MXPA99008750A - Antimicrobial prevention and treatment of human immunedeficiency virus and other infectious diseases - Google Patents

Abstract

An improved medical treatment and medicine is provided to quickly and safely resolve HIV and other microbial infections. The inexpensive medicine can be self administered and maintained for the prescribed time. 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 and a nutrient. In the preferred form, the medicine comprises:Echinacea and Commiphora myrrha phytochemicals, benzalkonium chloride, a sterile water solution, and folic acid.

Description

ANTIMICROBIAL PREVENTION AND TREATMENT OF VIRUSES HUMAN IMMUNODEFICIENCY AND OTHER INFECTIOUS DISEASES BACKGROUND OF THE INVENTION The present invention relates to the human immunodeficiency virus and more particularly to medical treatments and prevention for the human immunodeficiency virus and other microbial infections. It has been reported that there are currently approximately 22 million people infected with the human immunodeficiency virus (HIV) around the world. The largest proportion of cases given HIV originated in Africa and the Caribbean. The typical progression of HIV infection is divided into different stages: (1) viral transmission; (2) acute retroviral syndrome; (3) sero conversion; (4) clinical latent period with or without persistent generalized lymphadenopathy (PGL = Persistent Generalized Lymphadenopathy); (5) early symptomatic HIV infection previously known as AIDS related complex or ARC = AIDS Related I Complex) and more recently referred to as "B symptoms" according to the 1993 CDC classification); (6) Acquired Immune Deficiency Syndrome (AIDS) (AIDS)) the AIDS indicator condition (AIDS) according to the CDC criteria of 1987 and the revised CDC criteria of 1993 that include a CD4 cell count below 20O / cubic millimeter; and (7) advanced HIV infection, characterized by a CD4 cell count of less than 50 / cubic millimeter; CD4 cells are lymphocytes targeted by HIV. In 1993 the CDC changed the definition of AIDS to include all patients with a CD4 count of less than 200 / mm3; this definition includes patients in stages 4 to 7, regardless of the symptoms. The initial acute retroviral syndrome is accompanied by a precipitous decrease in CD4 cell counts, high viraemia of arable plasma and high concentrations of HIV RNA in the plasma. Clinical recovery occurs and the high level of HIV RNA plasma viraemia is reduced with the development of cytotoxic T lymphocyte (CPL) response. The CD4 cell count gradually decreases for several years and then shows an accelerated decline of 1.5 to 2 years before a diagnosis that defines AIDS. Concentrations of HIV RNA in plasma are relatively stable until HIV is in a late stage when the CD4 count is less than 200 / mm3, and the clinical course is characterized by infections, selected tumors, weakening (progressive weakening and thinning) and neurological complications. In general, approximately 10% of patients develop a diagnosis that defines AIDS before the CD4 count falls to 200 / mm3. The median time present to a complication that defines AIDS after the CD4 count of 200 / mm3 is 12 to 18 months. In the absence of targeted therapy against HIV or PCP prophylaxis, the average time of viral transmission to a diagnosis defining AIDS is approximately 10 years, and survival after a complication defining AIDS was previously approximately one year. The entire sequence of events for an average patient in the absence of treatment directed against HIV, is approximately 10 years from sero conversion to death. The median time from sero conversion of HIV to AIDS has been reported to be approximately 7 years for transfusion recipients, 10 years for hemophiliacs, 10 years for drug addicts and 8 to 12 years for homosexuals. The rates of advancement seem similar by sex, race and risk category, if adjusted for the quality of care. For patients aged 16 to 24 years in seroconversion, the median time was 15 years, for those with more than 35 years in the sero conversion was 6 years. HIV infection can be acquired through sexual intercourse, drug transfusions with contaminated blood, drug addicts with infected needles or perinatal transmission. Primary and symptomatic HIV infection also referred to as acute retroviral syndrome has been reported in the preceding risk categories with a frequency of 50 to 90%. This syndrome has also been noticed in 7 out of 8 health care workers, with HIV transmission that follows the occupational exposure. The time of exposure to the onset of symptoms is usually 2 to 4 weeks, but incubation can be as long as 6 weeks. Typical symptoms are: fever, adenopathy, pharyngitis, hives that include maculopapular erythematosus with lesions of 5 to 10 mm on the face and trunk, sometimes on the extremities including the palms and soles of the feet or mucocutaneous ulceration in the mouth, esophagus or genitals, nelgias or arthralgia diarrhea, headaches, hepatosplenomegaly, thrush, nausea and vomiting. Neurological symptoms may include: meningo encephalitis, peripheral neuropathy, facial paralysis, Guillain-Barré syndrome, brachial neuritis, radiculopathy, cognitive imbalance and psychosis. Acute disease is usually accompanied by high-level HIV viremia with p24 antigenemia, plasma viremia, and high HIV titers in peripheral blood mononuclear cells. The cytotoxic lymphocyte T (CTL) response is first and usually precedes the detectable humoral response by several weeks. The CTL response is accompanied by a 3 to 5 log decrement in concentration of HIV in peripheral blood. The high level of viremia during this acute phase of the disease may be associated with the spread of the virus to the CNS and lymphatic tissue. The lymph tissue serves as the main container for HIV loading and replication. The infection of non-lymphoid organs with high levels of HIV seems to occur in late stages of HIV. The presence of symptoms instead of asymptomatic seroconversion as well as a prolonged illness longer than 14 days seem to correlate with a faster progression to AIDS. Seroconversion with HIV positive serology is usually carried out 6 to 12 weeks after transmission such as transfusion or needle injury to a health care worker. The median interval is 63 days. The CTL response is associated with a marked reduction in quantitative viral load in the blood, clinical recovery of acute retroviral syndrome and return of the CD4 cell count to higher levels that are often in the normal range for most laboratories. The HIV patient becomes clinically asymptomatic and generally without findings on physical examination except for persistent generalized lymphadenopathy (PGL) that includes enlarged lymph nodes. Studies of lymph nodes show high concentrations of HIV as extracellular virus trapped in the processes of follicular dendritic cells within the germinal centers and as an intracellular virus predominantly in a latent form. Lymph tissue serves as a major reservoir for HIV, follicular dendritic cells filter and trap free viruses and infected CD4 cells, and viral load in peripheral blood mononuclear cells is relatively low. With progressive disease, the configuration of the lymph nodes is interrupted by HIV. Virological studies in patients with asymptomatic HIV infection, show high rates of HIV replication with production of an average of 109 virions daily. Viral replication is accompanied by massive destruction and the production of 109 CD4 cells daily. The lifespan of CD4 cells represents 6 to 7% of the total CD4 cells in the body, so that the entire supply has a lifetime of every 15 days. AIDS has been considered a consequence of a continuous high-level replication of HIV-1, leading to immune-mediated termination and CD4 lymphocyte virus. Advanced HIV infection occurs in a patient with a CD4 cell count less than 50 / mm3. Patients have a limited life expectancy with a median survival of 12 to 18 months. Virtually all patients who die from HIV-related complications are in this stratum of the CD4 cell count. Food and Drug Administration of the U.S.A. (FDA = Food and Drug Administration) has tested many reverse transcriptase (RT) inhibitors. RT enzymes convert viral RNA into DNA. RET inhibitors can interrupt this process. The RT AZT inhibitor, which is sold under the Retrovir and zidovudine brands by Glaxo Wellcome, was approved by the FDA in 1987. The RT ddl inhibitor, sold under the trademarks with Videx and didanosine by Bristol-Myers Squibb, was approved by the FDA in 1991. The RT ddC inhibitor sold under the brands of HIVID and dideoxycytidine by Hoffman-LaRoche was approved by the FDA in 1992. The RT d4T inhibitor sold under the trademarks of Zerit and stavudine by Bristol-Mayer Squibb approved by the FDA in 1991. The RT ddC inhibitor sold under the Epivir and lamivundine brands by Glaxo Wellcome was approved by the FDA in 1995. The TR Nevirapine inhibitor, sold under the trademark of Viramune by Boehringer Ingelheim, was approved by the FDA in 1996. The Food and Drug Administration (FDA) has now approved three protease inhibitors for the treatment of human immunodeficiency virus (HIV) infection. Saquinavir sold under the Invirase brand by Hoffman-LaRoche Laboratories was the first protease inhibitor agent approved by the FDA. Ritonavir, another protease inhibitor, sold under the brand name Norvir by Abbott Laboratories, received approval from the FDA in March 1996 as well as indinavir sold under the Crixivan brand by Merck & amp; amp;; Co. The protease inhibitors have a different mechanism of action than that of previously approved anti-HIV drugs, such as the nucleoside analogs AZT and 3TC which are sold under the trademarks of Sidobvudine and Lamivundine by Glaxo Wellcome, ddl and d4T which it is sold under the didanosine and stavudine brands by Bristol-Myers Squibb, and ddC that is sold under the dideoxycytydine brand by Roche Laboratories. Protease inhibitors block the enzyme that requires HIV to complete its cycle of replication and form viable new viruses. Without the protease enzyme, the viral structural proteins can not be manufactured properly and a defective non-infectious virus is formed. The nucleoside analogs block a different enzyme-reverse transcriptase. This action can prevent viral RNA from producing viral DNA that can then be incorporated into the DNA of human cells. Combining one or more reverse transcriptase inhibitors with a protease inhibitor, sometimes referred to as a "coctail", is claimed to attack HIV replication at two points in the replication sequence. Clinical trials that combine saquinavir with AZT, ddC or both, show a much greater decline in the number of HIV particles in the blood, sometimes referred to as viral load, and a greater increase in CD4 (T lymphocytes) than observed previously with reverse transcriptase inhibitors alone. Occasionally, cocktails have been toxic and ineffective for some patients. The clinical benefit in terms of improved survival or reduced speed in disease progression, however, has not yet been fully demonstrated for the combination (cocktails) of RT inhibitors and protease inhibitors. Doctors however begin to consider HIV as a manageable chronic disease rather than a death sentence. The saquinavir protease inhibitors have been approved by the FDA for use in combination with reverse transcriptase inhibitors in patients with advanced AIDS (AIDS). Saquinavir protease inhibitors may be tolerated by some patients without the neurological or hematological toxicities encountered with nucleoside analogues. Certain prescription drugs, including rifampin, rifabutin, phenobarbital, dilantin, and dexamethasone, can significantly lower plasma levels of saquinavir protease inhibitors and should be avoided in patients taking saquinavir. Viral resistance to protease inhibitors saquinavir as with other anti-HIV drugs has been reported. The protease inhibitors ritonavir and indinavir appear to be more potent against HIV than the current saquinavir formulation. Ritonavir protease inhibitors require refrigeration. The ritonavir protease inhibitors are currently used in combination with nucleoside analogues (drugs such as AZT) or as monotherapy. An early study treated 32 patients with ritonavir plus AZT plus ddC. After 20 weeks, the median CD4 cell count increased from 83 cells / cubic millimeter in the baseline to 106 cells / cubic millimeter. The viral load, a measure of the number of viral copies in the blood, decreased almost 100 times. Ritonavir is dosed 600 mg orally twice a day, which may require 12 capsules per day. The drug is available in capsules of 100 mg. Side effects are quite common including: gastrointestinal symptoms with nausea, vomiting and diarrhea. Other side effects include numbness and tingling, particularly around the mouth, and inflammation of the liver that comprises a form of hepatitis.

