45 replies to this topic

[MrHappy]

Has anyone else noticed noopept as triggering HSV replication?
Since starting noopept, I've basically had a constant outbreak, although it's gradually moving from the first damaged/infected epithelial cells to neighbouring cells and the original area is now healthy. I'm applying topical sodium hypochlorite to the affected area for about 3-5 minutes as a means of selective chemotherapy. I'm going to add some of the internal treatments mentioned to the mix, as well.

I'm suspecting (assuming I've identified the correct cause) that it's because of noopept's effect on stress-induced protein kinase.
http://www.ncbi.nlm....pubmed/21395007

Edited by MrHappy, 22 July 2012 - 01:11 AM.

[niner]

I'm wondering if emodin is really that good of an anti-herpetic. Looking at the abstract in the first post, note the dosage:

J Ethnopharmacol. 2011 Jan 27;133(2):718-23. Epub 2010 Nov 2.

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

Xiong HR, Luo J, Hou W, Xiao H, Yang ZQ.

State Key Laboratory of Virology, Institute of Medical Virology, Research Center of Food and Drug Evaluation, School of Medicine, Wuhan University, 185 Donghu Road, Wuhan 430071, PR China.

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.

PMID: 21050882

These are absolutely mammoth doses of emodin. A lot of people get diarrhea from milligram doses of emodin. Imagine if you were eating a pound a day! I don't know how they can say that the antiviral activity of emodin is equivalent to acyclovir in vivo on the basis of this data, unless there's something in the full text that they aren't mentioning in the abstract. In the cell culture experiment, 50 mcg/ml is a lot more reasonable, but the bioavailability of emodin in humans is likely to be very poor, along the lines of resveratrol, so hitting this level would be hard, and would probably require a lot more emodin than anyone could tolerate.

[MrHappy]

These are absolutely mammoth doses of emodin. A lot of people get diarrhea from milligram doses of emodin. Imagine if you were eating a pound a day! I don't know how they can say that the antiviral activity of emodin is equivalent to acyclovir in vivo on the basis of this data, unless there's something in the full text that they aren't mentioning in the abstract. In the cell culture experiment, 50 mcg/ml is a lot more reasonable, but the bioavailability of emodin in humans is likely to be very poor, along the lines of resveratrol, so hitting this level would be hard, and would probably require a lot more emodin than anyone could tolerate.

Agreed. There is another discussion here with a lot of other potent substances - PUFAs, etc.

[Logic]

I have been taking a supplement that contains 100 mg Resveratrol twice a day. (50% Knotweed extract)
I contacted the company who said it contained only 2% Emodin??? Can this be?
http://www.solaltech...&productId=5177

I stopped for a couple of days while taking Astragalus and had my 1st fever blister in ages FWIW.

I am now back on the Resv and Coconut Oil to try kill it completely. I suppose the only way to know if it worked is to stop taking everything, which I am loth to do ATM as I feel that I will have to take the regimen for at least 6 months to have any chance of completely killing HSV?

Do you think its worth adding acocliver? BHT?
Anything else?

[Logic]

"...Exposing the infected cells to the licorice ingredient, glycyrrhizic acid, shuts down LANA. That starts a chain reaction of biochemical changes in the white blood cells, leading to their suicide and the virus' death. The uninfected cells showed no detrimental effects from glycyrrhizic acid..."
http://www.phschool....ice_herpes.html

Note the references.

More info:
http://www.herpes-co...nd.30579/page-2

[Astroid]

Recently I had the feeling an outbreak was about to start.. and rubbed C60 on the area.  The next day everything felt and appeared normal. I reapplied it for insurance and never had an outbreak.

 

The reason I tried this was reading C60 is antiviral.   

[Astroid]

I took BHT for several weeks last year.. probably a total of 250 grams.. Can not say I noticed for sure anything. However, looking back I don't seem to have as many outbreaks for what it is worth.

