If you’ve followed this ASP2151 thread, you may know that I’ve been taking amenamevir (Amenalief) for about two months. In these two months, I have had absolutely no symptoms and no side effects to speak of. I’m ordering blood work soon to confirm that there are no major changes in important biomarkers (kidney, liver, heart, etc.) but I haven’t experienced any side effects that I could observe myself (headaches, diarrhea, insomnia, mood changes etc.) However, there is no data about the effectiveness of valacyclovir + amenamevir on reducing HSV recurrences. Two months of being on this combination is not enough to tell how well it works.
As a community, what we need is a functional cure. There’s a lot of excitement surrounding pritelivir in this regard. Pritelivir, like amenamevir, is a new drug inhibits the HSV helicase-primase complex. This is a different target than valacyclovir, which is why combining the two has major potential to be a functional cure. If you’ve read Josh Bloom’s article on the possibility of using pritelivir and valacyclovir together as a sort of HIV-like cocktail, then you’ve probably realized this combo is the only way in the foreseeable future that we will have a functional cure.
Here’s the reality of the situation.
There will not be a vaccine in the foreseeable future (barring a miracle that allows GEN-003 to continue. I wouldn’t count on that).
There will not be a CRISPR treatment in the foreseeable future.
The only HSV drug that is going through clinical trials (past pre-clinical) is pritelivir. That means that aside from amenamevir and pritelivir, there will not be any new drugs on the market for at least ten years.
You are not getting much help from the pharmaceutical companies. It’s the truth. Many people here are already aware of this. Look at the HSV pipeline. Other than the helicase-primase inhibitors, there is little to no progress being made, and the failure rate is incredibly high.
If you want, you can wait ten years hoping that the pharmaceutical companies come out with something. The only alternative is to conduct our own trials and gather some data.
There are plenty of drugs/supplements with studies that have some evidence to support their use in preventing HSV recurrences, but there’s not much consensus on whether they actually improve anything. A lot of them have been tested in animals, but not in humans for the purpose of reducing HSV recurrences. Others have been tested in early-stage trials with very small sample sizes and don’t achieve statistical significance, even if the results are promising:
Aspirin & other COX-2 inhibitors Another link
and plenty more.
Some people have also speculated that diet changes (ketogenic diet, intermittent fasting, etc.) also lead to dramatic improvement in symptoms. There is plenty of reason to be skeptical about these claims, especially when they only come from a small number of people. The sample size simply isn’t large enough.
And, of course, there’s a new drug that we know to be a strong inhibitor of HSV replication: amenamevir. Just as famciclovir has the same effect on HSV as valacyclovir, amenamevir has the same effect on HSV as pritelivir. And, as some of you know, amenamevir is approved in Japan and can be purchased online.
In many cases, valacyclovir by itself is not enough to stop all symptoms/recurrences. Additionally, valacyclovir doesn’t reduce shedding as much as it should. But research has found a strong correlation between number of recurrences and shedding. If we get recurrences down to zero, chances are that shedding is close to zero. At the very least, it means with very high probability that shedding has been significantly reduced.
Clearly, to achieve a functional cure, valacyclovir is not enough. But when combined it with other drugs/supplements/diets, it could achieve a functional cure or at least eliminate all outbreaks (which all but guarantees a very low level of shedding). Hypothetically, valacyclovir might reduce the average number of outbreaks per year from 3 to 1. Taking amenamevir in combination with valacyclovir might reduce that number to .5. Taking glutamine with amenamevir and valacyclovir might reduce that number to .2 (this is just a hypothetical example). Many of these combos may have a synergistic effect, meaning that using both drugs together would have a stronger effect than the effects of each individual drug combined. And how will we actually figure this out? By doing our own clinical trial.
We need a significant amount of participants. A trial will have at least sixty participants (more is better, but sixty is doable) for a three month period. I’ve created to gather some basic information about people (nothing personal or potentially identifying. Just things like age, time of diagnosis, frequency of outbreaks in the past year, whether or not they currently take medication. This data will help group the study participants properly) and a spreadsheet for a trial participant to record when they get an outbreak and to briefly describe the symptoms. The group will be split in half, with thirty participants taking only valacyclovir and the other half taking valacyclovir along with whatever we want to study in combination with valacyclovir. Other standard study procedures such as randomization of the groups will be incorporated into the trial. All the participants have to do is take the pills and record any outbreaks they have, briefly describe the symptoms, and write down when they are fully healed from the outbreak.
At the end of the trial, we will have three months of data for sixty participants. That’s ninety months, or seven and a half years of data, in each group. If the valacyclovir group had a total of ten outbreaks, then the average number of recurrences per year would be about 1.3. If the combo group had a total of five outbreaks, then the average number of recurrences would be about .7. Finally, we test to see if the combo led to a statistically significant reduction in outbreaks compared to the valacyclovir only group. The larger the study group, the more statistically significant the findings will be, which is why a large number of participants is crucial.
Finally, we finalize the trial by performing any other important data analysis. For example, we could see if there is any correlation between age and efficacy of the treatment. We generate graphs and charts and write a brief “paper” presenting the findings.
The only one of these trials that would actually “cost” a lot of money would be an amenamevir trial (amenamevir, although available, is pretty expensive). However, if enough people are willing to participate in one, we could get data on what looks to be the most effective treatment that is currently available.