The indinavir protease inhibitors received accelerated approval from the FDA based on studies showing average increases in CD4 counts of approximately 100 cells / cubic millimeter and reductions in viral load of almost 100-fold, in combination with AZT plus 3-c plus indinavir. Indinavir is dosed at 800 mg orally three times a day (two capsules, three times a day). In contrast to ritonavir, indinavir can be taken on an empty stomach to improve absorption. Indinavir causes fewer gastrointestinal side effects than ritonavir and appears to be better tolerated in total by some patients. The main side effect of protease inhibitors indinavir is in the development of kidney stones. The drug is partially excreted in the urine and can crystallize to form stones if proper hydration is not maintained. Indolevir protease inhibitors can also affect the liver, causing an increase in blood levels of bilirubin, ie a bile pigment formed from the breakdown of red blood cell cells. Indinavir protease inhibitors can also cause drug interactions. The analysis of resistance to protease inhibitors has not yet been completely determined. The protease inhibitors saquinavir and ritonavir can currently cost the patient approximately US $ 600. per month. Indinavir protease inhibitors are priced approximately 30% lower than this level. A combination of three AZT plus 3TC drugs plus ritonabir protease inhibitors may cost a patient more than 1,000 US dollars per month. Combinations (cocktails) of RT inhibitors and protease inhibitors can cost as much as 25,000 US dollars. by year. Although protease inhibitors can help, the medical community and society have not yet resolved the patient's cost problems for these expensive drugs. The herpes simplex virus (HSV = Herpes Simplex Virus), commonly referred to as "herpes virus" or "herpes", is an infectious disease that has also reached crisis proportions nationally, with estimated numbers of people infected from 70 to 80% of our population as reported by the Association of Health of the American Society (ASHA = American Societal Health Assosiation) and grow more than 500,000 people. There are two common types of herpes: herpes simplex virus 1 (HSV1) and herpes simplex virus 2 (HSV2). Herpes enters the human body through tiny ruptures or faults in the epidermal tissue usually by contact with an infected host and is marked by the eruption of one or more vesicles, usually in groups, following an incubation period of approximately 4 days. Typically, the course of the infectious outbreak begins with the prodromal stage; advancing to the vesicular eruption; followed by ulceration, coalescence, resolution and the latency period. The outbreak may last several weeks and on average lasts two to three weeks. In some immunocompromised individuals, the outbreak may last for months. Vesicles can appear anywhere on the skin or mucosa, typically arising on the lips such as cold sores, glands, oral mucosa, conjunctiva and cornea, genitals and mucosa and perianeal tissue. Herpes symptoms include: inguinal swelling, pain, fever, malaise, headaches, muscle aches and swollen glands. Some individuals who have the trigeminal nerve compromised with oral herpes, have extreme facial pain, difficulty swallowing, eating and facial swelling. Individuals with the affected sacral nerve have severe pain in the upper part of the legs, swollen and enormous difficulty walking. The infection of herpes simplex virus (HSV) increases, residing in the ganglia of the nerves, then recur due to some stimuli not yet known. Recurrent herpetic infections can be precipitated by almost anything including: overexposure to sunlight; nutritional deficiencies; tension, menstruation; immuno suppression, certain foods; drugs, febrile disease; etc. Recently, the herpes virus was isolated from cardiac tissue. HSV1 and HSV2 infections present very serious threats to health often causing: blindness; and increased risk of cancer in the cervix; aseptic meningitis and encephalitis; neonatal deaths; viremia; etc. The devastating effects of this disease go beyond the medical scope of human suffering. HSV is responsible for serious psychological and emotional distress as well as substantial economic loss for the nation and the world. Various herpes treatments have been proposed and have included topical application of agents such as povodone-iodine, idoxuridine, trifluorothymidine or acyclovir. These treatments have been found with varying degrees of success. Most previous treatments have proven to be disappointing. Acyclovir, which is taken orally for systemic treatment of HSV is somewhat effective. However, acyclovir is only successful in interrupting the replication of the virus. It is not successful to treat an infectious outbreak either systemically or atopically. Strains resistant to acyclovir have been reported. Individuals with Autoimmune Deficiency Syndrome (AIDS) are seriously compromised and suffer especially debilitating HSV outbreaks. Additionally, individuals with AIDS can carry strains resistant to aciclovir HSV, which can make acyclovir ineffective for these individuals. Therefore, it is convenient to develop a safe and successful medical treatment to help treat and avoid the very serious problems of HIV and other infectious diseases. SUMMARY OF THE INVENTION [0002] Improved medicine and medical treatment are provided which, when administered systemically, inhibit the binding or binding of the human immunodeficiency virus (HIV) to target cells and prevent the spread of HIV. Advantageously, the use of novel medical and medical treatment can help prevent the sexual transmission of HIV and other viruses. Significantly, improved medicine and medical treatment are safe, less expensive and effective. The improved medicine, also referred to as Viracea 2 HIV-4, comprises novel medical composition, formulation, antimicrobial compound and solution. The new antimicrobial medical treatment and microbicide medicine are successful in treating HIV, primarily in systemic form and can be used to treat other microbial infections including but not limited to varicella zoster virus (herpes zoster) and cytomegalovirus. In some circumstances, it may be convenient to use novel medicine topically. While the novel antimicrobial compound and medicine are particularly useful in dramatically inhibiting the infection of human immunodeficiency virus (HIV), they may be useful in treating other microbial diseases (diseases that cause microbes) such as: Epstein Barr, papilloma virus, cellulitis, staphylococci, streptococci, mycobacteria, influenza, parainfluenza, adenovirus, encephalitis, meningitis, arbovirus, arenavirus, anaerobic bacilli, picornavirus, coronavirus and syncytial virus, as well as herpes simplex virus, varicella zoster virus and cytomegalovirus. While medicine and medical treatment are particularly useful for inhibiting HIV and other infectious diseases, in humans (humans) (homo sapiens), they may also be useful for veterinary purposes to treat viral and bacterial infections and infectious diseases in animals such as dogs. , cats, birds, horses, cows, sheep, pigs (pigs and pigs), and other farm animals, as well as rodents and other animals that are seen in zoos.

