Medical Forum / Diseases and Disorders / Herpes / March 2004
Novitra: Zincum Oxydatum 2X, benzalkonium chloride , etc
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Perl Molson - 15 Jan 2004 20:44 GMT Together with viroxyn http://viroxyndirect.com/ExecutiveSummary.pdf
and viracea, http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9 754950&dopt=Abstract
this product seems very promising.
Recently I've read about the echinacea pure essential oil as a perfect candidate to the herpes cure, together with benzalkonium chloride and zinc oxide. http://www.pharmcast.com/Patents/Yr2002/Mar2002/031202/6355684_Herpes031202.htm http://www.herbmed.org/Herbs/Herb6.htm
I repeat, for the skeptiks (I am also a skeptic, like youself), one consideration regarding the "cure" in my opinion is that, once there are no more herpes viruses situated in the asymtomatic areas where it usually will remain, the herpes, even though having traces in ganglia, will not be capable of being carried out on the usual surfaces where it causes OBs.
The virus needs, presumably, those viruses located in the asymptomatic areas to "guide them" on the path along the nerve.
Perl Molson
NOVITRA(TM) Cold Sore Medicine Provides Relief in Time for Cold and Flu Season; Breakthrough Non-Prescription Medicine Proven to Shorten the Duration of Cold Sore Outbreaks Triggered by Weakened Immune Systems. PR Newswire, Nov 20, 2002
SANTA ROSA, Calif. -- The return of cold weather means the start of cold and flu season. To add to the misery of feeling under the weather, a weakened immune system can trigger unsightly cold sore outbreaks on or around the mouth that can last up to two weeks. While there is no cure for cold sores, there is a breakthrough non-prescription medicine that uses an active zinc formulation to fight the cold sore infection at its source. NOVITRA(TM), available nationwide at drug stores, mass merchants and supermarkets, is clinically proven to shorten the duration of cold sores, and it goes to work immediately to reduce the severity of symptoms, including tingling, itching, blistering, soreness and pain.
"Studies in the U.S. demonstrate that NOVITRA(TM) is not only clinically proven effective but also represents an exciting new usage of zinc that fights the cold sore infection," said Dr. David Riley, board certified internist and editor of a medical journal. "The active zinc in NOVITRA(TM) is unique in that it works to promote healing and shorten the duration of the cold sore rather than just suppress symptoms."
Consumer research indicates that cold sore sufferers are ready for a medicine that works quickly and effectively. According to an August 2002 survey, more than 50 percent of adults feel miserable, embarrassed or unattractive when they have a cold sore, and nearly half of all respondents admitted to changing their diet, avoiding social interactions or calling in sick to work when suffering from a cold sore outbreak.(1)
An estimated one-in-five Americans endure a cold sore outbreak each year, while more than 80 percent of the U.S. population has been exposed to and carries the virus. Most cold sore sufferers experience 2-3 outbreaks per year, which can be triggered by stress, fatigue, fevers, colds, the flu, sun exposure, hormonal changes or local mouth irritations caused by laser treatments, dental work or shaving.
Clinically Proven
NOVITRA's(TM) active zinc formulation has been proven as an effective medicine. In studies it has been demonstrated that NOVITRA(TM) shortens the duration of cold sores and goes to work immediately to reduce the severity of cold sore symptoms, including tingling, blistering, itching, soreness and pain. The clinical study results showed an average of a 36-hour reduction in cold sore duration and a decrease in symptoms compared to placebo.
The results of a recent in vitro study supports that zinc ions effectively inhibit viral propagation of Herpes Simplex 1 (HSV-1), the cold sore virus. The study was conducted to isolate the interaction between the active zinc in NOVITRA(TM) and HSV-1 to confirm whether active zinc is responsible for inactivating the cold sore virus.(2)
The active zinc technology in NOVITRA(TM) is designed to release free zinc ions, which are absorbed into the infected skin to fight the cold sore virus, protect healthy cells and promote healing. The active zinc is combined with an amino acid, which improves the body's absorption of zinc and ensures that the right amount of active zinc penetrates the cold sore to speed up and ease the healing process. "Consumers are often unaware that most non-prescription cold sore medications work to temporarily suppress the symptoms of a cold sore infection instead of supporting healing," said Riley. "NOVITRA(TM) is an effective treatment for cold sores that promotes healing as well as provides symptomatic relief."
