophosphate (acyclo-GMP) by viral thymidine kinase, which is far more effective (3000 times) in phosphorylation than cellular thymidine kinase. Subsequently, the monophosphate form is further phosphorylated into the active triphosphate form, acyclo-guanosine triphosphate (acyclo-GTP), by cellular kinases. Acyclo-GTP is a very potent inhibitor of viral DNA polymerase; it has approximately 100 times greater affinity for viral than cellular polymerase. As a substrate, acyclo-GMP is incorporated into viral DNA, resulting in chain termination. It has also been shown that viral enzymes cannot remove acyclo-GMP from the chain, which results in inhibition of further activity of DNA polymerase. Acyclo-GTP is fairly rapidly metabolised within the cell, possibly by cellular phosphatases.
« Last Edit: November 19, 2007, 08:59:26 PM by bimazek »

Offline Tim Horn

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Bim:

All very interesting, but without any data showing that acyclovir specifically inhibits the activity of HIV's reverse transcriptase enzyme -- the virus's very own polymerase -- we risk going in totally confusing circles of discussion (keep in mind, there are plenty of drugs that target other viral polymerases, such as those of hepatitis B virus and hepatitis C virus, that have no known activity against HIV's reverse transcriptase enzyme).

IMHO, this is an important -- and somewhat basic -- question for bench scientists to work out. Reading between the lines of articles on Wikipedia isn't going to do us much good. Fact of the matter is, what we're seeing here is a potentially clinically significant reduction in viral load among HIV-positive patients with herpes simplex virus-2 coinfection. As there's much more known about the effects of HSV-2 coinfection on HIV viral load and transmission and well established anti-HSV activity associated with use of acyclovir -- with little, if any, evidence that acyclovir has a direct effect on HIV's life cycle -- I'm more inclined to keep this conversation in focus.

Tim Horn

Offline risred1

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I spoke to my specialist about the study sited here and the findings that Valtrex can by acting against HSV help lower VL of HIV.

His concern is that using Valtrex in an immune suppressed person long term possibly could create HSV mutation. It should be noted that Valtrex is not recommended in people with essentially AIDS.

I know we are seeing a fair bit of media encouraging HSV folks to get on a daily regimine. But for those with fully functioning immune systems, there is less concern that Valtrex can cause HSV mutation.

He is interested in the results, but also stated that this idea is not new, not that is all that important. As usual, more information is needed to see if partially impacted immune systems and valtrex is a good match to lower viral load with more or less long term usage.

risred1 - hiv +
02/07 CD4 404 - 27% - VL 15k
10/07 CD4 484 - 31% - VL 45k
05/08 CD4 414 - 26% - VL 70k
01/09 CD4 365 - 23% - VL 65k
05/09 CD4 291 - 23% - VL 115k - Started Meds - Reyataz/Truvada
06/09 CD4 394 - ?% - VL 1200 - Boosted Reyataz with Norvir and Truvada
07/09 CD4 441 - ?% - VL 118 - Boosted Reyataz with Norvir and Truvada
09/09 CD4 375 - ?% - VL Undetectable - Boosted Reyataz with Norvir and Truvada
12/09 CD4 595 - ?% - VL Undetectable - VIT D 34 - Reyataz/Truvada/Norvir

Offline Jake72

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  • Posts: 145
This may be a stupid question, but how would Valtrex work on someone who has already achieved long-term viral suppression on conventional HAART?  Could Valtrex monotherapy keep an already undetectable viral load undetectable?  At first glance, this would seem easier than, say, bringing a VL of 100000 down to undetectable, but I'm not a medical expert. 

And would it theoretically work on people who do not have HSV types 1 or 2?  Granted there are a lot of 'ifs' here, but it's an interesting subject, especially given that Valtrex would presumably not have the side effects associated with HAART (in addition to being much cheaper!).

Thanks for your input!

Jake

Offline Winiroo

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  • Positive since 1991
I was on a unsupervised drug holiday and went back to the docs after I noticed I had shingles. I started taking norvir, truvada and reyataz at the same time taking the 1 gm tablets of valcyclovir 3 times a day for the shingles.
My viral load went from 750,000 + to undetectable and my tcells went from 21 to 77 in one month.


Offline risred1

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This is my understanding, and I would hope for other commentary especially if there is another point of view on this.

The idea is that those coinfected with both HIV and HSV essentially have two things to deal with. By treating HSV with Valtrex and suppressing HSV, the body can then just deal with HIV, which may then result in a lowering of Viral load.