Advantageously, the improved medicine and medical treatment of the present invention produce unexpected, surprisingly good results. This easy-to-use microbicidal solution can provide improved absorption rate in parenteral administration. Before administration, there may be a slight itching effect. In minutes of application, you can experience a light medicinal taste in the mouth. Initially, in vitro testing of novel medical and medical treatment demonstrates extremely surprising inhibitory effects in HIV virus. Conveniently, novel medicine is made from easily available, over-the-counter chemicals or products (OTC = Over The Counter) and provides a safe and comfortable economic treatment. Conveniently, novel medicine (medical composition) includes inhibitors of microbes that inhibit, suppress and stop microbial infections by diseases that cause microbes. The microbial inhibitors comprise antimicrobial isolates, botanical extracts or phytochemicals from at least a portion of one or more of the plant species below. Microbial inhibitors may comprise viral inhibitors to inhibit viral diseases such as: HIV, herpes simplex virus 1 (HSV1) herpes simplex virus 2 (HSV2), varicella zoster virus (herpes zoster), cytomegalo virus, Epstein Barr, papilloma virus, viral influenza, viral parainfluenza, adenovirus, viral encephalitis, viral meningitis, arbovirus, arenavirus, picornavirus, coronavirus and syncytial virus. Microbial inhibitors may also comprise inhibitors of bacteria, to inhibit bacterial diseases such as cellulitis, staphylococci, streptococci, mycobacteria, bacterial encephalitis, bacterial meningitis and anaerobic bacilli. In some circumstances, the microbial inhibitors may include fungal inhibitors. Better results can be obtained if Echinacea and Commophora (also referred to as Commiphora) or other plants, are not used in raw, untreated medicine and in the uncut state. Even for best results, the medicine can exclude: Arabinose, betaine, cellulose, copper, fructose, fatty acids, galactose, glucose, iron, potassium, protein, resin, sucrose and xylose. The improved medical treatment provides a novel method and process for use in treating the above infectious diseases. For some infectious diseases, microbial inhibitors can be applied and maintained in the infected microbial area or the infected area (region or surface), until the external symptoms and physical manifestations of the infection disappear, reside or resolve with respect to the infected area. The medicine can be administered by syringe injection, intramural sublingual, spraying, applying with touches, sprinkling, application with swab, application with sponge, application with brush, emptying, supply, coverage or strong coating with the medicine in the infected microbial areas such as : lymph nodes, lymphatic system, T cells, oral mucosa, nasal mucosa, vaginal tissue, labial tissue, rectal tissue and anal tissue, perianal tissue, lips, cutaneous tissue, ocular tissue, conjunctiva and eyelids of the eyes. Preferably, the microbial inhibitors or the antimicrobial compound are applied systemically with a syringe in the rectal channel or vagina, to treat or prevent the sexual transmission of HIV. The microbial inhibitors or the antimicrobial compound can be applied in the above form 4 to 20 times per day for 4 to 18 consecutive days to substantially decrease the viral load of patients infected with HIV, ie to decrease the amount of HIV virus and AIDS in the body. Preferably, the improved medicine, medical composition or microbial compound is a phytochemical concentrate that is combined and applied simultaneously or concurrently with a surfactant, a nutrient and a carrier, solvent or diluent, to provide a microbicidal medicinal solution. The nutrient serves as a catalyst, activator7 phytochemical initiator, nutritional supplement and auxiliary carrier. The nutrient may comprise one or more of the following: a water-soluble vitamin, a fat-soluble vitamin, vitamin A, vitamin B complex (vitamin B complex), vitamin D, vitamin E, vitamin K, vitamin Bl, vitamin B2, vitamin B5, vitamin B6, vitamin B12, vitamin B15 and preferably folate or folic acid. For this purpose, the interesting microbicidal solution comprises an antimicrobial detergent surfactant with botanical extracts. The surfactants are preferably cationic surfactants which may comprise in simple form or any amount of quaternary ammonium chloride having 6 to 18 carbon atoms such as alkyl benzyl dimethyl ammonium chloride, mixtures of alkyl benzyl dimethyl ammonium chloride, alkyl chloride dimethyl / ethyl benzyl ammonium, N-alkyl dimethyl benzyl ammonium chloride, diisobutyl phenoxy ethoxy ethyl dimethyl benzyl ammonium chloride, M (ClzC iC16) dimethyl benzyl ammonium chloride, benonium chloride, octyl decyl dimethyl ammonium chloride, didecyl chloride dimethyl ammonium, dioctyl dimethyl ammonium chloride, dialkyl dimethyl ammonium chloride, dialkyl methyl benzyl ammonium chloride, octyl decyl dimethyl ammonium chloride, dimethyl benzyl ammonium chloride, lauryl dimethyl benzyl ammonium chloride, o-benzyl-p-chlorophenol, didecyl dimethyl ammonium chloride, dioctyl dimethyl ammonium chloride, dialkyl (C14C12C16) dimethyl benzyl ammonium chloride, preferably comprises and alkyl benzyl dimethyl ammonium, particularly preferably benonium chloride. The activity range of the cationic surfactant can be from 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, sulfuric surfactants and non-ionic surfactants. The surfactants may comprise detergents, wetting agents, emulsifiers, defoamers and / or agents for reducing surface tension. They are useful carriers to mix the constituents, keep the constituents in solution, and provide an easy method of application to the affected area, either by spraying, dripper or applicator. While an aqueous solution, preferably a sterile aqueous solvent carrier, is preferred for best results, in some circumstances it may be convenient 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, talcum, corn flour, beeswax, canova wax, betacharacter, garlic oil, camphor oil, soluble vitamins, soluble minerals, rapeseed oil, nut oils, olive oil, liposomes, ascorbic acid, donkey herb oil, piogenol, grapeseed oil, lanolin, Ethocyn, collagen, aloe vera, bee pollen, royal jelly, chondroitin sulfate A, marine vegetables, EDTA, fatty acids, herbs, lecithin, bioflavanoids, oils or grain powders, algae, teas, vinegars, acidophilus, cell salts, ascorbic acids, hydra 5, glandular is, amino acids, psyllium, plant derivatives or other sterile carriers. The botanical extracts, isolated antimicrobials or phytochemicals contained in these new medical treatment and medicine, can be constituted by: myrrh gum resin, sesquiterpenes, cursenone, dihydrofuanodien-6-one, 2-methoxyl furandiene, elemol, acetic acid, -amirone , araminose, a-bisabolene, gamma-bisabolene, sadinene, campesterol, cholesterol, cinnamaldehyde, comiferin, comorphic acid, beta-comophoric acid, gamma-comorphic acid, comiforinic acid, m-cresol, cumic alcohol, cuminaldehyde, dipentene, elemol, 3-epi-a-amidine, eugenol, furanodiene, furan, dienone, galactose, gum, heerabolene, a-heerabomirrol, beta-heerabomirol, heeraborecene, limonene, 4-0-methyl glucuronic acid, N-nonacesan, beta cytosterol, xylose, caprolens, (carofilenes), linderestirene (lindestirene), arabinose, betaine, copper, echinacea, Echinacin B, echinacoside, equinolone, enzymes, fructose, fatty acids, galactose, glucose, glucuronic acid, inulin, inuloid, iron, pentadecadiene, polyacelene compounds, polysaccharides, such as, but not limited to, arabinogalactan, potassium, protein, resin, rhamnose, sucrose, sulfur, tannins, vitamins A, C and E, alkylamides, apigenin, arabino galacta, ascorbic acid, behenic acid - ethyl acid, betaine, borneol, bornyl acetate, caffeic acid, 2-0-caffeoyl acid 3- (5-a-ca rboxibeta) 3,4-dihydroxyphenyl, 2-0-caffeoyl-3-0-cumaroyl taraic acid, 3-0-caffeoquin echinacoside, 2-O-caffeoyl 3-0-feruloyl tartaric acid, 2-0-caffeoyl tartaric acid, carbonate calcium, ß-carotene, carofileno-epoxide, chloride, chlorogenic acid, cyclic acid, methyl ester of cyclic acid, cobalt, cyanadin-3-0- (beta-d-glycopyranoside), cinadin-3-6-0-malonil beta-d-glycopyranoside, cynarin, deca (2e, 4e, 6e) linolenic-isobutyl amide, 3-rhamnosylverbascoside, 3-5-dicaphenoylquinic acid, 4,5-0-dicaphenyl quinic acid, acid 2,3-0 - tartaric diferolol, do-deca (2e, 4e) dienoic-isobutyl amine, 2-deca-2,4-dien-l-isovalerate, do-deca (2e, 6z, 8e, 10e) tetrahenoic-isobutylamine acid, episode , betafarnecene, 2-O-feruloyl tartaric acid, germacrene, hepta deca (8z, llz) diendosone, heteroxylan, humulene 8-12, (e) -10-hydroxy-4, 10-dimethyl-4, 11-dodecadien-2 -one, 13-hydrooctadeca-9z acid, lie, 15z (trienoic, inulin, iron, acid is ochlogenic, isoramnetin-3-rutinoside, isotusilagine, caemferol, caemferol-3-glucoside, caemferol-3-nitunoside, limonene, lutolin, liutolin-7-glucoside, magnesium, manganese, 2-methyl-tetradeca-5,12s-diene, 2-methyl-tetradeca 6,12-diene, methyl-p-hydroxycinnamate, marcene, niacin, palmitic acid, pentadeca- (8z, llz) -dien-2-one, pentadeca- (8z, 13z) -dien-ll- lin-2-one, pentadeca-8-en-2-one, pentadeca- (8z) -en-2-one, pentadeca- (8z) -in-ll, 13-dien-2-one, 1-pentadecene, penta- (l, 8z) -diene, phosphorus, a-pinene, beta-pinene, polyacetylene, pontic epoxide, potassium, protein, quercetagetin-5-one-glucoside, quercetin, quercetin-3-galactoside, quercetin-3-glucoside , quercetin-ter-robinoside, quercetin-xyloside, quercetin-3-xylosyl galactoside, rhamno rabinogalactan, riboflavin, rutin, rutoside, selenium, silicate, beta-sitosterol, sitosterol-3-beta O-glucoside, sodium, stigmasterol, sulfate, tartaric acid, tetradeca- (8z) -in-ll, 13-dien-2-one, thia ina, n-triacontanol, tr ideca-l-en-3, 5,7,9, 10-pentaine, tusilagina, vanillin, verbascoside. For best results, the phytochemical concentrates include the aforementioned phytochemicals, excluding arabinose, betaine cellulose, copper, fructose, fatty acids, galactose, glycosa, iron, potassium, protein, resin, sucrose and xylose. Botanical extracts, isolated antimicrobials and phytochemicals can be separated, extracted and isolated from plant parts such as: pimpinella anisum, myroxylon, aretostaphylos, carum, capsicum, eugenia mytacea, coriandrum, inula, allium, gentiana, juniperus, calendula, origanum , mentha labiate, commiphora, plantago, rosmarinus, route, lamiaceae, meliosa, baptisa, artemisa, sago, mentha, partenium integrifollium, eucalyptus, asteriacea and preferably: (1) of the genus Echinacea of the family Astericaea, ie Echinacea purpurea, Echinacea angustofollium, (Echinacea pallidae), Echinacea vegetallis, Echinacea atribactilus and their Echinacea pallidum and crops; as well as the Commophora genera Commophora myrrha, Commophora molmol, Commophora erythraea, and their crops. For best results, phytochemicals and antimicrobial isolates are extracted from Echinacea purpurea, Echinacea angustifolium and Commophora myrrha. The technology, treatment and medicine of the invention produce very attractive unexpected results and surprisingly good and consistent results. Tests show that the microbicidal solution (medicine) and medical treatment are extremely useful for controlling HIV infection, inhibiting the binding of the HIV virus to target cells, acting as a preventive mycobiocide, extending periods of HIV latency and other diseases and inhibiting dramatically HIV and other viruses, while in general it is safe for the patient and the environment. A more detailed explanation of the invention is provided in the following description and appended claims. DESCRIPCT? W nCT? T.T.Ar > A r »F. PREFERRED MODALITIES A microbicide and treatment is provided to inhibit the human immunodeficiency virus, also referred to as human immunodeficiency virus or HIV. Conveniently, the HIV microbicide and the treatment completely inhibit HIV, as well as other infectious microbial diseases and are safe and non-toxic to humans, animals and the environment. The HIV medicine and microbicide may comprise a surfactant and a herbaceous botanical compound that provides a botanical, phytochemical, antimicrobial isolated, antiviral isolate, microbial inhibitor and viral inhibitor extract. The preferred microbicidal composition may comprise: a surfactant; an aqueous diluent; a nutrient and botanical herbaceous genus Echinacea (E) of the Asteraceae family, species: purpurea, angustifolia, pallidae, vegetables, atribactilus and crops as well as botanical herbaceous genus Commiphera species: Commiphora myrrha, Commiphora molmol, Commiphora erythraea, and crops, preferably the herbanáceos botanicals are extracts and isolates comprising Commiphora phytochemicals and Echinacea phytochemicals as found in and extracted from Commiphora myrrha, Echinacea purpurea, Echinacea angustifolia and Echinacea pallidae. For best results, medical treatment and microbicide (medicine) include: a cationic surfactant; the phytochemicals of Echinacea purpurea, Echinacea angustofolia and Commiphora myrrha, a sterile aqueous diluent and folacin. The ratio of Commiphora myrrha to Echinacea purpurea and Echinacea angustofolia is preferably in the range from 1: 2 to 1: 4. The surfactant provides some debridement at the cell surface level with a broad spectrum of antimicrobial action. Surfactants of this nature may comprise quaternary ammonium salts containing 6 to 18 carbon atoms. Preferably, the quaternary ammonium salt surfactant, is a mixture of chlorides benzyl alkyl dimethyl ammonium, which can be: benzalkonium halide, benzalkonium bromide, of benzaltonio chloride and most preferably benzalkonium chloride. The HIV treatment can comprise a 100% active aqueous solution, but it can also be used in concentrated form. The solution may comprise by weight various concentrations of surfactants such as .55% to .08%, preferably .02% to .30% and more preferably .02% to .26%. The phytochemicals in botanical Echinacea have shown impressive activity against bacteria, viruses and some fungi. The exact mechanism is unknown. When the microbiocide of the invention was tested topically in HIV and HCV 1 and 2, it is effective in treating infectious outbreaks of herpes simplex. When tested in vitro shows inhibitory activity against HIV-1 and HCV 1 and 2. The phytochemical concentrate composition comprises the following isolated constituents, botanical extracts, microbial inhibitors, and antimicrobial isolates: polysaccharides, equinaceno, echinaceine, echinacoside (caffeic acid ester ), echinolone, equinadiol, enzymes, glucuronic acid, inuloid, pentadecadiene, polyacetylene compounds, arabino galactan, rhamnose, PS1 (1.4-0-methyl-glucurono-arabinoxylan, Mt 35 kD) and PS II (one acid rhamnoarabinogalactan, Mt 450 kD), cynarin, 1,5-di-ion-0-caffeoyl quinic acid), chicoric acid (2,3-0-di-caffeoyl tartaric acid) and derivatives, alkyl amides, keto-alkynes and -alkenes; quinones, oils including borneol, bornyl acetate; pentadeca-8 (z _) - en-2-one, germacrene D; caryophyllene; caryophyllene epoxide, anthocyanins, pyrrolizidine alkaloids; lipophilic amides, isobutylamides; polyacetylenes, myrrh gum resin; curzerenone (of the furahoeudesmano type), dihydro fuanodien-6-one; 2-methoxyfuranodiene (type furan elemeno); elamol; lindestireno (furano germacrano type); alkylamides; apigenin, arabinogalacta, ascorbic acid, behenic acid-ethyl acid, betaine, borneol, bornyl acetate, caffeic acid, 2-p_-caffeoyl-3- (5) -a-carboxy-β- (3,4-dihydroxyphenyl) acid , 2-0-safeoil-3-0_-coumaroyl taráico, 6-0-caffeoyl echinacoside, 2-0-caffeoyl-3-0-feruloyl tartaric acid, 2-0-caffeoyl tartaric acid, calcium, carbonate, beta carotene, carofileno, carofileno epoxide, chloride, clorgénico acid, sicórico acid, methyl ester of cichórico acid, cobalt, cianadin-3 -? - ß-de-glycopyranoside (cinadin-3-) 6-Q-malonil-ß-de-glycopyranoside (cinarin, deca isobutyl amide-deca (2, 4e, 6e,) trienoic acid, des-rhamnosyl verbascoside, 3-5-dicaphenoylquinic acid, 4-5-0-dicaphenoylquinic acid, acid 2, 3-Q- diferulol tartaric, isobutyl amide dodesa acid 2-dk (2e, 4e) -dinoic acid, dodeca-2,4-dien-l-yl isovalerate, isobutyl amide of dodeca (2e, 6z, 8e, lOe) tetraenoic acid, epishobunol, ß -farmecene, acid-2 -? - feruloyl tartaric, germacrene, hepta deca (8z, llz) -dien-2-one, heteroxylan, humulene 8-12, (e) -10-hydroxy-4, 10-dimethyl-4,1-dodecadien-2-one, 13-hydroxy-octadeca acid (9z, lie, 15z) trienoic, inulin, iron, chlorogenic acid, isoramnetin-3-ritunoside, isotusilagina, caemferol, caemferol-3-glucoside, caemferol-3-nanoside, limonene, luteolin, luteolin-7-glucoside, magnesium, manganese, 2-methyl-tetradeca-5,12-diene, 2-methyl-tetradeca-6-12-diene, ethyl-p-hydroxycinnamate, marcene, niacin, palmitic acid, pentadeca- (8z, llz) -dien-2- ona, pentadeca- (8z, 13z) -dien-ll-lin-2-one, pentadeca-8-en-2-one, pentadeca- (8z) -in-2-one, pentadeca- (8z) -in- ll, 13-dien-2-one, 1-pentadecene, penta- (1, 8z) -diene, phosphorus, α-pinene, β-pinene, polyacetylenes, pontic epoxide, potassium, protein, quercetagetin-7-glucoside, quercetin , quercetin-3-galactoside, quercetin-3-glucoside, quercetin-3-robinoside, quercetin-3-xyloside, quercetin-3-xylosilgalactoside, rhamnoarabino galactane, riboflavin, rutin, rutoside, selenium, silicate, β-sitosterol, sitosterol-3-β-o-glucoside, sodium, stigmasterol, sulfate, tartaric acid, tetra-deca- (8z) -in 11, 13-dien-2-one, thiamin, n- triacontanol, trideca-l-en-3, 5,7,9, 10-pentaine, tusilagin, vanillin, verbascoside, sesquiterpenes, acetic acid, -amirone, arabinose, a-bisabolene,? -bisabolin, cadinen, campesterol, cholesterol, cinnamaldehyde, comiferin, α-comiphoic acid, β-comiforic acid, α-comorbic acid, comiforinic acid, m-cresol, cumic alcohol, cuminaldehyde, dipentene, elomol, 3-etr-a-amidine, eugenol, furanodiene, furanodienone, galactose, heerabolene gum, a-heerabomirrol, ß-heerabomirrol, heeraborescene, limonene, 4-O-methyl-glucuronic acid, n-nonacesan, ß-sitosterol, xylose, carofilenes (carofileno), gum resin, obsenone, furanodien -6-one and 2-methoxy furandiene. For best results, the antimicrobial isolates of the phytochemical concentrate comprise by weight (based on the total weight of the inventive medical composition): 0.3 to 9% equinacoside; 0.1 to 7% PS I (-4-0-methylgluconoaranylaxylane, M ^, 35 kD) and PS II (a ramnoarabinogalactan acid, ffc 450 kD); .1 to 10% cynarin (1,5-di-O-caffeoylquinic acid) and chicoric acid (2,3-0-di-caffeoyl tartaric acid) and derivatives; .2 to 4% equinolone; .2 to 8% equinacin B; 0.1 to 6% equinacein; .2 to 7% of antosianins comprising cyanidin 3-O-β-D-glucopyranoside and 3-0- (6-Q-malonyl-β-D-glucopyranoside); .01 to .06% pyrrolizidine alkanoids comprising tusilagine and isotusilagina; .003 to .009% isomeric dodecaisobutylamides and 2E, 4E, 8Z, 10E / Z-tetraenoic acid; .01 to 2% of cariopilenos; as well as Commophora myrrh phytochemicals comprising: myrrh gum resin, cursenone, dihydro furan dien-6-one, 2-ethoxy furandiene, linderstirene (lindestreno) sesquiterpenes, acetic acid, aA-a-irona, arabinose, -bisabolene, ? -bisaboleno, gama-bisaboleno, cadineno, campesterol, cholesterol, cinnamaldehyde, comiferina, a-comifórico acid, beta-comoric acid, acid? -comorphic, comiforinic acid, n-cresol, cúmico alcohol, cu inaldehyde, dipenteno, ele ol, 3-epi-a-amyrin, eugenol, furanodiene, furanodienone, galactose, heerabolene gum, -heerabomirrol, ß-heerabomirrol, heeraboresin, limonene, 4-0-methyl glucuronic acid, n-nonacesan, ß-sitosterol, xylose, caropilenes, (caropilenes) and linderestireno (lindestireno). The phytochemical concentrate can comprise by weight 2 to 90% of the chemical composition and solution and preferably comprises not less than 15% of the composition and solution and for better results comprises 40 to 60% of the medical composition and solution. The diluent dissolves the benzalkonium chloride (surfactant) and the phytochemical concentrates and can act as a carrier in sprays, tubes and dropper bottles. The preferred diluent is an aqueous diluent and is preferably a sterile aqueous diluent. The ratio of water in the aqueous solution to benzalkonium chloride can be in the range from 30,000: 1 to 250: 1 and preferably from 5,000: 1 to 750: 1. The ratio of water to the combined benzalkonium chloride and phytochemical concentrates can comprise a range of 2: 1 to 100: 1, with a preferable range of 4: 1 to 40: 1 and for best results can comprise a ratio of 6: 1 to 20: 1. For better results, the medicine (microbicide) and improved microbicide treatment for herpes, comprise by weight: 0.02% to .3% of benzalkonium chloride and to avoid toxicity preferably less than 0.26%, 40% to 60% of the phytochemicals of Echinacea and Commophora; .01% to 25%, more preferably 2% to 12% nutrient; and 20% to 60%, more preferably 29.74% to 59.8% sterile water. The medicine (microbicide) conveniently comprises a vitamin nutrient that serves as a nutritional carrier and provides a synergistic effect when combined with Commophora myrrh, Echinacea purpurea, and Echinacea augustifolia. The nutrient may comprise one or more of the following: Vitamin A, vitamin B complex, vitamin D, vitamin E, vitamin K, a water-soluble vitamin, a fat-soluble vitamin, vitamin Bl, vitamin B2, vitamin B5, vitamin B6, vitamin B12, vitamin B15 and preferably folate or folic acid. While water is the preferred diluent and aqueous carrier, it may conveniently be in some circumstances to use other carriers in order to propel the concentrate through a syringe or sprayer, or for greater solubility and efficacy, it may be desirable in some circumstances to Include a viscosity control agent. In addition, while it is estimated that the shelf life or shelf life of the improved medicine is two years, it may be necessary to add an appropriate conservator. For preferred use, as a preventive microbicide against HIV, the medical solution (medicine) should be applied systemically, vaginally or rectally. The method of application of medicine can be by: application by syringe, spraying, application by touch, drip or other methods. The application or coating of the solution (medicine) should be maintained during intercourse. Anionic soaps and anionic detergents and especially soaps with protein content may be contraindicated. Preferably, the application area should be washed, cleaned and dried before application of the medicine. For treatment as an HIV antiviral, the medicine can be applied by syringe from the dosing treatment to the rectum or vagina or by other methods. BENZALCONIUM CHLORIDE A preferred surfactant is benzalkonium chloride. Benzalkonium chloride in aqueous solution is commercially available under the trade name Zephiran "distributed by Zanophy Winthrop Pharmaceuticas (formerly Winthrop Labs.) Benzalkonium chloride is a fast acting anti-infective surfactant., with a moderately long duration of action. The surfactant is active against bacteria and some viruses, fungi and protozoa. Bacterial spores are considered resistant. The benzalkonium chloride solutions are bacteriostatic or bacteriocidal according to the concentration. The exact mechanism of bacterial action of benzalkonium chloride is unknown but is considered to be due to the inactivation of enzymes. The activity of benzalkonium chloride generally increases with increasing temperature and pH. Gram-positive bacteria are more susceptible to benzalkonium chloride than gram-negative bacteria. Unfortunately, benzalkonium chloride is inactivated by soaps, anionic detergents, serum and certain proteins. Benzalkonium chloride has fallen out of favor in many laboratories for the above reasons. When benzalkonium chloride is used alone and tested topically in vivo, it was ineffective for infectious outbreaks of herpes simplex. When testing in vi tro in HIV and HSV 1 and 2, benzalkonium chloride showed undesirably high levels of cell toxicity, even at high dilutions, which is medically unacceptable. The chemical formula of benzalkonium chloride is illustrated below. Other types of benzalkonium chloride can be used.