 

I don't remember the dosage but tried to take it twice a day.

[Logic]

Researchers have discovered a protein that switches HCMV between dormancy and reactivation. They found this protein to be bound to the HCMV genome in latently infected hematopoietic stem cells and, upon a variety of external stimuli, to undergo a modification that allows for viral activation. Furthermore, the researchers were able to control this switch with a drug called chloroquine, usually used against malaria. When they treated hematopoietic stem cells containing dormant HCMV with chloroquine, the virus reactivated and became exposed, opening the door to maneuvers aimed at eliminating virus-infected cells.
http://www.longecity...virus/?p=722894

I dont know if chloroquine will work for the related HSV, but it may be worth a try.

 

Anecdotal:  

PABA + VCO and PABA + BHT kicked the ass (and fast) of fever blister outbreaks better than VCO and BHT have done in the past, although there aren't any outbreaks for me in the 1st pace when on either or both VCO and/or BHT.

I have not tried PABA on its own.

Edited by Logic, 12 April 2015 - 12:05 AM.

[ta5]

Creatine might be another:

 

 

Med Hypotheses. 2001 Sep;57(3):310-2.

Does supplemental creatine prevent herpes recurrences?

Ness SR1, McCarty MF.

While functioning as a general practitioner at the Camp Pendleton Marine Base, the first author treated numerous patients with recurrent genital herpes. Beginning in 1998, a number of these patients failed to return for periodic acyclovir therapy. Inquiries revealed that these patients had all commenced supplemental creatine after their last outbreak, and had experienced no further outbreaks. A literature search uncovered a report that cyclocreatine, a synthetic compound structurally and functionally homologous to creatine, inhibits the replication of cytomegalovirus, varicella-zoster, and herpes simplex types 1 and 2, in low millimolar concentrations; furthermore, dietary cyclocreatine reduces morbidity and mortality in mice infected with HSV-2. The fact that both creatine and cyclocreatine exert neuroprotective and cancer-retardant effects in rodents, encourages the speculation that creatine shares the anti-viral activity of cyclocreatine. Pilot studies to assess the impact of creatine loading on recurrence of oral and genital herpes appear warranted; the impact of creatine on shingles occurrence in high-risk patients could also be explored. Although initially conceived as an aid to athletic performance, creatine loading may prove to have broad preventive and therapeutic applications.

PMID: 11516222

[ta5]

Maybe Curcumin:

 

Virology. 2008 Apr 10;373(2):239-47. 

Curcumin inhibits herpes simplex virus immediate-early gene expression by a mechanism independent of p300/CBP histone acetyltransferase activity.

Kutluay SB1, Doroghazi J, Roemer ME, Triezenberg SJ.

Curcumin, a phenolic compound from the curry spice turmeric, exhibits a wide range of activities in eukaryotic cells, including antiviral effects that are at present incompletely characterized. Curcumin is known to inhibit the histone acetyltransferase activity of the transcriptional coactivator proteins p300 and CBP, which are recruited to the immediate early (IE) gene promoters of herpes simplex virus type 1 (HSV-1) by the viral transactivator protein VP16. We tested the hypothesis that curcumin, by inhibiting these coactivators, would block viral infection and gene expression. In cell culture assays, curcumin significantly decreased HSV-1 infectivity and IE gene expression. Entry of viral DNA to the host cell nucleus and binding of VP16 to IE gene promoters was not affected by curcumin, but recruitment of RNA polymerase II to those promoters was significantly diminished. However, these effects were observed using lower curcumin concentrations than those required to substantially inhibit global H3 acetylation. No changes were observed in histone H3 occupancy or acetylation at viral IE gene promoters. Furthermore, p300 and CBP recruitment to IE gene promoters was not affected by the presence of curcumin. Finally, disruption of p300 expression using a short hairpin RNA did not affect viral IE gene expression. These results suggest that curcumin affects VP16-mediated recruitment of RNA polymerase II to IE gene promoters by a mechanism independent of p300/CBP histone acetyltransferase activity.