Why this is would be speculation on my part. But I believe the application that we are looking for is for those with elevating viral loads who have coinfection, and instead of reaching for HART, may be able to bring VL down by applying Valtrex. By reducing VL, we may be able to delay HARRT.

So if your on HARRT today, I don't know why Valtrex would be applied, but there may be a scenario for that.

If your on a Drug Holiday, it may be an option one may want to utilize to keep VL down during the holiday.

If you do not have HSV, and this is my guess, Valtrex won't do anything for you in reducing VL. (???)

--------

So while those who are getting close to having to go on meds, if your coinfected, Valtrex is an appealing idea to buy more time before committing to HARRT. But the down side is, and this is why we need more information, Valtrex, which is not for people with severely impacted immune systems, may in fact cause HSV mutation. This according to my specialist. I'm going to emphasize the "may" option. But my doc has stated that the idea of using Valtrex is not new, which means that some ground work has already been laid in this area. Additionally, at the University of Pennsylvania ID practice, they are fairly collaborative as a team of doctors. So I'm not going to say what my doc says goes. But as i spoke to him about this, he is interested, but as usual, we need more information to help us understand if this is a good choice over starting HARRT.

I don't know what the risk of HSV mutation is, but my Doc was not at all happy about it. Which is what gives me pause on this option.

The "ray" of hope on this issue is if your CD4 is say above 350 or 500, or whatever, can long term use of Valtrex be of benefit with little risk of HSV mutation? Perhaps Valtrex can be applied in those scenarios long term.


« Last Edit: November 27, 2007, 05:08:03 PM by risred1 »
risred1 - hiv +
02/07 CD4 404 - 27% - VL 15k
10/07 CD4 484 - 31% - VL 45k
05/08 CD4 414 - 26% - VL 70k
01/09 CD4 365 - 23% - VL 65k
05/09 CD4 291 - 23% - VL 115k - Started Meds - Reyataz/Truvada
06/09 CD4 394 - ?% - VL 1200 - Boosted Reyataz with Norvir and Truvada
07/09 CD4 441 - ?% - VL 118 - Boosted Reyataz with Norvir and Truvada
09/09 CD4 375 - ?% - VL Undetectable - Boosted Reyataz with Norvir and Truvada
12/09 CD4 595 - ?% - VL Undetectable - VIT D 34 - Reyataz/Truvada/Norvir

Offline risred1

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I found this commentary on Valtrex and suitability for Immune Suppressed Individuals. (From thebody.com)

    VALTREX AND HIV
Feb 21, 2004

Why is that HIV positive people are advised against taking Valtrex? Does Valtrex suppress the immune system and, if so, to what degree? How would a healthy person's immune system who took supressive doses of Valtrex be affected by the medicine?

Sincerely,

HIV-HERPES-HAVER-WHO-WANTS-VALTREX

      Response from Dr. Frascino

Hello HIV-Herpes-Haver-Who-Wants-Valtrex, (I'll call you HHHWWV for short or perhaps even H3W2V?)

The warning for Valtrex is for those with severe immunodeficiency. That would include advanced HIV (not just HIV disease). The reason for the warning can be traced to the clinical trials that were done when Valtrex was in development, awaiting FDA approval. Some patients in those clinical trials, who had severe immunodeficiency (those with advanced HIV disease, allogenic bone marrow transplant recipients, renal transplant recipients) developed a condition called Thrombotic Thrombocytopenic Purpura/Hemolytic Uremic Syndrome. Valtrex does not "suppress the immune system." Talk to your HIV/AIDS specialist. He/she will let you know what your best options would be for herpes, whether it's to prevent outbreaks or treat an active infection.

Well H3W2V,hope that helps!

Dr. Bob
risred1 - hiv +
02/07 CD4 404 - 27% - VL 15k
10/07 CD4 484 - 31% - VL 45k
05/08 CD4 414 - 26% - VL 70k
01/09 CD4 365 - 23% - VL 65k
05/09 CD4 291 - 23% - VL 115k - Started Meds - Reyataz/Truvada
06/09 CD4 394 - ?% - VL 1200 - Boosted Reyataz with Norvir and Truvada
07/09 CD4 441 - ?% - VL 118 - Boosted Reyataz with Norvir and Truvada
09/09 CD4 375 - ?% - VL Undetectable - Boosted Reyataz with Norvir and Truvada
12/09 CD4 595 - ?% - VL Undetectable - VIT D 34 - Reyataz/Truvada/Norvir

Offline risred1

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  • My Source for Supps - www.newyorkbuyersclub.org
I found this on HSV Resistence! I now conclude that my doc is pretty up to date and know stuff!! ;)

What this means is, if you take Valtrex and are immune supressed, Mutation can result in HSV. This is a sobering thought regarding what would be a trade off. Use Valtrex to lower VL and delay HARRT and risk HSV mutation.