PHYTOCHEMICALS Whereas Echinacea not isolated unprocessed and untreated raw, it is generally not convenient to treat HIV and herpes intramurally, when properly filtered, intramural administration may be feasible. Significantly, it appears that some, though not all, isolated constituents and botanical extracts of Echinacea and Commiphora (as described above) provide phytochemicals, antimicrobial isolates, botanical extracts, and inhibitors of microbes that have or exhibit antimicrobial activity, which It seems to be effective in treating HIV, herpes virus and other infectious diseases. As previously stated, the phytochemical concentrate composition comprises the following isolated constituents, botanical extracts, microbial inhibitors and antimicrobial isolates: polysaccharides, echinacen, Echinacein, Echinacoside (esters of caffeic acid), Echinolone, Echinadiol, enzymes, glucuronic acid, inuloid, pentadecadiene, compounds of polyacelylene, arabinogalactan, rhamnose, PS I (-4- 0.-methylgluconoarabinoxylan, M, 35 kD) and PS II (a ramnoarabinogalactan acid, tfc 450 kD), cynarin (1,5-di-O- acid) quinico cafeoil) chicoric acid (2,3-O-di-caffeolyl tartaric acid) and derivatives, alkylamides, keto-alkynes and -alquenos; quinones, oils including: borneol, bornyl acetate, penta deca-8 (z) -en-2-one, germacrene D; carofileno; carofylene epoxide, anthocyanins pyrrolizidine alkaloids; lipophilic amides; isobutyl amides; polyacetylenes; myrrh gum resin; curzerenone (furahoeudesmano type), dihydro fuanodien-6-one; 2-methoxy furanodiene (type furanoelemeno); elamol; lindestreno (type furanogermacrano); alkyl amides, apigenin, arabinogalacta, ascorbic acid, behenic acid-ethyl acid, betaine, borneol, bornyl acetate, caffeic acid, 2-0-caffeo1-3- (cyclo-a-carboxybeta) 3,4-dihydroxyphenyl, acid 2-0-caf oíl-3-0-cumaroyl tartaric, 6-O-caffeoyl echinacoside, 2-0-caffeoyl-3-0-feruloyl tartaric acid, 2-O-caffeoyl tartaric acid, calcium, carbonate, beta-carotene , carofileno, carofileno-epoxide, chloride, clorgénico acid, cichórico acid, acid cichórico-metiléster, cobalt, cianadin-3-0- (ß-d-glyco-pyranoside), cinadin-3- (6-0-manolin-β -d-glocipiranoside), cinarin, deca (2E, 4E, 6E) isobutyl amide trienoco, deramnosyl verbascoside, 3,5-dicaphenoylquinic acid, 4-5-O-dicaphenoylquinic acid, 2,3-O- acid diferulol tartaric, isobutyl amine of 2-deca- (2E, 4E) -dienoic acid, dodeca-2,4-dienyl-l-yl isovalerate, isobutyl amine of dodeca (2e, 6z, 8e, l0e) -tetraenoic acid, epishobunol , ß-farmecene, 2-O-feruloyl tartaric acid, germacrene, hepta deca- (8z-llz) -en-2-one, hetereoxylan, umulene 8-12, (e) -10-hydroxy-4, l? -dimethyl-4, 11-dodecadien-2-one, acid 13-hydroxy-hepta- (9z, lie, 15z) -noic, inulin, iron, isoclorogenic acid, isoramnetin-3-rutinoside, isotussilagino, caemferol, caemferol-3-glucoside, caemferol-3-nutinoside, limonene, luteolin, luteolin -7-glucoside, magnesium, manganese, 2-methyl-tetradeca-5, 12-diene, 2-methyl-tetradeca-6, 12-diene, methyl-p-hydroxycinnamate, marcene, resin, palmitic acid, pentadeca- (8z, llz) ) -dien-2-one, penta deca- (8z, 13z) l-dien-ll-lin-2-one, penta deca-8-en-2-one, penta deca- (8z) -en-2- ona, penta deca- (8z) -in-ll, 13-dien-2-one, 1-pentadecene, penta- (1, 8z) -diene, phosphorus, -pinene, β-pinene, polyacetylenes, pontic epoxide, potassium, protein, quersetagetin-7-glucoside, quercetin, quercetin-3-galactoside, quercetin-3-glucoside, quercetin-3-robinoside, quercetin-3-xyloside, quercetin-3-xylosyl galactoside, ramnoarabino galactane, riboflavin, rutin , rutoside, selenium, silicate, ß-sitosterol, sitosterol-3-ß-0-glucoside, sodium, stigmasterol, sulfate, tartaric acid, tetra deca- (8z) -in-ll, 13-dien-2-one, aunt ina, n-triacontanol, trideca-l-en-3, 5,7,9, 10-pentaino, thialagen, vanillin, verbascoside sesquiterpenes; acetic acid, -amirone, arabinose, a-bisabolene,? -bisabolin, cadinen, campesterol, cholesterol, cinnamaldehyde, co-serine, a-comiforic acid, beta-comorphic acid, acid? -comorphic, comiforinic acid, m-cresol, alcohol cumic, cuminaldehyde, dipentene, elemol, 3-epi-a-amyrin, eugenol, furanodieno, furanodienona, galactose, gum, heerabolene, a-heerabomirrol, ß-heerabomirrol, heeraboreceno, limonene, 4-0.-methyl-glucuronic acid, D-nonacesan, ß-cytosterol, xylose, caropilenes (carofilenes), linderestireno (lindestireno), caropilenos (carofilenos), resin of myrrh gum, cursenone, dihydrofrianodina-6-one, 2-methoxyfurandiene and linderstireno (lindestireno).

The chemical formula of some of the botanical extracts of Echinacea is illustrated below.

Equinacoside Chloric acid Equinacein Equinolone The chemical formula of some of the botanical extracts of Commiphora myrrha is illustrated below.

Curzerenone 4, 8-Dihydrofuranodien-8-one 2-Methoxyfuranodienc (Type Furanoeudesmano) (Type Furanoelemano) Lindestreno Elemol (Type Furanogermacreno) Myrrh is also sometimes referred to as: myrrh, irre and myrrhis, gummi myrrha, myrrha vera, myrrh gum, Commiphora resin, gruggal gum, gruggal resin, myrrh myrrh, myrrh myrrh, myrrh myrrh , Opopanax and Hirabol myrrh. Myrrh can comprise gum resin obtained from cuts made in the bark of trees of the genus Commifora myrrha, that is, the myrrh tree. Myrrh also includes balsamic juices from Balsamodendrom myrrha, that is to say the Arab myrtle, a bourgeois tree. Myrrh can also be used as Osmorhiza or Washingtonia, which is sometimes referred to as Sweet Odorous Chervil (s eet cicely). The myrrh tree is native to Eritrea, Abyssinia, Somalia, Yemen, Sudan and elsewhere. The Commiphora species that produces myrrh are shrubs or small trees with large thorns with sharp points on the trunk. The unequal trifoliate leaves are alternated and small flowers are arranged in terminal panicles. When it is damaged, the schizogenic resin ducts produce the drug myrrh. Myrrh is an air-dried rubber oil resin that exudes from the bark of the Commiphora species. The material comprises lumps or irregular round grains of varying sizes with holes and a range of color from dark brown and almost black to light or orange-dark brown; some parts may be yellow or colorless to pale yellow. The surface is primarily covered with a gray to yellowish gray powder, the fracture is conchoidal and produces thin translucent fragments. Myrrh can also have a sweet fragrance and an aromatic smell. Myrrh can have a vinegary and aromatic flavor. Myrrh can be acrid and can stick to the teeth when chewing. Commiphora molmol and other Commiphora species in terms of the chemical composition of its resin-gum is comparable to that of myrrh DAB 10. There is considerable confusion in the literature regarding the sources of myrrh and the identity of the Commiphora species involved. Common myrrh (or hirabol) seems to derive from Commiphora myrrha. Somali myrrh is said to come from Commiphora molmol. However, the systematic (taxonomic) relationship between Commiphora myrrh and Commiphora molmol is unclear. The source of Abyssinia myrrh is Commiphora madagascarlensis or Commiphora abyssinica. Opopanax, which is also referred to as myrrh bisabol or perfumed bdellium is considered to originate either from Commiphora erythraea (Ehrenb) or from Opopanax. The composition of the myrrh is very complex and it is only known that partially 40 to 60% of the myrrh is soluble in ethanol and comprises a resin and an essential oil, the myrrh consists almost entirely of sesquiterpenes. The main components of sesquiterpenes are: furan sesquiterpenes of the germaran types elemano, eudesmano and guayano. In addition, there are sesquirterpene hydrocarbons, for example β and β-ememene, β-burbonene, β-caryophyllene, humulene and sesquiterpene alcohols for example elemol. Preferably, some of the furan esquirterpenos are characteristic of the myrrh pharmaceutical product. Crude myrrh or raw mucilage gum includes 20% proteins and 65% carbohydrates that are made up of galactose, 4-0-methyl glucuronic acid and arabinose. The chemical products of Comophora myrrhaphyto, include: acetic acid, α-amyrone, arabinose, α-bisabolene, α-bisabolene, carinene, campesterol, cholesterol, cinnamaldehyde, comiferin, α-comiforic acid, β-comoric acid, α-comic acid , comiforinic acid, -cresol, cumic alcohol, cuminaldehyde, dipentene, elemol, 3-epi-a-amyrin, eugenol, furanodieno, furanodienona, galactosa, gum, heerabolene, a-heerabomirrol, ß-heerabomirrol, heeraboresin, limonene, 4-0-methyl-glucuronic acid, n-nonacesan, β-sitosterol, xylose, caprolenes, (carofilenes), resin myrrh gum, burzenone, dihydro fuanodien-6-one, 2-methoxy-furandiene and linderstirene (lindestirene). Myrrh tincture can have an anti-inflammatory effect. Myrrh macro and microscopically may appear as a cafetic yellow powder characterized by yellowish splinters of spherical grains with varying sizes, together with fine granular material that swells in water. In chloral-hydrate mountains, there are only a few fragments of tissue from the source of the plant: reddish brown cork fragments, individual and groups of petrified polyhedral cells to oblong, partially with enormously thickened, pitted or hollowed walls, and lignified and cafetosa contents: fragments of sclerenqui-atherosclerotic and thin-walled parenchyma fibers and prismatic to irregular polyhedral crystals of 10 to 25 μm calcium oxalate. Myrrh should be protected from light and moisture in tightly closed containers. It is better with a dehydrator, since the carbohydrate part of the drug easily absorbs water. Preferably, myrrh should not be stored in powder form. FOLIC ACID The preferred nutrient is folic acid to improve results. Folic acid also referred to as folacin, pteroyl glutamic acid, foldin, folemin, foliamine, folicet, folipac, follets, folsan, folvite, incafólico, milefol or citofol is a water soluble, yellow, crystalline vitamin of the B complex group essential for growth and reproduction of cells. Folic acid works as a co-enzyme with vitamins B12 and vitamin C in the breakdown and utilization of proteins and in the formation of nucleic acids and heme in hemoglobin. Folic acid also increases appetite and stimulates the production of hydrochloric acid in the digestive tract. Folic acid is stored in the liver and can be synthesized by the bacterial flora of the gastro-intestinal tract. Folic acid deficiency can result in poor growth, gray hair, glossitis, stomatitis, gastrointestinal lesions and diarrhea, and can lead to megaloblastic anemia. The deficiency is caused by inadequate absorption of the vitamin's diet, malabsorption or metabolic abnormalities. The need for folic acid increases as in pregnancy, childhood and tension. Folic acid is both labile to heat and light and considerable loss of the vitamin occurs when it has been stored for a long time. Folic acid is non-toxic and effective in treating specific deficiency states. The chemical formula of folic acid is illustrated below: Folic acid (pteroylglutamic acid) The structure of folic acid is presented below: pteroic aa do Pteroylglutamic acid (folic acid) The folic acid molecule contains glutamic acid, p-amino benzoic acid and pterin; The combination of pterin and p-amino benzoic acid is called pterósido acid. The structure shown is the pteroyl glutamic acid of the liver. Folic acid produced by bacteria contains three glutamic acid residues combined in a? -glutamyl bond. Many animal tissues contain pteroyl heptaglutamic acid, the glutamic acid residues are again in the y-glutamyl bond. Synthetic polyglutamic pterool acids in which the glutamic acid molecules are in a-glutamyl bonds, are active in bacterial growth assays; pteroyl -? - glutamic acids are effective both in bacteria and in the treatment of macrocytic anemia in humans. An enzyme in animal tissues hydrolyzes the pteroyl polyglutamate compounds of natural origin in pteroyl monoglutamic acid and free glutamic acid. Another structural form of pteroyl glutamic acid (PteGlUi) is illustrated below: pte monoheptaglu + ama + o congener radical position N »- < H3 C «2H, PitGlu Metilietrahi drofolate N! -CHO S-CHOH.ritGlu Folic Acid (factor W-CHO lCCHOK teGI.1O-formiidecahydroFcJaio N »-? - U- S.HJ.i? ^ FeG! 5,1 O-meth enyltetrahydrofolate MS-io-x ..- iA t / ULHfuG1m 5.1.1 O-methylenetetrahydroFolate NJ - HCH CHNHH ~ P ^ cGk? Farmininolfefrahydrofolate K! "- CK-OH HjOHH ^ itC ^ h idrtací ethyltetrahi drofoiato The structures and nomenclature of pteroyl glutamic acid (folic acid).

