45 replies to this topic

[Lufega]

Expanding on two (1, 2) previous posts on the general antiviral actions on Emodin, it also seems to be very effective for Herpes Simplex 1. What I find interesting though, is that it's capable of actually reducing the viral load in the brain and other organs. Given the recent association of neurodegenerative diseases and Herpes infections, I think this could have some important applications. Most substances that kill the herpes virus are virucidal only against the free virus. That is, they don't affect the total viral burden inside the cell. Only the extracellular virions are affected and this makes them great topical agents. If you want to eradicate the virus completely (*cough, cure ?) you need to reduce the viral load inside the cells. I thought this was impossible but I found a few substances that can do this. Emodin is one.

There are 6 hits on Pubmed for "herpes" and "emodin". One is an in vivo study.

http://www.ncbi.nlm....emodin%20herpes

My question to all the Resveratrol gurus on this forum is how to go around the laxative effect of emodin. Is any emodin absorbed at all ? Also, has anyone tusing anything less than 99% Resveratrol noticed a reduction in Herpes outbreaks ?

The effect of emodin, an anthraquinone derivative extracted from the roots of Rheum tanguticum, against herpes simplex virus in vitro and in vivo.

AIM OF THE STUDY:

Herpes simplex viruses (HSV-1 and -2) are important pathogens for humans and the discovery of novel anti-HSV drugs with low toxicity deserves great efforts. Rhubarb is one of the oldest and best-known traditional Chinese medicines. We initiated this study to test if emodin is the active ingredients from Rheum tanguticum (R. tanguticum, one of the Chinese Rhubarb) against HSV infection and to investigate its antiviral activity on HSV infection in tissue culture cells and in a mouse model.
MATERIALS AND METHODS:

Emodin (3-methyl-1,6,8-trihydroxyanthraquinone) was extracted and purified from R. tanguticum (cultivated at high mountainous area in Qinghai) and the purity was determined by high performance liquid chromatography. The antiviral experiments of emodin against HSV infection were performed in vitro and in vivo. In vivo, the HSV-infected mice were orally administered with emodin beginning at 24 h post-HSV exposures with dosages of 3.3 g/kg/day, 6.7 g/kg/day, and 11.3 g/kg/day, respectively, for 7 days.
RESULTS:

Emodin was found to inhibit the replication of HSV-1 and HSV-2 in cell culture at the concentration of 50 μg/ml with antiviral index of 2.07 and 3.53, respectively. The emodin treatment increased the survival rate of HSV-infected mice, prolonged survival time and showed higher efficacy of HSV elimination from brain, heart, liver and ganglion, compared to the viral controls. In addition, the antiviral activity of emodin was found to be equivalent to that of acyclovir in vivo.
CONCLUSIONS:

Our results indicate that emodin has the anti-HSV activity in vitro and in vivo and is thus a promising agent in the clinical therapy of HSV infection.

Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.

Emodin has three mechanisms of action including the direct inhibition of UL12 alkaline nuclease activity, casein kinase 2 (CK2) inhibition and directly disrupting the phospholipid bilayer. It's interesting that UL12, is conserved in all species of Herpesviridae. This could also be effective for treating HSV-2, CMV, epstein barr, etc.

The doses used in the study above seemed kind of high. This sounds a little more hopeful.

Serum profiles after oral administration of emodin at a dosage of 2gkg⁻¹ in mice showed that the peak serum concentration of emodin is 700μM (Mengs et al., 1997). We revealed that emodin at a concentration of 21.5μM was sufficient to reduce 50% virus yields without cytotoxic effect. Moreover, there is no evidence or equivocal evidence of carcinogenic activity of emodin in rats or mice.

Edited by Lufega, 30 December 2011 - 08:39 AM.

[Psychonaut]

Lufego having had ME/CFS for around 10 years now I find this very interesting since many of the herpes viruses, CMV, parvo are all potentially involved in the onset of many people who end up with the diagnosis, many times several of these will be present in a patient. I am still not quite sure why having several of these positive at a given time is not enough for a doctor to give an alternative diagnosis other than CFS which is not a real diagnosis at all; because they are present in a lot of the population anyway?