Allterra, Inc. and B & T Pharmaceuticals have joined in a licensing agreement to make NOVITRA(TM), a homeopathic medicine, available to consumers. Allterra, Inc., established exclusively for the research and development of antiviral formulations that successfully use zinc to treat common illnesses, developed and patented NOVITRA's(TM) active zinc formulation. B & T Pharmaceuticals manufactures, distributes and markets the product.
B & T Pharmaceuticals
B & T Pharmaceuticals, headquartered in Santa Rosa, Calif. has been manufacturing and distributing non-prescription medicines for over 165 years. NOVITRA(TM) is currently available nationwide at drug stores, mass merchants and supermarkets. For more information about NOVITRA(TM), please visit the newly launched Web site at http://www.novitra.com/.
(1) August 2002 survey conducted by Tele.Nation for B & T Pharmaceuticals. (2) The published results of the in vitro study conducted by Washington University School of Medicine will be available in January 2003.
Make Your Opinion Count - Click Here http://tbutton.prnewswire.com/prn/11690X55517484
CONTACT: Jennie McCann of Porter Novelli, +1-415-975-3328, or jmccann@porternovelli.com
Web site: http://www.novitra.com/
COPYRIGHT 2002 PR Newswire Association, Inc. COPYRIGHT 2002 Gale Group
http://www.findarticles.com/cf_dls/m4PRN/2002_Nov_20/94439431/p1/article.jhtml
additional, from the site I've mentioned above,
http://www.pharmcast.com/Patents/Yr2002/Mar2002/031202/6355684_Herpes031202.htm
Title: Antimicrobial treatment for herpes simplex virus and other infectious diseases
United States Patent: 6,355,684
Inventors: Squires; Meryl (Elmhurst, IL) Assignee: Squires; Meryl J. (Barrington Hills, IL)
Appl. No.: 646988 Filed: May 8, 1996
Abstract
An improved medical treatment and medicine is provided to quickly and safely resolve herpes and other microbial infections. The inexpensive user-friendly medicine can be applied and maintained on the infected region until the physical symptoms of the disease disappears and the patient is comfortable and has a normal appearance. The attractive medicine comprises an antimicrobial concentrate comprising microbe inhibitors, phytochemicals or isolates. Desirably, the effective medicine comprises a surfactant and an aqueous carrier or solvent. In the preferred form, the medicine comprises Echinacea phytochemicals and benzalkonium chloride in a sterile water solution.
SUMMARY OF THE INVENTION
An improved medical treatment and medicine are provided which, when applied in the topical manner, rapidly relieves pain and heals lesions of herpes virus. Advantageously, the improved medical treatment and medicine are safe, inexpensive and effective. The improved medicine, also referred to as Viracea, comprises a novel medical composition, formulation, antimicrobial compound and solution. The new antimicrobial medical treatment and microbicidal medicine are successful in treating primarily herpes simplex virus (HSV 1 & HSV 2) topically and can be useful in treating other herpes related microbial infections including, but not limited to: varicella zoster virus (herpes zoster) and cytomegalovirus. In some circumstances, it may be useful to use the novel medicine systemically.
Advantageously, the improved medical treatment and medicine of the present invention yielded unexpected, surprisingly good results. Initial, topical, in vivo testing, demonstrated relief from pain in minutes and speedy total resolution of vesicular eruption in all individuals tested. When the inventive medical treatment and medicine are applied at the prodromal stage, the infection is interrupted and no further outbreak occurs. In vitro testing of the novel medical treatment and medicine demonstrated extremely surprising inhibitory effects on herpes virus. Desirably, the novel medicine is made from readily available, over the counter (OTC) chemicals or products and provides a safe comfortable, economical and user-friendly treatment.
While the novel medicine and antimicrobial compound is particularly useful in dramatically inhibiting herpes virus simplex, it may be useful in treating other microbial diseases (microbe-causing diseases)such as: human immunodeficiency virus infection (HIV), Epstein barr, papilloma virus, cellulitis, staphylococci, streptococci, mycobacteria, influenza, parainfluenza, adenoviruses, encephalitis, meningitis, arbovirus, arenavirus, anaerobic bacilli, picornavirus, coronavirus and synsytialvirus, as well as varicella zoster virus and cytomegalovirus.