Main portions of the folic acid molecule include a pteridine ring linked by a methylene bridge with paraminobenzoic acid which is linked by an amide bond with glutamic acid. While pteroylglutamic acid is the common pharmaceutical form of folic acid, neither is the main congener in folate nor active co-enzyme for intracellular metabolism. After absorption, PteGlu ,. it is rapidly reduced in positions 5, 6, 7 and 8 in tetrahydrofolic acid (H ^ PteGlu) which then acts as an acceptor of a number of units of a carbon atom, these are connected in any position 5 or 10 of the piperidine ring or bridges these atoms to form a new 5-membered ring Vitamin B12 and folic acid are essential dietary products for humans A deficiency of any vitamin results in defective synthesis of DNA in any cell that attempts chromosomal replication and division. that the tissues with the fastest life-time of cells show the most dramatic changes, the hematopoietic system is especially sensitive to deficiencies of these vitamins.Clinically, the earliest sign of deficiency is a megaloblastic anemia, where the reduction in DNA synthesis results in morphological abnormality characteristic of precursor cells in the bone marrow. Abnormal macrocytic reds are the product and the patient becomes severely anemic. Methylcobalamin supports the methionine synthetase reaction which is essentially for the normal metabolism of folate. Methyl groups contributed by methyl tetrahydrofolate (CHsHyPteGlUj.) Are used to form methyl cobalamin, which then acts as a methyl group donor for the conversion of ho ocitein to methionine. This folate-cobalamin interaction is pivotal for normal synthesis of purines and pyrimidines and therefore DNA. The methionine synthetase reaction is substantially responsible for controlling the recycling of folate cofactors; the maintenance of intracellular concentrations of folyl poly glutamates; and through the synthesis of methionine and its product, S-adenosyl methionine, the maintenance of a number of methylation reactions. Since methyl tetrahydrofolate is the main congener of folate delivered to the cells, the transfer of the methyl group into cobalamin is essential for the adequate supply of tetrahydrofolate, the substrate for a number of metabolic steps. Tetrahydrofolate is a precursor for the formation of intracellular folil polyglutamates; it also acts as the acceptor of a one carbon unit in the conversion of serine to glycine, with the resulting formulation of 5, 10-methylene tetrahydrofolate (5,10-CH 2 H 4 PteGlu). The latter derivative donates the methylene group in deoxyuridylate for the synthesis of thymidylate-an extremely important reaction in DNA synthesis. In the process, 5, 10-CHaHiP eG1 is converted to dihydrofolate H, PteGlu.

The cycle is then completed by the reduction of H2PteGlu in H4PteGlu by dihydrofolate reductase, the stage which is blocked by folate antagonists such as methotrexate. Other routes also lead to the synthesis of 5, 10 -methylene tetrahydrofolate. Table A: Biosynthesis of Folic Acid The biosynthesis of folic acid is illustrated below. The ppp symbol represents triphosphate. Synthesis Folate can be transported to tissues such as CHjEUPteGlu, .. The liver actively reduces and compounds PteGlu ,. (and H2 or HiPt GlUa.) and then transport the CHgHiPteGlu ,. in the bile for reabsorption by the intestine and subsequent supply to tissues, CHsHí t GlUa. it acts as a methyl donor for the formation of methyl cobalamin and as a source of H4PteGlu1 and other similar folate as previously described. Folate is stored inside the cells as polyglutamates. SURFACTANTS While benzalkonium chloride is the preferred surfactant for best results, in some circumstances it may be convenient to use other quaternary ammonium surfactants or other surfactants. The quaternary ammonium compound may be dicocodimonium chloride, which is also known as dicoco alkyl dimethyl chlorides or dicoco dimethyl ammonium chloride or Di-C8-18-alkyl dimethyl chloride. This can be used in combination with isopropanol such as 20 to 30% isopropanol. The preferred source of quaternary compound comprises 70 to 80% quaternary ammonium compound and less than 0.03% methyl chloride, and an approximate specific gravity of 0.87 at 46 ° C (115 ° F), a vapor pressure of 33 mm / Hg at 20 ° C (68 ° F), an initial boiling point of 82 ° C (180 ° F) at 760 mm / Hg and a volatility at 20 to 30%, and is produced under the brand name CarSpray 300 by Witco Corporation, Dublin, Ohio, USA The quaternary compound can provide disinfectant qualities and serves as a fungicide to treat fungal and yeast infections. Other quaternary ammonium compounds may be useful such as those produced under the brand Jet Quat 2C-75 by Jeteo Chemicals Inc., of Corsicana, Texas, USA, or produced under the trademarks CarSpray 400 and Carnabua Spray 200 by Witco Corporation, Dublin, Ohio, USA or containing 9% denatured ethyl alcohol such as that sold under the trademark BTC 2125M by Stephan Company, Northfield, Illinois, USA, or the following MAQUAT products comprising n-alkyl dimethyl benzyl ammonium chloride, produced by Mason Chemical Company, Arlington Heights, Illinois, E.Ü.A. , LC-12S (67% C12, 25% C14, 7% C16, 1% C18), MC 1416 (5% C12, 60% C14, 30% C16, 5% C18), MC1412 (40% C12, 50% C14, 10% C16), stearil paste or flakes SC-18 (5% C16, 95% C18), TC-76 O MQ-2525 (5% C12, 60% C14, 30% C16 and 5% C18) AND MC6025-50% / 25% C12, 60% C14 and 15% C16). Jet Quat 2C-75 comprises: 50 to 75% dicoco dimethyl quaternary ammonium chloride, 20 to 50% isopropyl alcohol has a specific gravity of .88 and a boiling point of 82 ° C (180 ° F). CarSpray 400 comprises: 55 to 65% of quaternary ammonium compounds, 20 to 30% of amines, ethoxylated 20% isopropanol, unsaturated alkyl, with C14-18 and C16-18 and less than 0.3% of methyl chloride, and has a specific gravity of approximately 0.88 to 23.9 ° C (75 ° F), a vapor pressure of 33 mm / Hg at 20 ° C (68 ° F), an initial boiling point of 82 ° C (180 ° F) at 760 mm / Hg and a volatility of 10 to 20%. Carnauba Spray 200 comprises: 50 to 60% of quaternary ammonium compounds, 10 to 20% of isopropanol, 15 to 25% of water, 1 to 10% of alkylated carnauba wax, and less than .03% of methyl chloride, and has an approximate specific gravity of .90 to 26.7 ° C (80 ° F) a vapor pressure of 33 mm / Hg at 20 ° C (68 ° F), an initial boiling point of 82 ° C (180 ° F) ) at 760 mm / Hg and a volatility of 20 to 40%. Nonionic surfactants are surfactant compounds that do not ionize in solution in water. Often, these possess hydrophilic characteristics by virtue of the presence of an oxygenated chain (for example a poly-oxyethylene chain), the lyophilic portion of the molecule is derived from fatty acids, phenols, alcohols, amides or amines. Exemplary compounds are the poly (ethylene oxide) condensates of alkyl phenols, for example the condensation product which is formed from one mole of nonyl phenol and 10 moles of ethylene oxide and the condensation products of aliphatic alcohols and ethylene oxide , for example the condensation product which is formed of 1 mol of tridecanol and 12 mol of ethylene oxide. The nonionic surfactants may comprise phenols ethoxylates containing a condensed product of ethyl oxide and an alkyl phenol or an aliphatic alcohol. Nonionic surfactants preferably comprise nonylphenol ethoxylate such as T-DET and / or octaphenol ethoxylate. Nonionic surfactants are reaction products of ethylene oxide and nonol phenol and / or octafenol. The ratio of phenol to ethylene oxide may be in the range of 2:20 to 4:16 and preferably of about 2:12. The nonionic synthetic surfactants may comprise nonionic detergents. Synthetic nonionic surfactants can also be formed by condensing ethylene oxide with a hydrophobic base that is formed by the condensation of propylene oxide with propylene glycol. The hydrophobic portion of the molecule which of course exhibits insolubility in water, has a molecular weight of about 1200 to about 2500. The addition of polyoxyethylene radicals to this hydrophobic portion tends to increase the water solubility of the molecule as a whole and the character The product liquid can be retained to the point where the polyoxyethylene content is about 50% of the total weight of the condensation product. Other synthetic nonionic surfactants may include the polyethylene oxide condensates of alkyl phenols, for example the condensation products of alkyl phenols or dialkyl phenols, wherein the alkyl group contains from about 6 to 12 carbon atoms, either in the configuration of Straight chain or branched chain with ethylene oxide. The ethylene oxide may be present in amounts equal to 8 to 25 moles of ethylene oxide per mole of alkyl phenol. The alkyl substituent of these compounds can be derived from polymerized propylene, diisobutylene, n-octene or n-nonene. Nonionic surfactants can also be produced from the condensation of ethylene oxide with the reaction product of propylene oxide and ethylene diamine, for example compounds containing from about 40% to about 80% polyoxyethylene by weight and have a molecular weight from about 5,000 to about 11,000, which results in a reaction of ethylene oxide groups with a hydrophobic base comprising the reaction product of ethylenediamine and excess propylene oxide.; the base has a molecular weight in the order of 2,500 to 3,000. Other nonionic surfactants include the condensation product of aliphatic alcohols having 8 to 18 carbon atoms in either straight chain or branched chain configuration, with ethylene oxide, for example a condensation product of ethylene oxide coconut alcohol , and the fraction of coconut alcohol having 10 to 14 carbon atoms. Additional nonionic surfactants include long chain tertiary amine oxides corresponding to the following general formula: LRZ J? O wherein RL is an alkyl radical with from about 8 to 18 carbon atoms and Ra and R3 each are methyl radicals or ethyl. The arrow in the formula is a conventional representation of a semipolar link. Examples of amine oxides suitable for use include: dimethyl dodecylamine oxide, dimethyl octylamine oxide, dimethyl decylamine oxide, dimethyl tetracylamine oxide and dimethylhexadecylamine oxide. Other nonionic surfactants may include: long chain tertiary phosphine oxides corresponding to the following general formula: RR'R "P? 0 wherein R is an alkyl, alkenyl or monohydroxyalkyl radical in the range of 10 to 18 carbon atoms. chain length carbon and R 'and R "each are alkyl or monohydroxyalkyl groups containing from 1 to 3 carbon atoms. The arrow in the formula is a conventional representation of a semipolar link. Examples of suitable phosphine oxides are: dimethyl dodecyl phosphine oxide, dimethyl tetradecyl phosphine oxide, ethyl methyl tetradecyl phosphine oxide, cetyl dimethyl phosphine oxide, dimethyl stearyl phosphine oxide, cetyl ethyl propyl phosphine oxide, diethyl dodecyl phosphine oxide , diethyl tetradiethyl phosphine oxide, dipropyl dodecyl phosphine oxide, bis- (2-hydroxymethyl) dodecyl phosphine oxide, bis- (2-hydroxyethyl) dodecyl phosphine oxide, (2-hydroxypropyl) methyl tridecyl phosphine oxide, dimethylolethyl phosphine and dimethyl (2-hydroxydecyl) phosphine oxide. In some circumstances, it may be useful to employ other surfactants such as other cationic surfactants, ampholytic surfactants or a zwitterionic surfactant. Cationic surfactants may include cationic detergents. Cationic surfactants comprise compounds that ionize in an aqueous medium to give cations containing the lyophilic group. Typical of these compounds are the quaternary ammonium salts containing an alkyl group of about 12 to about 18 carbon atoms, such as lauryl benzyl dimethyl ammonium chloride. Ampholytic surfactants are compounds that have both anionic and cationic groups in the same molecule. Examples of these compounds are aliphatic amine derivatives containing a long chain of about 8 to about 18 carbon atoms and an anionic water solubilizing group, for example carboxy sulfo, sulfo or sulfate. Examples of ampholytic detergents are: 3-dodecyl amino propane-sodium sulfonate, n-methyl sodium taurate and related substances such as amino acids disubstituted with higher alkyl, betaines, nipples, sulphated long chain olefinic amines and sulfated imidazoline derivatives. Zwitterionic surfactants may include synthetic detergents. Zwitterionic surfactants are in general derivatives of aliphatic quaternary ammonium compounds, wherein the aliphatic radical can be straight or branched chain and wherein one of the aliphatic substituents contains from about 8 to 18 carbon atoms and one contains a solubilizing group of anionic water, for example carboxy, sulfo or sulfate. Examples of compounds falling within this definition are: 3- (N, N-dimethyl-N-hexadecylammonium) -propane-1-sulfonate and 3- (N, N-dimethyl-N-hexadecylammonium) -2-hydroxy-propane -l-sulfonate. CLINICAL PHARMACOLOGY When the phytochemicals Echinacea and Commiphora (antimicrobial isolates, botanical extracts and microbial inhibitors) were mixed, combined and applied with: a surfactant, preferably benzalkonium chloride, a nutrient carrier, preferably folic acid; and a sterile aqueous carrier, the results were unexpected and surprisingly good at solving (treating) HIV, and other infectious diseases and the effectiveness of the medicine (microbicide) is dramatically increased. Significantly when tested in vitro, the single compound demonstrates unexpected and surprisingly good antiviral activity against HIV including inhibition of HIV connection to the target cells. When synergistic medicine was tested topically in vivo, herpes simplex infections were immediately stopped. When the synergistic medicine was tested in vitro, the benzalkonium chloride surfactant was substantially less toxic and within a safe level and there was a higher level of inhibitory activity against HIV and HSV 1 and 2. The interaction of synergy and the mixing of the phytochemicals of Echinacea and Commiphora, folic acid and surfactant, was demonstrated and observed upon seeing the rapid solubility of the components when mixed and the slight adhesive quality created by the properties in solution. In addition, the chemical properties of the Echinacea and Commiphora phytochemicals, carrier of surfactant nutrient (nutrient) and the increased reactivity and improved stabilization of aqueous carrier, which are useful for treating infectious diseases.