Will have to do some checking and see if it has been discussed by the communities before and maybe repost this info to them.

Edited by Psychonaut, 30 December 2011 - 12:20 PM.

[Hebbeh]

I use 98% resveratrol now but in years gone by, I used gram doses of the 50% extracts several times per day for extended periods of time and never ever experienced any adverse gastrointestinal issues of any kind. I no doubt a few did as some can have food sensitivities but I always felt the emodin issue was way over blown...at least from my experience.

[MrHappy]

That is a very good catch, Hebbeh!
Interesting that the phenol is also in knotweed, where resveratrol is usually extracted from. Also has anti-cancer effects. Chronic usage concerns/unknown.

Updated anti-herpes stack:
Resveratrol
BHT
Coconut Oil
Emodin
L-Lysine

[Lufega]

That is a very good catch, Hebbeh!
Interesting that the phenol is also in knotweed, where resveratrol is usually extracted from. Also has anti-cancer effects. Chronic usage concerns/unknown.

Updated anti-herpes stack:
Resveratrol
BHT
Coconut Oil
Emodin
L-Lysine

If you're serious about getting rid of Herpes (I definitely am), I found a couple of other interesting substances that can potentially cure the problem. I can post about the if you like. Emodin was the most impressive since it's the most recognizable. I am starting to believe that it is definitely possibly to eradicate Herpes forever. We just need a way to test this. I have antibodies for HSV1 but I've never had lesions. Maybe after treatment, antibody titers will decrease or maybe they will disappear altogether, but I can't be sure. How will we know the virus is completely gone ?

It's disheartening to think that a few IV doses a Emodin could potentitally eradicate this plague and yet, no one will ever produce such medication. I bet big pharma is in the process or tweaking the molecule to come up with a patentable derivative of emodin. Only time will tell.

[MrHappy]

Bavituximab is one that falls into that category. Monoclonal = profitable.

I'd definitely love to hear what else you know about it. I think its damage is a problem that is much bigger than the public is aware of and not as widely researched.

[Lufega]

PABA.

[Action of para-aminobenzoic acid and its combination with acyclovir in herpetic infection].

Abstract

The effect of para-amino benzoic acid (PABA) on the virus of Herpes simplex (VHS-1, strain L2) was studied and it was shown to be active in vitro and in vivo. The action of PABA was virucidal in the culture of the cell-free virus-containing material. It lowered the death rate of the laboratory mice with experimental herpetic encephalitis (intraperitoneal contamination) at the average by 40 per cent and increased the mean life-span of the animals significantly decreasing the virus titre in the mouse brain. PABA was not toxic with respect to the Vero cells thus not preventing the virus-induced cytopathic effect in the cultures. However, PABA showed high ability to potentiate the antiherpetic action of acyclovir (Zovirax, acycloguanosine) in the infected cultures when acyclovir was used in inactive concentrations.

PMID: 8660116 [PubMed - indexed for MEDLINE]

By itself it's only virucidal against the free virus but very potently so. The part about potentiating acyclovir is also interesting. I like PABA in that it's cheap and readily available. The pontentiating mechanism is due to PABAs ability to induce interferon. Interferons are able to interfere with viral replication inside the host cell. That's very cool.

[Actipol in treating stromal herpetic keratitis].