This scenario in my mind would then limit the time you would use Valtrex. If one needed to get ones lipids or Liver functioning better prior to starting HARRT, maybe one would use Valtrex Short term to lower VL, while your getting in shape, but you may not want to stay on Valtrex for more than a few months. (???)

This really does not bode well for long term use of valtrex to keep VL down. It sounds like in the case sited below that HSV mutation is not a good thing. Not having something like Valtrex to knock down a bout with HSV may lead to other issues down the line with HIV coinfection, in my opinion.

Recurrent Antiviral-Resistant Genital Herpes in an Immunocompetent Patient
Author(s)    John D. Kriesel, Spotswood L. Spruance, Mark Prichard, Jacqueline N. Parker, and Earl R. Kern
Identifiers    The Journal of Infectious Diseases, volume 192 (2005), pages 156–161
DOI: 10.1086/430612
PubMed ID: 15942905
Availability    This site:   PS  |  HTML  |  PDF (603.9k)
Copyright    © 2005, the Infectious Diseases Society of America.
Abstract    Herpes simplex virus type 2 (HSV-2) resistance to antiviral drugs has been described primarily in immunocompromised patients. We report an apparently immunocompetent, human immunodeficiency virusndashnegative male patient who has experienced repeated HSV-2 genital outbreaks despite receiving antiviral prophylaxis with several different drugs. Several of the HSV-2 genital isolates from this patient have been confirmed as resistant to acyclovir and penciclovir. Antiviral resistance occurred in the setting of long-term prednisone treatment and intermittent acyclovir prophylaxis at suboptimal doses and persisted despite the cessation of oral steroid treatment. The patient's genital herpes outbreaks were not controlled by high-dose prophylaxis with acyclovir, valacyclovir, and famciclovir. Cessation of antiviral prophylaxis resulted in reversion of this patient's HSV-2 isolates to acyclovir and penciclovir sensitivity, although resistant virus reappeared when antiviral prophylaxis was resumed. Transmission of a sensitive HSV-2 strain from this patient to a female sex partner was observed. These observations confirm previous reports that resistance to acyclovir may develop during prophylactic therapy in an otherwise well, immunocompetent patient. These findings support the conclusion that both drug-sensitive and drug-resistant HSV-2 strains established latency in this patient and that both strains are capable of frequent reactivation.
risred1 - hiv +
02/07 CD4 404 - 27% - VL 15k
10/07 CD4 484 - 31% - VL 45k
05/08 CD4 414 - 26% - VL 70k
01/09 CD4 365 - 23% - VL 65k
05/09 CD4 291 - 23% - VL 115k - Started Meds - Reyataz/Truvada
06/09 CD4 394 - ?% - VL 1200 - Boosted Reyataz with Norvir and Truvada
07/09 CD4 441 - ?% - VL 118 - Boosted Reyataz with Norvir and Truvada
09/09 CD4 375 - ?% - VL Undetectable - Boosted Reyataz with Norvir and Truvada
12/09 CD4 595 - ?% - VL Undetectable - VIT D 34 - Reyataz/Truvada/Norvir

Offline bimazek

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wow lots of interesting stuff
i have a few things to write
i dont think that valtrex or aciclovir or any thing like that could ever get the VL down that much 50% was in the study but it would never never alone do anything like HAART,  HAART is the only thing that will bring VL to undetectable
-  there are 8 different herpes viruses and most people in world have most or all of them in thier bodies and the immune system has to constantly work to suppress these, esp. if it is a weakened immune system
understand that my reason for being on valtrex or actually now aciclovir because adap would not give valtrex first was that i had a tiny teany little sore in inside of my lip about the size of a well the letter o on this screen or maybe two   oo's

anyway it was small, but the body is also repressing the chickenpox virus a herpes virus in all of us 24x7
and many other herpes viruses see above

for me i am feeling much much better with the swelling under my neck and not sure if it is suppression of herpes virus or what exactly but i feel much much better

so who knows after time if this will help

i will get my VL in 2 months again

this is NOT a substitutute for HAART if you are under 350 i would get on HAART asap

but if not and you have antibody poz test for herpes or you ever had chicken pox -- a herpes virus -- and the Dr. suggests
every day treatment  with valtrex or aciclovir