A trial to assess the effect of any other drug, supplement, or diet would practically cost nothing. Aspirin, glutamine, lactoferrin, and propranolol are widely available and inexpensive, as are many of the other possible treatments, and these trials assume that participants are already taking valacyclovir whether it is covered by their insurance or not. And these trials do not require a major time commitment. The participant will have to verify at the beginning of the trial that they have the study drugs/supplements in their possession (just send a picture and blur out any personal info if there’s a prescription bottle). They take one or two pills a day and record any recurrences. In trials with potential side effects (e.g. lithium), the participant records any side effects. At the end of the study, the participant sends the spreadsheet over. That’s it.
These studies and data may not be as high quality as that of many clinical trials, but they are certainly useful. By obtaining this data, we give ourselves the ability to treat this disease better than ever before. Instead of shooting fish in a barrel and hoping some supplement works because one person on the internet said it did or because a supplement had an effect in an animal study, you’ll be able to rely on real data from humans. Not only that, but that data will be on a combination of valacyclovir and whatever else is being taken, which there are very few if any human studies on.
TL;DR: Doing crowdsourced trials on different combinations of valacyclovir and other compounds, we can see which compounds are effective for improving HSV. You can participate, and it is minimally time-consuming and costs next to nothing (unless you want to do an amenamevir trial). Participating will help us gather data to improve our conditions dramatically.
If you’re interested in participating, please fill out this form: https://goo.gl/forms/Q50PKY8I11tVMsLh2
I am not interested in anyone’s personal data. These studies are to remain anonymous and I will never ask for or attempt to collect any personal data. The only reason I ask for age in the form is because is a potential variable to account for in data analysis. You do not need to provide your age if you don't want to.
All communications should be done through this website’s messaging system or using an email that does not link to your identity. You can reach me at honeycombstudy at gmail.com or message me on this site.
Any questions and/or skepticism are more than welcome.
Finally, if anyone would like to contribute to this project please contact me! Let’s start taking action.
Since May I have been taking Valtrex. At first it was 500mg once a day then it increased to 1000mg once a day in June after frequent outbreaks persisted. I've had a total of 9 outbreaks since May and was diagnosed with hsv2 in March of this year. The past three weeks I've had severe dizziness, especially when lying down and getting up in the mornings. Today my doctor suggested taking acyclovir 400mg twice a day. Has anyone switched from acyclovir to valtrex and experienced better results/less breakouts?
So 4 weeks ago I tested positive for HSV 2. igg levels 1.36
took test about 1 maybe 2 days after my risky exposure which I suspect is where I contracted it I started taking Valtrex.
Anyways I was taking 500 mg of Valtrex since once a day. Also taking an assortment of l-lysine ginger root, oregano oil topical and pill vitamin c list goes on. I have always eaten very clean but for that month I really tried to fast primarily on vegetables and fruits. I also decided to work out a lot of cold showers etc..
So one month goes by I get tested Igg comes back igg .92 HSV2 that's a low positive right? would the Valtrex have made it go down to .92? Then they do a retrace test which I want to find out some more details on pretty sure that means they just run the blood through again and it came back negative this time I think its an igg negative.
So yeah I'm obviously very glad, this whole situation has made me change my life and it wasn't easy still isn't. I am thankful for that.
The doctor says she wants to run some more test again but said I should still be considered positive.
Also could have been exposed to this a few months ago as well just was thinking it was that time because of the burning urination. I got tested one day later after that exposure within 24 hours. would igg even come back 1.36 if it was from then?
Also if I have tested positive twice both being very low 1.36 and.92 should I get a WB.
Thanks for reading excited to hear some feedback.
I will get more testing done next week should know more then and share
Scenario, I had a sexual encounter with a person in early January, I was afraid of any STD did two weeks after i got a full panel test. All results, except HSV1 were negative (I've had HSV1 for a long time). I got tested again (independent anonymous lab) 5 weeks 4 days post exposure and this time the IGG results forHSV2 cane back as 1.03. Scared, the next week I went to my doctor AND to an anonymous lab (just for comparison). My Dr results were IGG 1.08 and other lab was 1.06. My doc said positive and I stated daily valtrex. Now, 12 weeks and 2 days after exposure, my HSV2 IGG is at .74. I've read a lot of conflicting information about this scenario... valtrex does affect blood work, valtrex doesn't affect bloodwork..
I've never had a "typical" outbreak, if at all. My first one, if that's even what it was, started with a folliculitis type rash in my pubic area, itchy scrotum, an increased urge to urinate, and an itchy feeling inside my urethra BUT NO TYPICAL LESIONS, like all the Dr's say will happen. I had a second possible ob, with the exact same symptoms a month later BUT NO LESIONS. It was just after clearing that I went to the doc.
So my question is..... can valtrex LOWER an IGG score that much? I've read that Terri Warren (although I couldn't find the direct post) said that it can delay seroconversion BUT can it change the numbers so dramatically? I'm scared to stop the valtrex because of my situation, im married and had an affair with the other woman. My wife knows, everything, and we are working through things BUT I must need piece of mind.
One would think that a drug with virtually no side effects, and a majority of ppl unknowingly carrying an sti would get some air time. I don't understand. The stigma and the ignorance is frustrating and I'm tired of carrying around a 'dirty little secret'!
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