Abstract

Actipol (0.007% paraaminobenzoic acid--PABA) is a new interferon (IFN) inductor. It was recently introduced into ophthalmological practice. Its efficiency in surface herpetic keratitis is proven. We studied the therapeutic efficiency of actipol in the treatment of stromal herpetic keratitis and compared the results with combined therapy with acyclovir

(ACV) and leukocytic IFN. The main group (141 patients) were treated with actipol and the reference group (40 patients) with ACV ointment and leukocytic IFN. Local injections of actipol in combination with its instillations into the conjunctival sac led to cure of 67.3% patients with stromal herpetic keratitis; this treatment was more effective than combined local ACV + leukocytic IFN therapy (clinical cure in 45% cases). Epithelialization in the actipol group was observed 2 days sooner, infiltration resorption and clinical cure 4 days sooner than in the reference group. Relatively high visual acuity in the actipol group was presumably due to the reparogenic effect on the corneal stroma and antithrombotic, fibrinolytic, and antioxidant activity of

PABA. Hence, actipol is an effective drug for the treatment of stromal herpetic keratitis, exerting virtually no side effects.

PABA is also an acetylcholinesterase inhibitor.

p-Aminobenzoic acid derivatives as acetylcholinesterase inhibitors.

Abstract

Because Alzheimer's disease (AD) is a medical problem characterized by progressive loss of memory and cognition that is associated with a deficient cholinergic system, this work aims to evaluate some p-aminobenzoic acid (PABA) derivatives as acetylcholinesterase inhibitors in vitro, in continuation with our last studies. The assayed compounds are low toxic, simple-structured and low cost.

PMID: 15935907

Emodin also appear to induce interferon production and CK2 inhibitors (emodin) enhance the action of interferons. So emodin and PABA might be synergistic if used together.

Edited by Lufega, 02 January 2012 - 10:19 PM.

[Lufega]

The dose needed to induce interferons is very small.

[Para-aminobenzoic acid--an interferon inducer].

Abstract

Para-aminobenzoic acid (PABA) was shown to be an early type interferon inductor. PABA (10 micrograms/ml) induced interferon production in vitro in the cells of human peripheral blood and in vivo in albino mice (10 mg/kg). The results of the study suggested that PABA was able to induce production of interferon-alpha/beta in various immunocyte populations. By its interferonogenic activity PABA was comparable with the known interferoninductors. One of the mechanisms of the previously described in vivo antiherpes action of PABA can be attributed to its interferon inducing activity.

PMID: 10483491 [PubMed - indexed for MEDLINE]

[Lufega]

Terminalia Chebula (found in triphala)

Full Study: http://www.ncbi.nlm....66/?tool=pubmed

Hydrolyzable tannins (chebulagic acid and punicalagin) target viral glycoprotein-glycosaminoglycan interactions to inhibit herpes simplex virus 1 entry and cell-to-cell spread.

Lin LT, Chen TY, Chung CY, Noyce RS, Grindley TB, McCormick C, Lin TC, Wang GH, Lin CC, Richardson CD.

Source

Department of Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia, Canada.

Abstract

Herpes simplex virus 1 (HSV-1) is a common human pathogen that causes lifelong latent infection of sensory neurons. Non-nucleoside inhibitors that can limit HSV-1 recurrence are particularly useful in treating immunocompromised individuals or cases of emerging acyclovir-resistant strains of herpesvirus. We report that chebulagic acid (CHLA) and punicalagin (PUG), two hydrolyzable tannins isolated from the dried fruits of

Terminalia

chebula

Retz. (Combretaceae), inhibit HSV-1 entry at noncytotoxic doses in A549 human lung cells. Experiments revealed that both tannins targeted and inactivated HSV-1 viral particles and could prevent binding, penetration, and cell-to-cell spread, as well as secondary infection. The antiviral effect from either of the tannins was not associated with induction of type I

interferon

-mediated responses, nor was pretreatment of the host cell protective against HSV-1. Their inhibitory activities targeted HSV-1 glycoproteins since both natural compounds were able to block polykaryocyte formation mediated by expression of recombinant viral glycoproteins involved in attachment and membrane fusion. Our results indicated that CHLA and PUG blocked interactions between cell surface glycosaminoglycans and HSV-1 glycoproteins. Furthermore, the antiviral activities from the two tannins were significantly diminished in mutant cell lines unable to produce heparan sulfate and chondroitin sulfate and could be rescued upon reconstitution of heparan sulfate biosynthesis. We suggest that the hydrolyzable tannins CHLA and PUG may be useful as competitors for glycosaminoglycans in the management of HSV-1 infections and that they may help reduce the risk for development of viral drug resistance during therapy with nucleoside analogues.