The medicine can be used in varying dilutions in: oral and nasal mucosa; vaginal tissue; labial tissue; anal and perianal tissue; penis tissue; cutaneous tissue; open subcutaneous tissue; and in higher dilutions in ocular infections and preferably rectal or vaginal administration. By varying the concentrations, the medicine can possibly be administered parenterally. The medicine can be contraindicated in the vaginal or anal passages; in a dressing compress; in the auditory canal; in occlusive coatings; parts emptied or ingested and this use may cause irritation or chemical burns.

It may not be advisable to use the medicine to treat anaerobic fungal infections, since some fungi may be resistant. EXAMPLES 1-7 In vivo Test In an initial topical application, the in vivo study that was performed to evaluate the effects of medical treatment and the medicine of the present invention on 7 human test subjects, who tested positive for HSV 1 or 2. The subjects were treated topically with the medicine comprising the benzalkonium chloride surfactant in an aqueous solution (in a ratio of 1: 750) in combination with the botanical herbaceous Echinacea purpurea in powder form containing the previously listed phytochemicals. The application of the composition was carried out by a two-stage procedure, first wetting the affected area or vesicles with the benzalkonium chloride surfactant in an aqueous solution when spraying, applying touches, or using a dropper; Then apply a coatings of the powdery phytochemicals on the wetted area, either by applying by touch or manually spraying the powder on the infected area. An important aspect of this treatment is to maintain full coverage of the area affected by the duration of the outbreak. Therefore, the shoot area remains covered with the medical composition upon reapplication as required. Of the seven subjects, six were women and one was a man. At the beginning of this study, the age of men was 38 years, women were 8, 27, 30, 32, 38 and 39 years old. There were twelve infectious outbreaks in approximately six weeks. Nine of the outbreaks were HSV 2, genital herpes and 3 were HSV 1, fires, thrush or cold sores. The 8-year-old girl and the 27-year-old woman exhibited HSV 1 (cold sores). The women of 30 years, 38 years and 39 years exhibited HSV 2 (genital herpes). The 38-year-old also had a HSV 1 cold sore. The man exhibited HSV 2 (genital herpes). All tested subjects had a well-established history of the disease and were able to identify the standard course of their disease. To obtain objective data, none of these test subjects knew anything about the trial treatment or any action of the medicine. In repeated tests, the subjects were told that there could be placebos mixed with the formula samples. In 7 cases, the antimicrobial compound (medicine) was applied directly to tissue in the prodromal stage. In 5 cases, the antimicrobial compound was applied directly in erupted vesicles. The antimicrobial compound was re-applied as necessary to maintain coverage. Observations: With each application of the medicine, each individual (test subject) reported an itching sensation for a few seconds. They also reported that there was a substantial degree of adhesion of the medicine compound (antimicrobial to the vesicle or affected area). The adhesion of the composition to the epithelial tissue remained to a degree even after bathing or rinsing with water from the area. Results: The results of the test of the seven subjects with medical treatment and medicine were unexpectedly surprising, good and very consistent.

In each case, the subject happily reported that once the composition (medicine) was applied to the affected area, the pain was completely stopped in 10 to 20 minutes when nothing in the past had previously reduced the pain. In all seven cases, when the compound (medicine) was applied in the prodromal stage, the subjects reported that the pain was stopped, all symptoms that had previously escalated to a complete outbreak ceased and the outbreak never occurred again. All external symptoms and physical manifestations of herpes disappeared within a few hours after the medicine was applied. In the five cases where the compound (medicine) was applied to the erupting vesicles, the subjects reported that the pain stopped in minutes and the sensations of burning, itching and irritation resolved two to four hours and the vesicles dried up and they disappeared in 21 hours. In all cases, the other more extreme and debilitating symptoms were stopped: fever, malaise, inguinal swelling, blisters, oozing sores and painful urine, once the medicine has been applied. When followed up, where the subjects had been provided with the composition (medicine) to test in future outbreaks, it was reported that if the initial signs of an outbreak were shown, indicating the prodomal stage of an outbreak, the compound (medicine) it was immediately applied by the subjects according to the instructions and the outbreak was completely stopped and resolved. Significantly, it was also reported by subjects who were accustomed to experiencing several outbreaks annually, which had markedly longer latency periods. At a 3-year follow-up with a person who reported several outbreaks monthly for four years before using the medicine, he reported that he had not had an outbreak in more than a year since he used the medicine. Additional Observations: A male human subject reported that after the initial application during the prodromal phase of an outbreak, he bathed and forgot to re-apply the composition (medicine) for a period of approximately 30 hours. Consequently, several vesicles erupted and began to coalesce. The subject proceeded to re-apply the composition (medicine) and subsequently kept the area well coated with the composition. Subsequently, the outbreak resolved in 21 hours in the same manner as described with the other human subjects. Another observation indicated that the composition (medicine) may be weakened or less effective in the presence of certain proteins or soaps. A woman may have been excessively jealous in cleaning the affected area before application of the composition (medicine). This happened during a third outbreak after having succeeded with the composition (medicine) in the two previous outbreaks. In this case, when the composition (medicine) was applied, there was no familiar itching sensation and there was no relief from the symptoms. Approximately 24 hours elapsed before he sought advice and the outbreak escalated to the stage of complete vesicular eruption with all the previous symptoms of the disease. He was instructed to thoroughly rinse any soap residue from the area to dry the area and reapply the composition (medicine). After following the instructions, he reported that the outbreak had been completely resolved as it would have been in the two previous outbreaks, when applying the medical composition. EXAMPLES 8 TO 13 Dermatological and veterinary tests. Animal tests were performed to determine any possible dermatological allergic reaction induced by the medical composition (medicine). Six animal subjects were used. The animals included 3 rabbits (unknown ages), two dogs (a two-year-old female and a 9-year-old male); a three year old neutered male cat. In these tests on animals, the previous composition (medicine) was applied, in the method previously established to the interior of the external ear of each animal.

In all cases, the area to be treated remains coated with the compound for 24 hours, corresponding to the time used by the human subjects. The test performed on the six animal subjects indicated that there were no signs of dermatological irritation or allergic reaction. EXAMPLE 14 The above medical compound containing viral inhibitors was also tested on a wart or small tumor caused by papilloma virus on the muzzle of a purebred, neutered, 2-year-old racing horse. Papilloma virus warts are difficult to treat. The wart measured 25 mm in diameter. The antimicrobial compound (medicine) was applied twice a day. The wart was then measured in each application. Results: Quite unexpectedly, the wart decreased dramatically in size by approximately 3 millimeters per day, while the medicine applied to the wart and the fifth day completely peeled off. It was observed that at first the superficial layers of the wart began to degrade, exposing large erythematous papules. Then, interestingly, the wart not only decreased in size when scaled or peeled off, but decreased at the point of connection in the subject's epidermis and some something intact without scarring sequelae came off. In a continuous long-term in vivo study of this invention, which began with the first seven subjects in April 1989 and has now lasted 7 years, approximately 100 infectious outbreaks have been treated with the medicine in different concentrations as described above. In all cases, the surprisingly good results were the same. The pain disappears in minutes; 2) no outbreak occurs when the composition is applied in the prodromal stage; 3) the outbreak resolves in 21 hours when it is applied in the vesicular stage. IN VITRO TEST Laboratory tests were performed in the University of Chicago, Clinical Microbiology Laboratories (Laboratories of Clinical Microbiology) to determine the in vitro inhibitory activity of medical treatment and composition (medicine). Laboratory tests were performed by the associate director, PhD and associate professor of pathology. The in vitro test of the medical composition referred to as the "drug" below produces surprisingly good results. It was determined that the unexpected surprising medical treatment and composition exhibited inhibitory activity in HSV 1 and HSV 2. It was established by the pathologist who tested "hundreds" of other compounds and had never seen anything as good as this composition. The following are the tests of the medicine that were performed and the results that were obtained in the University of Chicago. For ease of interpretation of some of the scientific data and test results, the following definitions apply: "MEM" refers to minimum essential medium. This is the culture medium used in laboratories for the growth of cells in which the tests are carried out. "FIBROBLASTO" is a mesenchymal human cell (a cell that is found in connective tissue, blood, bones, lymphatics and cartilage). "IC50" refers to the inhibitory concentration. For this test, a 50% endpoint is chosen, as is typical. The next number indicates the largest dilution less than 50%. Therefore, this is the definition of the endpoint. If an area under a dilution is left blank, indicates that there may be toxicity to that dilution, it may be that the test was not worth reading or that there were no interpretable data.

If an area under dilution is marked with a dash (-), it indicates that there are no plaques and that there is a successful inhibition of herpes (HSV). EXAMPLES 15 TO 17 In these in vitro tests, the following drugs (medicine) were used: Drugs # 1 = Surfactant benzalkonium chloride in an aqueous solution at a ratio of 1: 750. The surfactant in the aqueous solution is filtered before to use and dilute in an equal volume of 2X MEM to give a dilution 1: 1500 in IX MEM. Drugs # 2 - Echinacea powder (phytochemical) in an aqueous solution. This preparation is extracted by hot infusion in sterile water. The extracted phytochemicals are centrifuged and filtered before this use. The filtered phytochemicals were diluted in an equal volume of 2X MEM to give the preparation undiluted in IX MEM. Drugs # 3 = Echinacea powder (phytochemical) is extracted and combined with benzalkonium chloride surfactant by a cold infusion process. The combined preparation is centrifuged and filtered before use and diluted in an equal volume of 2X MEM to give the preparation undiluted in IX MEM. 1. Three plates of 24 compartments were inoculated with fibroblasts. Three different extractions (for comparison) in five concentrations of the composition, were used to classify antiviral activity in concentrations of: undiluted, 1: 2, 1: 4, 1: 8, and 1:16 in IX MEM. There were 4 control compartments in each plate containing MEM without drug. 2. The growth medium is removed from the compartments and 200 ul of HSV-1 is added to each compartment of the upper half of each plate. HSV-1 is diluted 1: 5000 (2.0 ul of HSV-1 material in 10 L of MEM). The virus titer was 3 x 106 x mL. Also, 200 ul of HSV-2 is added to each compartment of the lower half of each plate. HSV-2 is diluted 1: 2000 (5.0 ul of HSV-2 material) in 10 mL of MEM. The virus titer was 6 x 105 x mL. 3. Plates were incubated at 37 ° C for two hours. 4. The inoculum was removed and one mL of the MEM containing drugs # 1-3 was added to the four compartments. The concentration of the drug compared to the MEM is indicated below. Table 1 Concentration Undiluted 1: 2 2: 4 1: 8 1:16 Drug (ul) 4000 2000 1000 500 250 MEM (ul) - 2000 3000 3500 3750 5. Results: HSV-1, liquid superimposed layer, drug added immediately after absorption of the virus. Plate 1, drug # 1 contaminated without bacterial growth, probably waste. Plate 3, drug # 3 the results are indicated in Tables 2 and 3 below. Table 2-Drug # 3 HSV-1 test results Concentration Without diluting 1: 2 2: 4 1: 8 1:16 Plates 54 toxic toxic - 6 * 12 ** Plates 42 toxic toxic 4 * 16 ** Average 48 5 14 IC50 > 1:16 Table 3-Drug # 3 HSV-2 test results Concentration Without diluting 1: 2 2: 4 1: 8 1:16 Plates 46 toxic toxic - 22 * 32 ** Plates 49 toxic toxic - 21 * 28 ** Average 48 22 30 ICso = 1: 8 * slight toxicity. ** Very small plates. Comments: test with medicine (Drug # 3) provides excellent result. The cells look good without contamination. At the lowest dilutions, the preparation can be toxic to some of the cells.