TAKE the valtrex or aciclovir to suppress the chicken pox so you dont get shingles even if you have to be on it for years.... i did not and got shingles and it was painful

alot of what is posted above shows how little medicine knows about so many diseases... there are 8 different herpes viruses and each one probably has sub groups that have not even been discovered yet


this is my guess at % how common amoung  sexually active gay men in usa cities of these different types

1 - Herpes simplex virus type 1 (short version - see also cold sores):
How common? UK population, by age 30 around 50%. The rates are much higher in other countries 70% or higher in USA

2. Herpes simplex virus type 2 (short version - see also our Frequently asked questions):
How common? Around 25% of the sexually active UK population. Over the whole country between 3% and 10%. The rates are much higher in other countries.   5% or higher in USA

3. Varicella-zoster virus (short version - see also our shingles and post-herpetic neuralgia pages):
How common? Almost 100% of population by adulthood.

4. Epstein Barr virus (EBV, also called glandular fever, mononucleosis, mono, kissing disease):
How common? Virtually everybody worldwide. 100% of population

5. Cytomegalovirus (CMV)
How common? Half the population has CMV by a young age, with higher rates of infection in poorer areas. 88% to 100% of population

6. Human herpesvirus 6 (roseola infantum/exanthem subitum)
How common? By the age of 2, almost all babies have type 6B virus. 100% of population

7. Human herpesvirus 7:
How common? By the age of 3, almost all children have HHV-7.100% of population

8. Human herpesvirus 8 (also called Karposi's sarcoma herpes virus or KSHV) How common? This virus is quite common in some parts of the world. In Europe and the US it is not very common - under 10% have it.

i repost this since i want to make point that there is alot of different ones

i had a small one on my lip

i never ever had any on any of my sex organs


« Last Edit: November 28, 2007, 03:06:10 AM by bimazek »

Offline Paulette

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  • Posts: 112
I once had a large blister on my eardrum (called Bullas Myringitis ) and my ID doctor put me on the Valtrex  for a couple of months and it reduced my viral load, so he continued to give me valtrex for another three months; for he said that studies have shown that it can be used as a kicker to the HIV meds, and it worked, the only problem with it is that my insurance quit paying for it and it is expensive,  he supplied me with as much free samples as he could. But eventually he needed the samples for someone else who didn't have any insurance and couldn't afford their meds. which was the right thing to do.  Eventually i had to switch meds from Combivir / viracept  to Atripla(had an allergic reaction, only took for two days then switched to norvir, reyataz, and truvada which has made an amazing impact VL- undetectable  CD4- 880 . But back to the original question it was great and yes i noticed i felt better while taking the valtrex and my VL did go down. I hopes this helps. Almost forgot it brought my VL down from 6548 to 4180 .
Paulette
I have HIV; it doesn't me;)

Offline bimazek

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  • Posts: 781
paulette said
i noticed i felt better while taking the valtrex

on another subject

two factors. Firstly, cellular thymidine kinases phosphorylate the parent form significantly less rapidly than does the viral thymidine kinase, so the active triphosphate is present at much higher concentrations in virally infected cells than in uninfected cells. Secondly, the activated drug binds to viral DNA polymerase with a much higher affinity than to human DNA polymerases. As a result penciclovir exhibits negligible cytotoxicity to healthy cells.

i did a search for studies on thymidine kinase and hiv

http://www.google.com/search?hl=en&q=%22thymidine+kinase%22+hiv&btnG=Google+Search

Genes for virus specific thymidine kinases have been identified in Herpes simplex virus, Varicella zoster virus and Epstein-Barr virus.


ome drugs are specifically directed against dividing cells. They can be used against tumour and viral disease, as the diseased cells proliferate much more frequently than normal cells. The mechanism most often used is phosphorylation of a thymidine analogue by thymidine kinase. The monophosphate is further phosphorylated to the corresponding triphosphate and incorporated in the growing DNA chain, where it may stop the growth of the chain as it is chemically unable to bind a further base, or because it makes the resulting DNA chain defective. Several HIV drugs belong to this class including AZT. Some antiviral drugs make use of the wide specificity of viral thymidine kinase than that of human thymidine kinases.

ok i found a study tim from 1998 when science was still grasping for a great combo therapy

http://gateway.nlm.nih.gov/MeetingAbstracts/102187973.html

Institute of Medical Virology, JWG-University, Frankfurt, Germany.