[MrHappy]

That's pretty impressive!

So basically PABA will induce IFN and seems to bypass HSV's downstream IFN signal blocking, as well as cleaning up free HSV in the blood. Nice.

How it potentiates acyclovir is another question that needs more data. My understanding is that acyclovir works by messing up the DNA encoding of infected active/replicating cells. Maybe the presence of PABA / IFN triggers a 'panic' state in the virus and causes it to start replicating in case the first cell is destroyed.

What could make this even more effective is to ramp up production of T-cells and enhance the immune system during introduction of PABA + acyclovir.

Perhaps combining with isoprinosine would be a benefit.

http://www.lifespanm...oprinosine.html

Isoprinosine is a synthetic purine derivative with immunomodulatory and antiviral properties, which result from an apparent in vivo enhancement of host immune responses due to the drug.
The action of Isoprinosine can be summarized as follows:
--- Normalizes the cell-mediated immunity by stimulating the differentiation of T-lymphocytes into T-cytotoxic cells and T-helper cells and increasing lymphokine production
--- Increases production of IL-1 (interleukin-1) and IL-2 (interleukin-2) and IFN-? (gamma interferon)
--- Increases NK cell (natural killer cell) function
--- Increases the humoral immune response by stimulating the differentiation of B- lymphocytes into plasma cells and by enhancing antibody production
--- Increases the number of IgG and complement surface markers
--- Potentiates neutrophil, monocyte and macrophage chemotaxis and phagocytosis
--- Inhibits viral growth by suppressing viral RNA synthesis while potentiating depressed lympocytic
--- RNA synthesis and translational ability

Other benefits of Isoprinosine treatment: Studies have documented the ability of Isoprinosine to slow the progression of AIDS in HIV-infected persons by increasing the total number and activity of T-cells, T-helper cells and NK (natural killer) cells. The largest study, which was published in The New England Journal of Medicine on June 21, 1990 found that HIV infected people with CD4 cells count over 500 experienced significant benefits from Isoprinosine therapy. T-lymphocyte defects are common in cancer and AIDS patients according to a study in Medical Oncological Tumor Pharmacotherapy in 1989, which found that Isoprinosine and levamisole (another immune-boosting drug) mimic the actions of the thymic hormones to promote T-cell development. Combinations of Isoprinosine, low-dose Interleukin 1 and 2, and other immune-modulating hormones such as Melatonin are suggested as possibly effective cancer therapies.

[Logan]

Anyone know of a good source for a good terminalia chebula product out there???

[Lufega]

I found some stand-alone T.chebula on Amazon and a few other places online. I was researching chebula for other things a month month and decided to go with Triphala. It's one of the 3 ingredients. Most T. chebula supps offer around 400 mg per pill, triphala can give you that same amount at the recommened doses plus all the other digestive benefits.

[Lufega]

Thyroid hormones have a role in regulating the latent/replicative cycle of the herpes virus. It seems that patients who regularly have reactivations are probably not consuming enough iodine, or simply have a higher demand for it. The same applies for HIV. I myself realized that I had subclinical hypothyroidism recently, based on my symptoms, cold intolerance, morning temperatures, etc. I've been using 1000 mcg of iodine maybe 2 weeks now and I feel a lot better. I've also broken though my fat loss plateau.

It would seem prudent to optimize the bodies own mechanisms of dealing with herpes before trying out any other therapies. Some examples are Lysine, lithium and now Iodine. If these have a natural antiviral effect, then the body might be using up more of these elements faster than someone without herpes, creating a higher demand for them. I tested my serum lithium levels a couple of times and it was always undetectable. Even after months of using lithium orotate. So where is it all going ? I've also found great relief from anxiety by using Lysine. I can even go a few weeks without it before the anxiety comes back. So there is definitely a concentration-dependent cummulative effect.