This preparation was unexpectedly successful in its inhibitory activity. EXAMPLES 18-20 Three plates of 24 compartments were inoculated with fibroblasts and the following drugs. Test drug number 1A = to benzalkonium chloro surfactants in an aqueous solution, the benzalkonium chloro surfactant is prepared by making a 1: 375 dilution in water (32 ul in 12.0 L of sterile water) this was filtered before use . This was diluted in an equal volume of 2X MEM to give 1: 750 dilution in IX MEM. Dilution is done to maintain the proportion. Test drug # 2A = Echinacea purpurea powder (phytochemicals) in an aqueous solution. This preparation was a 50 mg / ml 300 mg solution in 6.0 mL of water (from Echinacea purpurea powder in sterile water.) The mixture is vortexed and refrigerated for 4 hours.The Echinacea powder preparation is centrifuged at 3500 rpm. 15 minutes at 10 ° C and filter before use and then dilute in an equal volume of 2X MEM to give the preparation undiluted in IX MEM. Test drug # 3A = Echinacea purpurea powder (phytochemicals) dissolved in surfactant and chlorine This preparation was a 50 mg / mL solution (300 mg in 6.0 mL of benzalkonium chloride, 1: 375) .The mixture is vortexed and refrigerated for 4 hours.The mixture of phytochemical and surfactant is centrifuged at 3500 rpm for 15 minutes at 10 ° C and filter before use and then dilute in an equal volume of 2X MEM to give the preparation undiluted in IX MEM 1.- 3 plates were used to classify the three drug preparations. concentrations required to classify anti activity viral were: 1: 2, 1: 4, 1: 8 and 1:16 in IX MEM. There were four control compartments in each plate containing MEM without drug. 2. - The growth medium is removed from the compartments and 200 ul of HSV-1 are added to each compartment of the upper half of each plate. HSV-1 is diluted to 1: 5000 (2-0 ul of HSV-1 material in 10 L of MEM). The virus titer was 3 x 106 x mL. 3.- The plates were incubated at 37 ° C for four hours. 4.- The inoculum was removed and 1 mL of the MEM containing the drugs # 1A-3A are added to the four components. TABLE 4 Concentration undiluted 1: 2 2: 4 1: 8 1:16 Drug (ul) 4000 2000 1000 500 250 MEM (ul) - 2000 3000 3500 3750 5.- Results: HSV-l, composition on liquid layer, the composition is added immediately after absorption of the virus. Table 5 - Drug # 1A-HSV Test Result Concent. 1: 2 1: 4 1: 8 1:16 1:32 plates 70 toxic toxic toxic toxic toxic plates 68 plates 58 plates 74 Average 70 IC50 Comments: These compartments have a fine precipitate on the cells. Benzalkonium Chloride probably rushes with the protein in the middle. Table 6 - Drug # 2A-HSV Test Result Concent. 1: 2 1: 4 1: 8 1:16 1:32 plates 72 9 * 12 * plates 74 7 8 plates 79 4 12 plates 71 7 11 Average 70 ICso >; 1:32 Comments: Although there were some plates, they were very small.

Table 7 - Drug # 3 -HSV Test Result Concent. 1: 2 1: 4 1: 8 1:16 1:32 plates 72 toxic toxic toxic toxic - * plates 68 plates 67 - plates 70 - average 70 IC50 > 1:32 Comments: Although there was some toxicity, this drug form was very successful in inhibiting the virus, there do not seem to be plaques. EXAMPLES 21-24 Four plates of 24 compartments were inoculated with fibroblasts. Test Drug # 1B = Benzalkonium chloride surfactant in an aqueous diluent. Benzalkonium chloride is prepared by making a 1: 1000 dilution in water (10 μl in 10.0 mL of sterile water). This was filtered before use and diluted in an aqueous volume of 2X MEM to give a 1: 2000 dilution in XMEM (500 μl of drug plus 500 μl of 2X MEM). Test Drug # 2B = Echinacea purpurea powder (phytochemicals) in an aqueous solution. This preparation was a solution 50 mg / mL (250 mg in 5.0 L of water) of Echinacea purpurea powder in sterile water. The mixture was vortexed and refrigerated for four hours. This pulverulent preparation of Echinacea was centrifuged at 3500 rpm for 15 minutes at 10 ° C and filtered before use and diluted in an equal volume of 2X MEM to give the preparation undiluted in 1XMEM (500 μl drug plus 500 μl of 2X MEM) . Test Drug # 3B = Echinacea purpurea powder (phytochemicals) dissolved in benzalkonium chloride surfactant. This preparation was a 50 mg / mL solution (250 mg in 5.0 mL of benzalkonium chloride, 1: 1000). this mixture was subjected to whirlwind and refrigerated for four hours. The Echinacea phytochemicals and surfactants were centrifuged at 3500 rpm for 15 minutes at 10 ° C and separated by filtration before use and then diluted in an equal volume of 2X MEM to give the preparation in 1XMEM (500 μl of drug plus 500 μl of 2X MEM). Test Drug # 4B = Echinacea purpurea powder (phytochemicals) in an aqueous solution (diluent) and then mixed with benzalkonium chloride surfactant in a ratio of 1: 1000. This preparation was a 50 mg / mL solution (250 mg in 5.0 mL of water) of Echinacea purpurea powder in sterile water. The mixture is vortexed and refrigerated for four hours. Aqueous photochemical products were centrifuged at 3500 rpm for 15 minutes at 10 ° C and separated by filtration before use. This preparation was diluted in an equal volume of benzalkonium chloride in a ratio of 1: 1000, to obtain the mixture of benzalkonium chloride-Echinacea. This mixture is diluted with an equal volume of 2X MEM to give the 1: 4 preparation in 1XMEM (500 μl drug # 1 and 250 μl drug # 2 plus 500 μl of 2X MEM). 1. Four plates were used to classify the four drug preparations. The concentrations required to classify antiviral activity were 1:20, 1:40, 1:80 and 1: 160 and 1: 320 in IX MEM. There were four control compartments in each plate containing MEM without drug. 2. The growth medium is removed from the compartments and 200 μl of HSV-1 is added to each compartment of the two upper rows of each plate. HSV-1 is diluted 1: 5000 (2.0 μl of HSV-1 material in 10 L of MEM). The virus titer was 3xl06 per mL. Also, 200 μl of HSV-2 is added to each compartment of the lower half of each plate. HSV-2 is diluted 1: 2,000 (5.0 μl of HSV-2 material in 10 mL of MEM). The virus titer was 6xl05 per mL. 3. The plates were incubated at 37 ° C for four hours. 4. The inoculum was removed and one mL of MEM containing drugs # 1-4 is added to the four compartments. TABLE 8 Concentrate 1:20 1:40 1:80 1: 160 1: 320 Drug (μl) 400 200 100 50 25 MEM (μl) 3600 3800 3900 3950 3975 . Results: HSV-1, on liquid layer, drugs added immediately after virus absorption. Table 9 - Drug # 1B- HSV-1 Concentrated Test Results 1:20 1:40 1:80 1: 160 1: 320 plates 37 toxic toxic toxic toxic 157 * plates 45 187 * Average 41 ICso Comments: Slightly toxic, Test was hard to read. HSV-2, on liquid layer, drugs added immediately after virus absorption. Table 10 - Drug # 1B- HSV-2 Test Results Concentrate 1:20 1:40 1:80 1: 160 1: 320 plates 38 toxic toxic toxic toxic 21 plates 42 17 Average 40 19 IC5O > l: 320 Comments: The test was too toxic to give a good reading. Table 11 - Drug # 2B- HSV-1 Concentrated Test Results 1:20 1:40 1:80 1: 160 1: 320 plates 39 2 * 8 * 23 * 24 44 plates 40 3 18 11 28 38 Average 40 3 13 17 26 IC5O > l: 80 Comments: Small plates. Table 12 - Drug # 2B- HSV-2 Concentrated Test Results 1:20 1:40 1:80 1: 160 1: 320 plates 48 21 33 plates 52 22 38 Average 50 21.5 35.5 ICSO > 1:20 Table 13 - Drug # 3B- HSV-1 Concentrated Test Results 1:20 1:40 1:80 1: 160 1: 320 plates 44 1 * 17 31 37 plates 46 - 16 28 27 Average 45 - 17 30 32 ICSO > 1:40 Comments: Although there was some toxicity, the drug was very successful, there seemed to be no plaques.

Table 14 - Drug # 3B- HSV-2 Concentrated Test Results 1:20 1:40 1:80 1: 160 1: 320 few cells 11 * 27 30 35 plates 44 10 32 Average 44 11 29.5 ICSO > 1:20 Comments: A difficult test to obtain a really good reading. However, the drug has successful inhibitory activity. Table 15 - Drug # 4B- HSV-l Concentrated Test Results 1:20 1:40 1:80 1: 160 1: 640 plates 47 toxic toxic toxic 33 plates 48 28 Average 48 30 IC5O > l: 320 Comments: Toxic to higher levels. However, the drug has successful inhibitory activity at 1: 320. Table 16 - Drug # 4B- HSV-2 Concentrated Test Results 1:20 1:40 1:80 1: 160 1: 640 plates 38 toxic toxic toxic 2 * 16 plates 40 4 20 • Average 39 3 18 IC5O > l: 640 Comments: The toxicity probably due to benzalkonium chloride. The drug at 1: 320 dilution showed very strong inhibitory activity.

The in vitro tests of Examples 21-24 use unrefined raw materials. However, the tests showed surprisingly good viral inhibitory activity and a probable synergy between the constituents. In previous in vitro tests where Drugs # 3, 3A and 3B, were Echinacea purpurea phytochemicals extracted and combined with benzalkonium chloride surfactant, the resulting medicine demonstrated the highest antiviral activity and most notably demonstrated a synergy between the Echinacea components purpurea and benzalkonium chloride. This can possibly be explained by a shared stability and improved reactivity between the two components. The benzalkonium chloride in the synergistic mixture exhibits a lower degree of toxicity and the synergistic combination (medicine) exhibits a higher degree of antiviral activity, particularly with HSV-2. HIV TESTS Viracea-1 and Viracea-2 were tested for anti-HIV activity evaluation in acute infection model trials. Additional trials were conducted to evaluate the range and mechanism of action of the two components. The compounds Viracea-1 and Viracea-2 are supplied as solutions. Formulations include filtering the solution and centrifugation. The high test concentration used in each test varied from a 1: 5 dilution to a 1: 100 dilution in tissue culture medium. Each component was stored at 70 ° C before use. In these tests, the following drugs (composition) were used. Viracea l = Viracea 2 = Propagation and Quantification of Cell Lines and Virus Materials Cells used in the compound classification assays were designated as the CEM-SS cell line. These cells are highly susceptible to infection with HIV, quickly form multinucleated syncytia, and eventually are killed by HIV. These cells are easily maintained (2-7 x 10 3 cells per ml) in RPMI 1640 tissue culture medium supplemented with 10% fetal bovine serum glutamine and antibiotics. The cells are passed twice weekly at 1:20 dilution. The number of steps is recorded each week and the cells are discarded after twenty weeks per step and fresh CEM-SS cells are thawed and used in the assay. CEM-SS cell materials were frozen in liquid nitrogen in NUNC ampoules of 1 ml in 90% fetal bovine serum and 10% dimethyl sulfoxide (DMSO). After thawing, CEM-SS cells are routinely ready for use in the primary classification assay after two weeks in culture. Before replacing a late passage cell line, the new CEM-SS cells are tested in the classification assay protocol using the current infectious virus and AZT material. If the infectivity of the virus is significantly different from the new cells or if AZT appears to be less active than expected, the new cells will not enter the classification program. Mycoplasma tests are routinely performed on all cell lines (see above). Virus deposits are prepared and titrated in CEM-SS cells, placed in 5 ml aliquots and frozen at -135 ° C. After thawing, unused viruses are discarded to avoid changes in infectious titer. Optimization assays have documented a reduction of un-log in virus titer before the first freeze-thaw cycle, and less drastic titer reduction with subsequent rounds of freeze-thaw. Virus deposits are prepared by the acute infection of 5 x 10s of CEM-SS cells with HIV in a volume of 200 μl at a multiplicity of infection determined to give complete cell death on day 7 after infection (approximately 0.05 for the isolated IIIB of HIV-1 and 0.01 for the RF isolate of HIV-1). The infection is allowed to proceed for one hour at 37 ° C and then the cells are transferred to a T25 flask and the volume is increased to 2 ml. On day 1 after infection the volume is brought to 5 ml and on day 2 the volume increases to 10 ml. Beginning on day 4, the cells are pelleted, the supernatant is saved and the cells resuspended in a fresh 10 ml aliquot of tissue culture medium. Complete media changes on a daily basis, instead of allowing growth of the cells in the medium for longer periods of time, allow the virus inoculum used in the primary classification to remain relatively depleted of nutrients when used to infect cells . The staining reaction used (XTT) requires that the glucose concentration remain high. Wells depleted of glucose by cell growth will not be allowed metabolic conversation of the tetrazolium dye to the formazan product. Cell-free supernatants from acutely infected cells are stored on day 4, day 5, day 6 and day 7. An aliquot of supernatant is stored separately in each day for use in titre determination. Titre determinations include reverse transcriptase activity assay, end-point titration or plaque assay (CEM-SS) quantification of infectious particles and quantification of cell kill kinetics. It has been determined that peak levels of infectious virus occur in acutely infected cultures, since the viability of the cells falls to the 50% level. Since the primary classification assay quantifies the protective effects of a compound for its ability to inhibit HIV-induced cytopathic effects, the amount of virus required to kill CEM-SS cells within 6 days is routinely used to determine the amount of virus required. per well in the primary classification trial. Each of the daily collections is titrated in the XTT protocol of primary classification when performing double dilutions of the virus starting at the high test concentration of 50 μl of virus per deposit. The XTT spotting method with tetrazolium dye is used to determine the exact amount of virus required to kill all CEM-SS cells in each well and this minimal amount of virus is used to perform all primary tests. Identical methods are used to prepare all virus isolates used in the laboratory, including laboratory-derived strains of HIV-1, HIV-2 and STV. Clinical isolates used are passed on fresh human cells and methods for the growth of these cells and the production of virus harvested, They described below.