This easy to use microbicide solution provides a moderately water resistant coating upon application to either the prodromal tissue or the erythematous vesicular herpes lesion. Upon contact, there is a slight tingling effect. Within minutes of application, the pain of the infection resolves. Gradually, inguinal swelling subsides, fever, malaise, body aches, and nerve involvement subsides. Typically, within twenty-one hours all external symptoms and physical manifestations of infection are resolved and the vesicle is dried and resolved. A particularly surprising, beneficial effect provided by this inventive medicine, is that when it is applied at the first sign of outbreak, the prodromal stage, all symptoms and signs of further infectious outbreak stops! No eruptions appear or any further escalation of symptoms of the infection. The outbreak literally stops!
Desirably, the novel medicine (medical composition) includes microbe inhibitors which inhibit, suppress and stop microbial infections from microbe-causing diseases. The microbe inhibitors comprise antimicrobial isolates, botanical extracts or phytochemicals, of at least a portion of one or more of the special plants listed below. The microbe inhibitors can comprise viral inhibitors to inhibit viral diseases, such as: herpes simplex virus 1 (HSV 1), herpes virus 2 (HSV 2), varicella zoster virus (herpes zoster) cytomegalovirus, HIV, epstein barr, papilloma virus, viral influenza, viral parainfluenza, adenovirus, viral encephalitis, viral menigitus, arbovirus, arenavirus, picornavirus, coronavirus, and synsytialvirus. The microbe inhibitors can also comprise bacterial inhibitors to inhibit bacterial diseases, such as: cellulitis, staphylococci, streptococci, mycobacteria, bacterial encephalitis, bacterial meningitis, and anaerobic bacilli. In some circumstances, the microbe inhibitors can include fungi inhibitors.
Better results are obtained if Echinacea or other plants are not used in the medicine in their raw, untreated and uncut state. For even better results, the medicine can exclude: Arabinose, betaine, cellulose, copper, fructose, fatty acids, galactose, glucose, iron, potassium, protein, resin, sucrose, sulfur, vitamin a, vitamin c, vitamin e and xylose.
The improved medical treatment provides a novel method and process for use in treating the above infectious diseases by applying the microbial inhibitors on the microbial infected area and maintaining the microbe inhibitors on the infected area (region or surface) until the external symptoms and physical manifestations of the infection disappear, reside or resolve about the infected area. The medicine can be applied by spraying, dabbing, dusting, swabbing, sponging, brushing, pouring, dispensing, covering, or heavily coating the medicine on the microbial infected areas, such as: oral mucosa, nasal mucosa, vaginal tissue, labial tissue, anal tissue, peri-anal tissue, lips, cutaneous tissue, sub-cutaneous tissue, ocular tissue, conjunctiva, and eyelids.
While the medical treatment and medicine is particularly useful for inhibiting herpes and other infectious diseases in persons (human beings) (homo sapiens), they can also be useful for veterinary purposes for treating viral and bacterial infections and infectious diseases in animals, such as: dogs, cats, birds, horses, cows, sheep, swine (pigs and hogs), and other farm animals, as well as rodents and other animals seen in zoos.
Preferably, the improved medicine, medical composition or microbial compound is a phytochemical concentrate which is combined and simultaneously or concurrently applied with a surfactant and a carrier, solvent or diluent to provide a microbicide medicinal solution.