PMID: 18191976

Full text

 

 

And a new Med Hypothesis article:

 

Med Hypotheses. 2015 Mar 14. pii: S0306-9877(15)00119-X.

Anti-herpesviral activity of curcumin may attenuate the development of Alzheimer's disease.

Mori I1.

Accumulating evidence has suggested that the reactivation of herpes simplex virus type 1 (HSV-1) in the brain is a potent risk factor of Alzheimer’s disease [1,2]. Amyloid-β (Aβ) is a major component of the senile plaques. It accumulates in the brain of elderly patients where it plays a significant role in the pathogenesis of Alzheimer’s disease. The internal amino acid sequence of HSV-1 gB is a homologue of the carboxyl-terminal of the Aβ peptide and it initiates and promotes the Aβ fibril formation [1].

PMID: 25804240

[ta5]

Maybe Limonene + β-pinene (or Limonene alone?).

 

Full text

 

Iran J Microbiol. 2014 Jun;6(3):149-55.

Antiviral activity of monoterpenes beta-pinene and limonene against herpes simplex virus in vitro.

Astani A1, Schnitzler P2.

Shahid Sadoughi University of Medical Sciences, Yazd, Iran ; Department of Infectious Diseases, Virology, University of Heidelberg, Heidelberg, Germany.

Department of Infectious Diseases, Virology, University of Heidelberg, Heidelberg, Germany.

BACKGROUND AND OBJECTIVES:

Essential oils are complex mixtures containing compounds of several different functional- group classes. Depending on the structure, we can distinguish monoterpenes, phenylpropanes, and other components. Here in this study two monoterpene compounds of essential oils, i.e. β-pinene and limonene were examined for their antiviral activity against herpes simplex virus type 1 (HSV-1) in vitro.

MATERIAL AND METHODS:

All antiviral assays were performed using RC-37 cells. Cytotoxicity was determined in a neutral red assay, antiviral assays were performed with HSV-1 strain KOS. The mode of antiviral action was evaluated at different periods during the viral replication cycle. Acyclovir was used as positive antiviral control.

RESULTS:

Beta-pinenene and limonenen reduced viral infectivity by 100 %. The mode of antiviral action has been determined, only moderate antiviral effects were revealed by monoterpenes when these drugs were added to host cells prior infection or after entry of HSV into cells. However, both monoterpenes exhibited high anti-HSV-1 activity by direct interaction with free virus particles. Both tested drugs interacted with HSV-1 in a dose-dependent manner thereby inactivating viral infection.

CONCLUSIONS:

These results suggest that monoterpenes in essential oils exhibit antiherpetic activity in the early phase of viral multiplication and might be used as potential antiviral agents.

PMID: 25870747

[YOLF]

Has there been any progress on this? Is anyone actively researching this?

 

Would research on this qualify for a NIH grant for orphan drugs? I'd love to see LongeCity getting some of this money. Anyone here want to write a study and grant proposal? Have any labs in mind? I'm thinking of some organizations in the LE community that do more supplement research than anyone else could run some clinicals if we do a project to get the money and predevelop the study. Such a product would ultimately bring more attention to our meme and mission. IIRC, something like 78% of the population has HSV1? And as you mentioned it is a major contributor to age related pathologies and will have to be cured at some point or we'll all wind up with it. 

[Logic]

Has there been any progress on this? Is anyone actively researching this?

 

Would research on this qualify for a NIH grant for orphan drugs? I'd love to see LongeCity getting some of this money. Anyone here want to write a study and grant proposal? Have any labs in mind? I'm thinking of some organizations in the LE community that do more supplement research than anyone else could run some clinicals if we do a project to get the money and predevelop the study. Such a product would ultimately bring more attention to our meme and mission. IIRC, something like 78% of the population has HSV1? And as you mentioned it is a major contributor to age related pathologies and will have to be cured at some point or we'll all wind up with it. 