Effects of thyroid hormone on HSV-1 gene regulation: implications in the control of viral latency and reactivation.

Abstract

ABSTRACT:

Thyroid hormone (TH) is involved in many biological functions such as animal development, cell differentiation, etc. Variation and/or disruption of plasma TH level often led to abnormalities and physiological disorders. TH exerts the effects through its nuclear receptors (TR). Literature showed that procedures resulted in TH alteration also linked to reactivation of several viruses including Herpes Simplex Virus Type -1 (HSV-1). Bioinformatic analyses revealed a number of putative TH responsive elements (TRE) located in the critical regulatory regions of HSV-1 genes such as thymidine kinase (TK), latency associated transcript (LAT), etc. Studies using neuronal cell lines have provided evidences demonstrating that liganded TR regulated viral gene expression via chromatin modification and controlled viral replication. The removal of TH reversed the inhibition and induced the viral replication previously blocked by TH. These results suggest that TH may have implication to participate in the control of reactivation during HSV-1 latency.

Full Study: http://www.ncbi.nlm....42/?tool=pubmed

Edited by Lufega, 03 January 2012 - 10:07 PM.

[MrHappy]

Could be that. You'll probably like this too:

http://www.ncbi.nlm....pubmed/2837144/

Antiviral activity of uridine 5'-diphosphate glucose analogues against some enveloped viruses in cell culture.

AuthorsGil-Fernández G, et al. Show all Journal
Antiviral Res. 1987 Dec;8(5-6):299-310.

Affiliation
Centro de Investigaciones Biológicas, Madrid, Spain.

Abstract
Twenty five analogues of uridine 5'-diphosphate glucose were screened against herpes simplex type 2, vaccinia virus, Sindbis virus and African swine fever virus. After screening, the compound 5'-[[[[(2",3",4",6"-tetra-O-benzoyl-alpha-D- glucopyranosyl)oxi]carbonyl]amino]sulfonyl]uridine (2), the synthesis of which has been reported (Camarasa et al., J. Med. Chem. 28, 40-46, 1985), was selected for further study. This compound showed in vitro activity against all viruses tested. The replication of herpes virus type 2 and African swine fever virus was completely inhibited at 100 micrograms/ml and 150 micrograms/ml respectively; vaccinia virus and Sindbis virus were inhibited to a lesser extent. The compound may inhibit several steps in the viral replication process.

PMID 2837144 [PubMed - indexed for MEDLINE]

[MrHappy]

It gets better:
http://www.ncbi.nlm....2837144/related

Mode of action of a new type of UDP-glucose analog against herpesvirus replication.

Authors
Alarcón B, González ME, Carrasco L, Méndez-Castrillón PP, García-López MT, de las Heras FG.
Journal
Antimicrob Agents Chemother. 1988 Aug;32(8):1257-61.

Affiliation
Departamento de Microbiología, Universidad Autónoma de Madrid, Spain.

Abstract
The mode of action of a new type of UDP-glucose analog against herpes simplex virus type 1 (HSV-1) replication was examined. The analog showed good selectivity and potent activity. At 10 micrograms/ml, P-536 inhibited the formation of infectious HSV-1 by more than 90%, whereas at 100 micrograms/ml it had no cytotoxic effects, as evidenced by phase-contrast microscopy. P-536 showed a wide spectrum of action and was active against HSV-1, adenovirus type 5, vaccinia virus, poliovirus type 1, encephalomyocarditis virus, vesicular stomatitis virus, influenza virus, and measles virus, irrespective of whether these viruses have lipidic envelopes or not. P-536 clearly inhibited protein glycosylation if added at the time when late viral proteins were being synthesized. Moreover, it also interfered with the synthesis of nucleic acids and the phosphorylation of nucleosides. If P-536 was present from the beginning of infection, HSV-1 replication was blocked at an early step and the infected cells continued to synthesize cellular proteins for long periods.