To this end, the interesting microbicide solution comprises an antimicrobial detergent surfactant, with botanical extracts. The surfactants preferably are cationic surfactants which can comprise singly or any number of quaternary ammonium chlorides having 6-18 carbons such as alkylbenzyldimethylammonium chloride, mixtures of alkylbenzyldimethylammonium chloride, alkyldimethyl/ethylbenzylammonium chloride, n-alkyldimethylbenzylammonium chloride, diisobutylphenoxyethoxyethyldimethylbenzylammonium chloride, N--(C12C14C16)dimethylbenzylammonium chloride, benzalkonium chloride, octyldecyldimethyloammonium chloride, didecyldimethylammonium chloride, dioctyldimethylammonium chloride, dialkyldimethylammonium chloride, dialkylmethylbenzylammonium chloride, octyldecyldimethylammonium chloride, dimethylbenzylammonium chloride, laurryldimethylbenzylammonium chloride, o-benzyl-p-chlorophenol, dideryldimethylammonium chloride, doctyldimethylammonium chloride, alkyl (C14 C12 C16) dimethylbenzylammonium chloride, and preferably comprises alkylbenzyldimethylammonium chloride most preferably benzalkonium chloride. The range of activity of the cationic surfactant can be 5% to 90% but for best results 8% to 20%. Quaternary ammonium salts are readily available commercially. In some circumstances it may be useful to use other surfactants, such as, but not limited to: DMSO, glycolic acid surfactants, enzyme surfactants, ampholytic surfactants, switterionic surfactants, and nonionic surfactants. The surfactants can comprise detergents, wetting agents, emulsifiers, defoamers, and/or surface tension reducing additives.
Carriers are useful for mixing the constituents, keeping the constituents in solution, and providing an easy method of application to the affected area whether by spray, dropper, or applicator. While an aqueous solution, preferably a sterile aqueous carrier and solvent is preferred for best results, in some circumstances it may be desirable to use other liquid or solid carriers, such as: glycerin, mineral oil, silica, cottonseed oil, coconut oil, vegetable oil, seed oil, fish oil, or animal oil, alcohol, talc, corn meal, beeswax, carnauba wax, beta carotene, garlic oil, camphor oil, soluble vitamins, soluble minerals, rape seed oil, nut oils, olive oil, liposomes, ascorbic acid, evening primrose oil, pycnogenol, grape seed oil, lanolin, Ethocyn, collagen, aloe vera, bee pollen, royal jelly, chondroitin sulfate A, sea vegetables, EDTA, fatty acids, herbs, lecithin, bioflavinoids, grain oils or powders, algae, teas, vinegars, acidophilus, cell salts, ascorbic acids, hydra 5, glandulars, amino acids, psyllium, plant derivatives, or other sterile carriers.
The botanical extracts antimicrobial isolates or phytochemicals contained in this new medicine and medical treatment can be comprised of: Arabinose, betaine, copper, echinacen, echinacin B, echinacoside, echinolone, enzymes, fructose, fatty acids, galactose, glucose, glucuronic acid, inulin, inuloid, iron, pentadecadiene, polyacetylene compounds, polysaccharides such as but not limited to arabinogalactan, potassium, protein, resin, rhamnose, sucrose, sulfur, tannins, vitamins a, c, and e, xylose. For better results, the phytochemical concentrates include the above phytochemicals, excluding Arabinose, bataine cellulose, copper, fructose, fatty acids, galactose, glicose, iron, potassium, protein, resin, sucrose, sulfer, xylose and vitamins a, c and e.
The botanical extracts, antimicrobial isolates and phytochemicals are separated, extracted and isolated from portions of plants, such as: pimpinella anisum, myroxylon, arctostaphylos, carum, capsicum, eugenia mytacea, coriandrum, inula, allium, gentiana, juniperus, calendula, origanum, mentha labiate, commiphora, plantago, rosmarinus, ruta, baptisa, artemisa, sage, mentha, parthenium integrifolium, eucalyptus, asteriacea, and preferably from the genus Echinacea of the family Asteriacea, namely, Echinacea purpurea, Echinacea angustofolium, Echinacea pallidae, Echinacea vegetalis, Echinacea atribactilus and their cultivars. For best results, the phytochemicals and antimicrobial isolates are extracts from Echinacea purpurea and Echinacea angustifolium.
The inventive technology, treatment and medicine yield very attractive, unexpected, surprisingly good and consistent results. Tests show the microbicide solution (medicine) and medical treatment to be extremely useful to: heal and control herpes outbreaks, viral shedding, extend the latency periods of the disease, and dramatically inhibit the virus, while being generally safe to the patient and the environment.