Study of thymidine kinase (TK) activity in  HIV-1-infected patients in dependence on virus load, CD4 cell count and therapy duration.   TK deficiency in HIV-1 infected patients developed with disease progression, in association with increased viral load and decreased CD4 cell count. In such patients some monophosphate prodrugs [valtrex, aciclovir] may be superior to AZT or d4T as anti HIV-1 drugs as demonstrated by their ability to bypass thymidine kinase in TK-deficient cell lines.

http://www.medscape.com/viewarticle/421019_4

Herpes Simplex Virus Infection
Human herpes virus infection is a common malady that is exacerbated by HIV infection. In the general United States population approximately 65% of adults have antibody to HSV-1 and 25% have antibodies to HSV-2.[58,59] HSV-2 behaves as a sexually transmitted disease with increased seroprevalence in post-pubescent adults. In homosexual and bisexual men with HIV infection, the rate of HSV-2 seropositivity is approximately 75%.[60,61]

Acyclovir is an acyclic guanosine analog; it is phosphorylated by a viral thymidine kinase into acyclovir-monophosphate. Later additional phosphates are added by cellular kinases to produce acyclovir triphosphate, a compound which has a high affinity for viral DNA polymerase and leads to premature termination during viral replication because of its acyclic structure.
http://pubs.acs.org/cgi-bin/abstract.cgi/jmcmar/1996/39/i08/abs/jm950605j.html








http://aidsonline.com/pt/re/aids/abstract.00002030-200503250-00003.htm;jsessionid=HNNWsHQ8pnM3fJ7VRLJsF2GM1xDhxnfKlHyPlDcm9v7nhNTQhSTq!-1601909834!181195629!8091!-1


THIS TO ME SAYS IT ALL... SOME HIV POZ PEOPLE HAVE LOTS OF THESE THINGS GOING ON  -- Thymidine kinase and deoxycytidine  -- THEY DONT KNOW WHY OR WHAT CAUSES IT,  BUT WE DO KNOW THAT VALTREX TREATS IT...  THAT is what i get from this article....

March 25, 2005, 19:5 > Thymidine kinase and deoxycytidine...
   
    Thymidine kinase and deoxycytidine kinase activity in mononuclear cells from antiretroviral-naive HIV-infected patients.

    BASIC SCIENCE
    AIDS. 19(5):473-479, March 25, 2005.
    Turriziani, Ombretta a; Butera, Ornella a; Gianotti, Nicola b; Parisi, Saverio G c; Mazzi, Romualdo d; Girardi, Enrico e; Iaiani, Giancarlo f; Antonelli, Laura f; Lazzarin, Adriano b; Antonelli, Guido a

    Abstract:
    Objective: To evaluate whether an inter-individual variability in the activity of thymidine kinase (TK) and deoxycytidine kinase (dCK), which are involved in the first step of phosphorylation of some nucleoside analogues, exists in antiretroviral-naive, HIV-seropositive patients.

    Design: Forty-five randomly selected antiretroviral-naive HIV-infected patients were recruited, together with 26 healthy volunteers with no concurrent infection and under no pharmacological treatment.

    Methods: Peripheral blood mononuclear cells (PBMC) were isolated from venous blood and their TK and dCK activities evaluated. CD4 T cells and HIV-RNA were measured in HIV-infected patients, too.

    Results: There was a broad range of variability in TK activity in HIV-infected individuals. Furthermore, the activity in PBMC was significantly higher in HIV-infected individuals than in healthy volunteers. dCK activity in seropositive patients was significantly lower than in healthy volunteers. A marked inter-individual variability in dCK levels was observed in the HIV-infected group. No correlations were found between TK or dCK activities and plasma viral load, CD4 cell count, sex or age of patients.

    Conclusions: A marked range of inter-individual variability of TK and dCK activities in PBMC exists in HIV-infected individuals but not in healthy volunteers, indicating that the activity of enzymes with key roles in drug activation could vary greatly from one patient to another. Furthermore, TK expression is greater in HIV-infected individuals than in healthy volunteers. Better understanding of the viral or cellular factors that contribute to this variability, as well as their effect on responses to antiretroviral treatment, may aid optimization of the management of HIV-infected patients.



A marked range of inter-individual variability of TK and dCK activities in PBMC exists in HIV-infected individuals but not in healthy volunteers, indicating that the activity of enzymes with key roles in drug activation could vary greatly from one patient to another. Furthermore, TK expression is greater in HIV-infected individuals than in healthy volunteers.


 


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