 

Can you point me to a similar 'study and grant proposal' document YOLF, so I can see what would be involved.  I may be interested if its not above my ability/qualifications.

 

I must say that a capsule/capsules that:

Activate virii to replicate inside cells and then kills off the virii once free

and/or

Kills them of inside cells

and/or

Kills the infected cell itself

does seem possible with the information available.

 

Getting hold of some of the newer compounds like DRACO may pose some challenges?

[YOLF]

Looks like I may have gotten carried away, the orphan designation is for rare conditions rather than promising treatments that aren't being developed. I imagine there should be a grant for something like this though... It sucks to see all of these possibilities and not see anything being done about them. Maybe it's just that we don't have enough scientists to develop every possibility out there yet... 

[Logic]

More on licorice ingredient, glycyrrhizic acid as no-one seems to have grasped the significance of this stuff's ability to kill HSV, VZV, CMV, EBV infected cells :

 

 

Glycyrrhizic acid alters Kaposi sarcoma–associated herpesvirus latency, triggering p53-mediated apoptosis in transformed B lymphocytes

In addition, GA and its derivatives were shown to be effective both in vitro and in vivo against herpes simplex virus 2 (29–31), varicella zoster (31, 32), human CMV (31, 32), and EBV...

...GA is now routinely used throughout Japan for the treatment and control of chronic viral hepatitis, and its transaminase-lowering effect is clinically well recognized (35–37). Several pharmacological actions of GA, such as an antiinflammatory effect (38, 39), are considered to be mechanisms by which GA lowers transaminase levels. In human T cell lines, GA treatment enhances Fas-mediated apoptosis without alteration of caspase-3–like activity (40)....

http://www.ncbi.nlm....les/PMC1051998/

 

Licking latency with licorice

...While GA is effective for killing PEL cells in vitro, there are several caveats for the treatment of patients with PEL with GA. First, since GA is rapidly hydrolyzed to glycyrrhetic acid in the gastrointestinal tract, glycyrrhetic acid would need to be shown to be effective against PEL cells in vitro or GA would need to be administered intravenously. After intravenous administration of GA for treatment of hepatitis, serum levels of GA have been shown to range from 40 to 100 μg/ml (20), compared with the millimolar concentrations needed to induce apoptosis of PEL cells in vitro. Thus, the levels of GA required for efficacy in vitro might not be achievable in vivo. Second, Curreli et al. (2) found that the effects of GA on downregulating LANA expression in PEL cells were reversible for up to 3–4 days of treatment; thus, continuous and/or prolonged courses of therapy with GA might be needed. Third, therapeutic levels of GA might be toxic for normal cells and tissues. Curreli et al. found that the ED50 of GA for PEL cells was 2–3 mM; however, levels of 5–6 mM were toxic for uninfected cells...

http://www.ncbi.nlm....les/PMC1052015/

 

[ta5]

Dr. Proctor has a patent on PBN for herpes:
http://www.google.co...s/US20120115905

 

(Not that a patent means anything. You can patent something that's completely ineffective.)
 
Abstract:

Nitrone, nitroso, and nitroxide spintraps and spin labels ... for the prevention and treatment of fibrocystic disease of breast, premenstrual dysphoric syndrome and associated symptomology, prevention and treatment of migraine headache, cyclic vomiting syndrome, rectal hemorrhoids, trigeminal neuralgia, peripheral vascular disease, influenza, peridontitis and gingivitis, herpes zoster, herpes simplex, and post-herpetic neuralgia.

 
Claim 4:

Treatment of herpes zoster and/or post-herpetic neuralgia or related conditions with a nitrone, nitroso, or nitroxide spin-trap or a spin label and/or the reduced form of such at a pharmacologically effective dose, administered topically and/or systemically.