Claim 1 of 20 Claims
What is claimed is:
1. A medical composition for use in treating diseases:
substantially greater than 0.01% to about 0.8% by weight aqueous benzalkonium chloride;
from about 40% to about 60% by weight Echinacea purpurea, in the absence of Echinacea angustofolia and raw untreated Echinacea;
said antimicrobial isolates of Echinacea purpurea being selected from the group consisting of: echinacen; echinacen B; echinaceine; echinacoside; caffeic acid ester; echinolone; enzymes; glucuronic acid; inulini; inuloid; pentadecadiene; polyacetylene compounds; polysaccharides; arabinogalactan; rhamnose; tannins; PSI (a 4-O-methylglucoronoarabinoxylan, Mr 35 Kd); PSII (an acid rhamnoarbinogalactan, Mr 450 kD); cynarin; 1,5-di-o-caffeoylquinic acid; acid; 2,3-O-di-caffeoyltartaric acid; borneol; bornyl acetate; pentadeca-8(z)-en-zone; germacrene D; caryophyllene; caryophyllene epoxide; anthocyanin, pyrrolizidine alkaloid, lipophilic amide; isobutylamide; polyacetylene; anthocyanin; 3-O-B-D-glucopyranoside; 3-O-(6-O-malonyl-B-D-glucopyranoside); tussilagine; isotussilagine; isomeric dodeca isobutylamide; tetraenoic acid; and carophylenes; and
said antimicrobial isolates of Echinacea purpurea cooperating with said aqueous benzalkonium chloride to provide a herpes-treating medicine for treatment of herpes selected from the group consisting of herpes simplex virus 1, herpes simplex virus 2, papilloma virus, varicella zoster virus (herpes zoster), and cytomegalovirus.
Another link to viracea Antiviral activity of Viracea against acyclovir susceptible and acyclovir resistant strains of herpes simplex virus.
Thompson KD.
Department of Pathology, The University of Chicago Medical Center, IL 60637, USA. thompson@midway.uchicago.edu
Viracea, a topical microbicide, is a blend of benzalkonium chloride and phytochemicals derived from Echinacea purpurea and is a proprietary formula from Destiny BioMediX Corp. Viracea was tested against 40 strains of herpes simplex virus (HSV): 15 strains (five HSV-1 and ten HSV-2) were resistant to acyclovir (ACV-R) and 25 strains (13 HSV-1 and 12 HSV-2) were susceptible to ACV (ACV-S). The median ED50 of Viracea for the five ACV-R strains of HSV-1 was a 1:100 dilution of the drug with a range of 1:50-1:400. The median ED50 of Viracea for the ten ACV-R strains of HSV-2 was 1:200 with a range of 1:50-1:3200. For the ACV-S strains of HSV-1 and HSV-2, the median ED50 of Viracea was 1:100 and 1:200, respectively. The cytotoxicity of Viracea was evaluated in a standard neutral red dye uptake assay in human foreskin fibroblasts. The cytotoxicity of Viracea approached only 50% at the highest concentration of the drug tested, a 1:2 dilution, indicating that Viracea is non-toxic in this cell cytotoxicity assay. Although the active component(s) in Viracea that has anti-HSV activity is not known, it appears that this extract has good antiviral activity against both ACV resistant and ACV susceptible strains of HSV-1 and HSV-2.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9 754950&dopt=Abstract
Tim Fitzmaurice - 16 Jan 2004 12:25 GMT > The virus needs, presumably, those viruses located in the asymptomatic > areas to "guide them" on the path along the nerve. Eh? AN asymptomatic outbreak is just one where the virus level of destruction doesnt reach a point where its noticeable. In HSV it seems episodic like the outbreaks. These virions dont talk to each other and the transport mechanism - well they get onto it and it sends them from cell body to sensory end points of the axons...its all one cell so no need for any guidiance from other virus particles - the pathway is already there for neuronal internal transport of substances.
Tim -- When playing rugby, its not the winning that counts, but the taking apart ICQ: 5178568
Perl Molson - 17 Jan 2004 09:17 GMT > > The virus needs, presumably, those viruses located in the asymptomatic > > areas to "guide them" on the path along the nerve. [quoted text clipped - 8 lines] > > Tim I guess, I will figure that one out, after awhile; I've tried this next one product, Orajel.
