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Medical Forum / Diseases and Disorders / Herpes / March 2004

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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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