PMID 2847650 [PubMed - indexed for MEDLINE]

Full text free..

[Lufega]

I also forgot to mention. The thyroid study above went on to say the reason why herpes can reactivate after exposure to surgery, stress, UV light, radiation etc. also involves altered thyroid hormones. So, there was a increased demand for thyroid hormone in these situations, making less available to maintain herpes in a latent phase.

For example, whole body hyperthermia was reported to reduce the level of serum TH by 50%, probably due to the suppression of thyroid stimulating hormone release, monodeiodination alteration of T₄ from TH to reverse T₃, and enhanced TH clearance [76]. Importantly, hyperthermia is regularly used by laboratories to trigger HSV-1 reactivation in the mouse latency model [72]. In addition, brain injury and trauma were reported to reduce TH levels [86] and also trigger viral reactivation. Therefore, TH is likely to participate in the regulation and maintenance of viral latency and reactivation. TH acts on almost every cell in the body including neurons. It is likely that TH contribute, at least in part, to the regulation of HSV-1 latency/reactivation.

Table1).

[mpe]

Lufega, Mr Happy and Niner,
Hi guys,

My 23 year old , 7 months pregnant daughter, has just had her first and particularly nasty herpes ( cold sore) outbreak . She was infected by the child's father.
Before the outbreak she had been feeling a bit run down and now finds she has hsv-1.
After reading this post and others, I believe she should supplement with coconut oil, L-lysine and iodine.
I'm also keen to recommend BHT and some of the others discussed in this thread, but am concerned about any possible effects on the unborn child.
I have not read of any pregnancy issues but I don't know whether to have her start now or wait until the baby is born.
I would greatly appreciate your comments and would prefer a cautious approach, after all it is my daughter and granddaughter.

Thanks
Mike

[maxwatt]

Topical application of resveratrol powder to cold sores and canker sores has in my experience healed them in a matter of hours. Capsicum (chili pepper extract) takes a day. I expect there could be a similar benefit with herpes sores? the viruses are related.

[Lufega]

I don't see the harm in using coconut products, lysine and a small amount of iodine to control the herpes outbreak, which could pose a larger threat to the fetus. I would be curious, however, to see her thyroid values in their current state. I would expect to find a normal T4/T3 and a normal-high TSH value.

[kevinseven11]

No specific supplements have been recommended for Emodin. Why is that? Also would this help with warts? And my knowledge of how herpes works is limited but would a strong penetrator (DMSO) and Product (emodin) work to eradicate, or is the virus throughout the body? Wiki says possible neurotoxic damage, lets counter this potential FIRST ha.

Also Emodin is a laxative soo?

Edited by kevinseven11, 01 April 2012 - 07:06 PM.

[panhedonic]

Slightly off topic: I started taking l-arginine as part of a pre-workout stack, and around my 3rd intake, I had a herpes outbreak in my mouth. Not very common, but I definitely had them in the past (on high stress days, they would develop almost immediately after the stress "moment")

I also started taking DMAE (took 2 doses only)

Do you guys think I should stop taking l-arginine *forever*? Since almost everybody is a herpes host, i suppose other people are taking l-arginine and not having this issue...

Anybody sees a link between DMAE and herpes outbreaks?

[Lufega]

I've taken 20 grams Arginine for a few weeks with no problem. I've never had lesions, however. If your case you could experiment by consuming more lysine and iodine to keep the herpes in check and then see if using arginine troubles you again. No link between herpes and DMAE that I'm aware not.

[Logic]

As t5his seems to be turning into an anti HSV stack trhead:

BHT

I did a search to put a BHT link here and long-chain unsaturated monoglycerides and alcohols also came up.

http://scholar.googl...ved=0CCQQgQMwAA

Thithish really good newsh..! Hic!

[kevinseven11]

Does anyone have any links of where to buy any of these anti herpes supplements?
BTW here is a list of plant based anti herpes compounds.
http://www.ars-grin....pl?Antiherpetic

Edited by kevinseven11, 14 May 2012 - 12:52 AM.