The best way to tell about a potential dependency of the viral activity and to the asymptomatic viruses, is to see total improvements in dealing with herpes. Once the old triggers will not be exist anymore triggers is a good sign already.
Time will tell the rest.
Chemical signalling or of some other sort, between the viruses can be a possibility.
Imagine a skin that is stressed, unhealthy, dry, kept in wind, cold, other factors; that would be a trigger only if the skin contains asymptomatic viruses, in my opinion.
It doesn't make sense otherwise.
There are no direct relation between the skin's health and related activity in the skin areas and the herpes viruses in the neuron.
If, on contrary, that would be the case, then by sitting in cold temperature would mean a continuous flow of herpes viruses towards the skin areas, right?
Is that the case, Tim? Imagine a homeless person having herpes in this context. That person, in conformity to your theory, would have to be covered in herpes lesions.
Perl Molson
Orajel Mouth Aid Cold & Canker Sore Medicine, Gel
http://www.drugstore.com/qxp15833_333181_sespider/orajel/mouth_aid_cold_and_cank er_sore_medicine_gel.htm
Ingredients: Active Ingredients: Contains: Benzocaine (20%), Benzalkonium Chloride (0.2%), Zinc Chloride (0.1%)
Inactive Ingredients: Allantoin, Carbomer, Edetate Disodium, Peppermint Oil, Polyethylene Glycol, Polysorbate 60, Propyl Gallate, Propylene Glycol, Purified Water, Providone, Sodium Saccharin, Sorbic Acid, Stearyl Alcohol
Perl Molson - 19 Jan 2004 02:39 GMT > > > The virus needs, presumably, those viruses located in the asymptomatic > > > areas to "guide them" on the path along the nerve. [quoted text clipped - 57 lines] > Propylene Glycol, Purified Water, Providone, Sodium Saccharin, Sorbic > Acid, Stearyl Alcohol Herpes virus, after the first infection, will cause OB's as often as a few times avery 3 months.
Perhaps, in such a teorethical ,context we can identify the relationship between the existance of the viruses in the dermal areas and the continuous reactivation of the virus.
People with herpes are most likely to shed the virus asymptomatically for up to three months after an outbreak, in conformity with some authors.
A little math will tell that, having further OB's on at least 3 months period, will maintain the asymtomatic viruses capable of recausing the following OB's.
Once we will succeed in eliminating the asymtomatic viruses through various methods presented here at ASH, the clearance of that area will assure the discontinuity of the herpes activity.
In other words, as I've mentioned in my previous posts in this topic, we can consider ourselves cured of herpes simplex as soon as the asymtomathic viruses will perish.
The transport mechanism is directly related to the asymtomatic shedding of the viruses.
The viral structures located in ganglia, have a structure uncapable of becoming active viruses, unless a chimical signal will be received from the viruses coming along the axon signal contained in the newly arrived viruses in the ganglia.
So, as a conclusion, if you will not notice any outbreaks for more then 100 days, means you that, you can consider yourself cured of herpes.
The traces of herpes cannot reactivate themselves without the help of new viruses arriving at the trigerminal or root ganglia locations, whichever type of herpes virus you have.
Be adviced, that some OB's can be quite hard to be identified due to the milder symtoms.
Perhaps, there are areas in the mucus-skin areas, where a certain ammount of herpes viruses can remain asymptomatic, for up to 100 days.
During this time, back and forth, from the ganglia to the dermal areas, viruses can travel in a certain temporal pattern.
Imagine now, in the dermal areas, during these 3 months, the viruses will be defeated by antivirals. Their number will follow a decrease; at one point in time, when the viruses will become less and less in number, in dermal area, this number will reach soon, zero.
The last viruses travelling from the ganglia towards the dermal area, will be killed and that means a herpes cure.
It all makes sense, when think that the virus is a bunch of dna and rna and proteins stuff; in the ganglia, the viral traces need the component of the virus received from the new viruses that will disintegrate in ganglia in such components.
There are no enough components in the ganglia's viral traces, in order to allow the traces of viruses to become fully functional, capable of travelling along the axon. I repeat, these viral traces NEED the parts from newly arrived viruses in ganglia.
Perl Molson
Perl Molson - 19 Jan 2004 03:00 GMT Related to messages number 4 and 3 at the above ( 3 articles from pubmed.com )
1)
Thymidine kinase-negative herpes simplex virus mutants establish latency in mouse trigeminal ganglia but do not reactivate.
Herpes simplex virus infection of mammalian hosts involves lytic replication at a primary site, such as the cornea, translocation by axonal transport to sensory ganglia and replication, and latent infection at a secondary site, ganglionic neurons. The virus-encoded thymidine kinase, which is a target for antiviral drugs such as acyclovir, is not essential for lytic replication yet evidently is required at the secondary site for replication and some phase of latent infection. To determine the specific stage in viral pathogenesis at which this enzyme is required, we constructed virus deletion mutants that were acyclovir resistant and exhibited no detectable thymidine kinase activity. After corneal inoculation of mice, the mutants replicated to high titers in the eye but were severely impaired for acute replication in trigeminal ganglia and failed to reactivate from ganglia upon cocultivation with permissive cells. Nevertheless, latency-associated transcripts were expressed in neuronal nuclei of ganglia from mutant-infected mice and superinfection of the ganglia with a second virus rescued the latent mutant virus. Thus, contrary to a widely accepted hypothesis, the thymidine kinase-negative mutants established latent infections, implying that neither thymidine kinase activity nor ganglionic replication is necessary for establishment of latency. Rather, thymidine kinase appears to be necessary for reactivation from latency. These results suggest that acyclovir-resistant viruses could establish latent infections in clinical settings and have implications for the use of genetically engineered herpesviruses to deliver foreign genes to neurons.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=pubmed_ pubmed&from_uid=14671133
2)
Failure of thymidine kinase-negative herpes simplex virus to reactivate from latency following efficient establishment.
Thymidine kinase-negative mutants of herpes simplex virus did not reactivate from latency in mouse trigeminal ganglia, even when their latent viral loads were comparable to those that permitted reactivation by wild-type virus. Thus, reduced establishment of latency does not suffice to account for the failure to reactivate.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?
3)
Latent herpesvirus infection in human trigeminal ganglia causes chronic immune response.
The majority of trigeminal ganglia (TGs) are latently infected with alpha-herpesviruses [herpes simplex virus type-1 (HSV-1) and varicella-zoster virus (VZV)]. Whereas HSV-1 periodically reactivates in the TGs, VZV reactivates very rarely. The goal of this study was to determine whether herpesvirus latency is linked to a local immune cell infiltration in human TGs. T cells positive for the CD3 and CD8 markers, and CD68-positive macrophages were found in 30 of 42 examined TGs from 21 healthy individuals. The presence of immune cells correlated constantly with the occurrence of the HSV-1 latency-associated transcript (LAT) and only irregularly with the presence of latent VZV protein. In contrast, uninfected TGs showed no immune cell infiltration. Quantitative RT-PCR revealed that CD8, interferon-gamma, tumor necrosis factor-alpha, IP-10, and RANTES transcripts were significantly induced in TGs latently infected with HSV-1 but not in uninfected TGs. The persisting lymphocytic cell infiltration and the elevated CD8 and cytokine/chemokine expression in the TGs demonstrate for the first time that latent herpesviral infection in humans is accompanied by a chronic inflammatory process at an immunoprivileged site but without any neuronal destruction. The chronic immune response seems to maintain viral latency and influence viral reactivation.
cmd=Retrieve&db=PubMed&list_uids=14671133&dopt=Abstract
coldsoregone.com - 09 Mar 2004 20:17 GMT > Together with viroxyn > http://viroxyndirect.com/ExecutiveSummary.pdf > > and viracea, http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9 754950&dopt=Abstract
Please note that Viroxyn's directions do not call for it to be used with any other medication.
Viroxyn is a tincture of Benzalchonium Chloride, delivered in a patented vial that carries the antiseptic deep into the lesion, killing the active virus by stripping it of its lipid coat.
It is important not to use any other creams, soaps, etc. with Viroxyn before application and within at least an hour after application.
The pain and burning from the cold sore is usually gone in 15-20 minutes. And after that, the medication usually heals the lesion with one application, taking only 3 to 4 days to heal it completely.
Interesting, huh?
for more info: www.ColdSoreGone.com
Allen
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