[kevinseven11]

I will be running an experiment very soon.
I plan to dissolve

DMSO ( 54mg/mL Emodin ) 100ml ≥~5000Mg Emodin

Rheum spp. contain anthranoid derivatives (approx. 3-4%) Link

Hopefully 5 grams of emodin will come out of this lb but perhaps less.

http://www.amazon.co...37571988&sr=8-1
Absorb those 100ml through wart infected skin.
5 ml a day.
for 20 days.
If any success I will report happily.

Any concerns with this idea? I have a feeling the DMSO could accoumlate alot more than just Emodin and perhaps could be dangerous to my health. Im still planning everything out, but this is my current plan.
I know oxalic acid is poisonious so Im also concerned with that.
I did the dissolving math sloppy in the hope that more emodin and less toxic stuff will be dissolved.

Edited by kevinseven11, 21 May 2012 - 03:57 AM.

[Lufega]

Another option could be a less potent extract of resveratrol powder. Maybe something like 50%. The rest should be emodin. Resveratrol itself has anti-herpes activity so the combo. should be synergistic. Not sure if resv. dissolves in DMSO but searching the forum should turn up an answer. We wont really know which of the two works better than the other, but who cares! As long as it works.

If possible, take before and after pictures.

[Delafuente]

aren't there safety concerns with BHT and acyclovir? They are relativley safe, but do have potential to cause damage. Acyclovir may cause DNA mutations and, if I remember correctly, long term BHT administration caused abnormal morphology of hepatocytes (liver cells) in rats among other things.

There seems to be so many safer alternatives. Unless BHT and acyclovir are the main HSV "killers", then I would suggest sticking to the safer stuff.

Also, I here are some anti-HSV substances that I didn't see mentioned on this thread:
High vitamin D levels, zinc, andrographis, lemon balm, echinacea, eleuthero.

[Werper]

Here's the most advanced HSV-2 vaccine : http://investorshub....ge_id=67410022#

Entering Phase 2 studies this fall, the study will only take 12 months.

FWIW

[Delafuente]

If you're serious about getting rid of Herpes (I definitely am), I found a couple of other interesting substances that can potentially cure the problem. I can post about the if you like. Emodin was the most impressive since it's the most recognizable. I am starting to believe that it is definitely possibly to eradicate Herpes forever. We just need a way to test this. I have antibodies for HSV1 but I've never had lesions. Maybe after treatment, antibody titers will decrease or maybe they will disappear altogether, but I can't be sure. How will we know the virus is completely gone ?

It's disheartening to think that a few IV doses a Emodin could potentitally eradicate this plague and yet, no one will ever produce such medication. I bet big pharma is in the process or tweaking the molecule to come up with a patentable derivative of emodin. Only time will tell.

I was going to respond to you with an idea that occured to me regarding HSV-1 eradication. However, the post ended up being very detailed and i figured it would derail this thread significantly. I decided to post it as a new topic.

Essentially, it consists in devising a way to eliminate latency within the host and then using antivirals to eliminate all HSV-1 virions.
Here is the link: http://www.longecity...ation-of-hsv-1/

[Lufega]

I was going to respond to you with an idea that occured to me regarding HSV-1 eradication. However, the post ended up being very detailed and i figured it would derail this thread significantly. I decided to post it as a new topic.

Essentially, it consists in devising a way to eliminate latency within the host and then using antivirals to eliminate all HSV-1 virions.
Here is the link: http://www.longecity...ation-of-hsv-1/

I completely agree with this method. I was going to suggest it earlier but figured it would be too inflammatory. There are a few things out there that effectively kill the virus when it's replicating but not when it goes into latency. The obvious solution is exactly what you suggest. Aside from sunlight, I think Arginine also comes into mind. Good job thinking outside the box.

So, regular outings at the beach eating lots of watermelon (rich in citrulline) and your favorite antiviral of choice makes for a great day!