XTT Assay Antiviral Microtitre Cell Preparation Cells CEM-SS or another established human cell line used in these experiments are passed in T-150 flasks for use in the assay. The day before the test, the cells divide 1: 2 to ensure that they would be in an exponential growth phase at the time of infection. On the day of the assay, the cells are washed twice with the tissue culture medium and resuspended in fresh tissue culture medium. The viability and total cell counts are performed using a hemacytometer and exclusion of triptan blue dye. The cell viability was greater than 95% for the cells to be used in the assay. The cells were pelleted and resuspended at 2.5 x 10 4 cells per ml in tissue culture medium. Cells were added to the drug containing plates in a volume of 50 μl. Preparation of Virus A pre-titrated aliquot of virus is removed from the freezer (-80 ° C) and allowed to thaw slowly at room temperature in a biological safety cabinet. The virus is resuspended and diluted in a tissue culture medium such that the amount of virus added to each wall of a volume of 50 μl will be the amount determined to provide complete cell killing at 6 days after infection. In general, those collected from viruses produced with HIV isolate IIIB require the addition of 5 μl of virus per well. Collected from RF viruses were five to ten times more potent requiring 0.5-1 μl per well. Calculation of TCID50 by endpoint titration in CEM-SS cells indicates that the multiplicity of infection of these assays ranged from 0.005-2.5. Plate format The format of the test plate has been standardized and contains cell control wells (cells only), virus control wells (virus plus cells), drug toxicity control wells (cells plus drug only), drug colorimetric control wells (drug only) as well as experimental wells (drug plus cells plus virus). EXAMPLES 25-48 Spotting XTT Classification Plates After 6 days of incubation at 37 ° C in a 5% C02 incubator, the test plates were analyzed by staining with the XTT-tetrazolium dye. XTT-tetrazolium is metabolized by mitochondrial enzymes of cells of metabolic activity into a soluble formazan product, allowing rapid quantitative analysis of the inhibition of cell killing induced by HIV by anti-HIV test substances. On day 6 after infection the plates were removed from the incubator and observed. The use of round bottom microtiter plates allows rapid macroscopic analysis of the activity of a test compound given by the evaluation of the size of the nodule. The results of the macroscopic observations were confirmed and improved by additional microscopic analysis. Solution XTT is prepared alone as a 1 mg / ml material in PBS. Phenazine methosulfate (PMS) solution is prepared at 15 mg / ml in PBS and stored in the dark at -20 ° C, XTT / PMS material is prepared immediately before use when diluting PMS 1: 100 in PBS and adding 40 μl for my XTT solution. Fifty microliters of XTT / PMS are added to each well of the plate and the plate is reincubated for 4 hours at 37 ° C. Adhesive plate sealers were used instead of the lids, the sealed plate was inverted several times to mix the soluble formazan product and the plate was read spectrophotometrically at 450 nm, with a plate reader from Molecular Devices Vaax. Using a Reduction% CPE, Cell Viability%, IC2S, so and 95- TC2S, so and 95 and other indices were calculated.

TABLE } 7 ANTIVIRAL RESULTS IN VITRO ESSAY XTT PARAVIRACEA 1 1 2 3 4 5 6 7 S 9 10 p 12 Bottom Plastic Reagent 10 0169 0160 0160 D 159 154 0.167 0.066 0.063 0.058 0.061 0063 0067 Tox cc / vc Experimental High Conc Tox Tox Experimental Ba | a Conc cc / vc Tox 1,498 1461 0196 0378 0.278 1,466 1474 0204 0211 020S 1517 1511 1,392 1 61 0.192 0.196 0.293 1414 1 79 0205 0247 0.185 1.496 1497 00 1.333 1.426 0.3 ÍS 1.410 J.372 1356 1.482 0242 0182 0215 1.478 1.519 -o 1208 0219 1,134 1181 1110 1,206 1,487 0219 020S 0.215 0.189 1512 1032 0.193 0940 0828 0968 0.944 1.4S0 0.192 0207 0254 0309 J.506 0656 0222 0596 0582 0.544 0.572 1464 0206 0254 0.186 0.184 1468 Colorimetric Background-High Concentrations Background Color? Metric? Co-Ba | as Concentrations 0.? S9 0 IS2 0168 0171 0166 0167 0.163 0.173 0172 66 0164 0180 20 TABLE 18 VIRACEA 1 o J5 TABLE 19 VIRACEA 1 15 TABLE 20 ANTIVIRAL RESULTS IN VITRO ESSAY XTT PARAVIRACEA2 1 3 4 5 6 7 8 9 10 11 12 Background Reagent Background Material 10 0.169 0.163 0.164 0166 0160 0.170 0074 0072 0067 0067 0.067 0.068 Tox cc / vc Exper mental High Conc. Tox Tox Exper mental Bap Conc. Cc / vc fox 1468 1421 0461 0.257 1.170 1467 1.501 0.207 0222 0.214 1506 1503 1321 1397 1 16 0.209 0191 1,340 1494 0.200 0.202 0.204 1446 1457 0906 1.345 0.249 0.764 0.836 0.953 1.4S5 0.227 0.179 0179 1453 1.500 0219 0.256 1.190 0.207 0.210 0.234 1491 0204 0.190 0228 0192 1 06 0168 0190 0161 0.161 0148 0157 1.503 0237 0195 0202 0186 1.501 0. 242 0223 023S 0239 0230 0242 1495 0.201 0.204 0227 0189 1503 Fon do Colonme stpco-High Concentrations Fo gone Colopmétpco-Low Concentrations 0.258 0.172 0.159 0165 0.163 0.165 165 0.166 0.166 0171 0159 0169 TABLE 21 VIRACEA2 •or fifteen twenty TABLE 22 VIRACEA 2 fifteen EXAMPLES 49-54 Reverse Transemittase Activity Assay A reverse transcriptase (RT) reaction based on microtitre is employed. Tritiated thymidine triphosphate (NEN) (TTP) is resuspended in distilled H20 at 5 Ci / ml. Poli rA and oligo dT are prepared as a material solution that is maintained at -20 ° C. The reaction buffer RT is prepared fresh on a daily basis and consists of 125 μl of MEGTA, 125 μl of dH203, 125 μl of Triton X-100, 50 μl of 1M Tris (pH 7.4), 50 μl of IMDTT and 40 μl of IMMgCl2. These 3 solutions were mixed together in a ratio of 1 part of TTP, 2.5 parts of poly rA: oligo dT, 2.5 parts of reaction, the reaction buffer and 4 parts of distilled water. 10 microliters of this reaction mixture are placed in a round bottom microtiter plate and 15 μl of supernatant containing virus is added and mixed. The plate is incubated at 37 ° C and incubated for 60 minutes. After reaction, the reaction volume is stained on filter mats, washed 6 times for 5 minutes each time in a 5% sodium phosphate buffer, 2 times for 1 minute each in distilled water, 2 times for 1 minute each in 70% ethanol and then dry. The dry filter mat is placed in a plastic sample bag. Betaplate scintillation fluid is added and the bag is then heat sealed. The incorporated radioactivity is quantified using a Wallac Microbeta flash counter.

TABLE 23 VIRACEA-1: PBMC / RED ~ l TABLE 24 VIRACEA-1: PBMC / RED 15 twenty TABLE 25 VIRACEA-2: PBMC / RED O co TABLE 26 VIRACEA-2: PBMC / RED fifteen twenty ELISA ELISA kits were purchased from Coulter. The test is carried out according to the recommendations of the manufacturers. Prior to the ELISA analysis, reverse transcriptase activity assays were routinely performed and the values were used for radioactivity incorporated in the RT activity assay, to determine the dilution of the samples required for ELISA. Control curves were generated in each assay to accurately quantify the amount of protein capsid in each sample. Data were obtained by spectrum-photometric analysis at 450 nm using a Molecular Devices Vmax plate reader. The P24 concentrations were calculated from the optical density values by use of the software package from Molecular Devices Soft Max. Infectious Particles Infectious virus particles were quantified using the CEM-SS plate assay and Quantitative infectivity assay for HIV-1 and HIV-2. Flat-bottomed 96-well microtitre plates were coated with 50 μl of poly-L-lysine at 50 μg / ml for 2 hours at 37 ° C. The wells were then washed with PBS and 2.5 x 10s CEM-SS cells were placed in the microtiter well where they were fixed to the bottom of the plate. Sufficient cells were added to form a monolayer of CEM-SS cells in each well. Virus containing supernatant is added from each well of the XTT phase, including viruses and cell controls and each serial dilution of the test substance. The syncytial number was quantified in the 96-well flat-bottomed microtiter plate with an Olympus CK2 inverted microscope at 4 days after infection. Each syncytium resulted from a simple infectious HIV virion. Anti-HIV Activity in Fresh Human Cells: Test in Fresh Human T-lymphocytes Fresh human peripheral blood lymphocytes (PBL) were isolated from voluntary Red Cross donors, seronegative for HIV and HBV. Blood subjected to leukophoresis is diluted 1: 1 with buffered saline with Dulbecco phosphate (PBS), layered on 14 mL of Ficoll-Hypaque density gradient in a 50 mL centrifuge tube. The tubes were then centrifuged for 30 minutes at 600 X.g. PBLs in bands were slightly aspirated from the resulting interface and subsequently washed 2X with PBS by low speed centrifugation. After final washing, the cells were numbered by exclusion of triptan blue and resuspended at 1 x 10 7 / mL in RPMI 1640 with 15% Fetal Bovine Serum (FBS). 2 mM of L-glutamine, 4 μg / mL of PHA-P and allowed to incubate for 48-72 hours at 37 ° C. After incubation, PBLs were centrifuged and reinitiated or readjusted in RPMI 1640 with 15% FBS, 2 mM L-glutamine, 100 U / mL penicillin, 100 μg / mL streptomycin, 10 μg / mL gentamicin and 20 U / mL of recombinant human IL-2. PBLs were maintained in this medium at a concentration of 1-2 x 10E6 / mL with medium changes every two weeks, until used in the assay protocol. For the PBL assay, cells stimulated with PHA-P from at least two normal donors were collected, placed in fresh medium at 2 x 10E6 / mL and applied in plates in the inner wells of a microplate with a round bottom from 96 wells to 50 μL / well. Dilutions of the test drug were prepared at a concentration of 2X in microtiter tubes and 100 μL of each concentration and placed in appropriate points in a standard format. 50 μL of a predetermined dilution of virus material are placed in each test well. Wells with cells and viruses alone were used for virus control. Separate plates were identically established without virus for drug cytotoxicity studies using an XTT assay system. In the standard PBL assay (MOI: 0.2), the assay is terminated on day 7 after collection of cell-free supernatant samples from the reverse transcriptase activity assay. In the low MOI PBL assay (MOI: 0.02), samples of supernatants were collected on day 6, day 11 and day 14 after infection and analyzed for Rl activity. Tritiated thymidine triphosphate (NEN) (TTP) is resuspended in H20 distilled at 5 Ci / l. Poly rA and oligo dT are prepared as a material solution that is maintained at -20 ° C. The reaction buffer RT is prepared fresh on a daily basis and consists of 125 μl IMEGTA, 125 μl of dH20, 110 μl of 10% SDS, 50 μl 1M Tris (pH 7.4), 50 μl 1M DTT and 40 μl 1M of MgCl2. These three solutions were mixed together in a ratio of 2 parts TTP, 1 part poly rA: oligo dT and 1 part of reaction buffer. Ten microliters of this reaction mixture are placed in a round bottom microtiter plate and 15 μl of supernatant containing virus is added and mixed. The plate is incubated at 37 ° C in a water bath with a solid support to avoid immersion of the plate and incubated for 60 minutes. After reaction, the reaction volume is stained on pieces of DE81 paper, washed 5 times for 5 minutes each in a 5% sodium phosphate buffer, 2 times for 1 minute each in distilled water, 2 times for 1 minute each in 70% ethanol and then dried. Opti-Fluor O is added to each sample and the incorporated radioactivity is quantified using a Wallac 1450 Microbetaplus liquid flash counter.

The incorporation of tritiated thymidine is measured in parallel cultures on day 7. Each well is pulsed with 1 μCi of tritiated thymidine and the cells were harvested 18 hours later in a Skatron cell harvester on filter papers with glass fibers. The filters are dried, placed in a blinking flask with 1 ml of flashing cocktail and the incorporated radioactivity is quantified in a Packard Tri-Carbb 1900 TR liquid flash counter. EXAMPLES 55-58 Fresh Human Cell Anti-HIV Activity: Assay in Fresh Human Monocyte Macrophages For isolation of adherent cells, 3 x 106 peripheral blood cells not stimulated with PHA were resuspended in Hanks buffered saline with calcium and magnesium supplemented with 10% human AB serum. The cells were placed in a 24-well microtiter plate at 37 ° C for 2 hours. Non-adherent cells were removed by vigorous washing six times. Adherent cells were cultured for 7 days in RPM1 1640 tissue culture medium with 15% fetal bovine serum. Cultures were carefully monitored for confluence during this incubation period. Infection of the cells is carried out with the BaL or ADA monocytotoxic HIV-1 strains and the coupled pair of AZT-resistant and AZT-sensitive virus isolates. Each of these virus isolates is obtained from the NLAID AIDS Research and Reference Reagent Program. High titre reservoirs of each of these viruses have been harvested from infected cultures of peripheral blood adherent cells and frozen in aliquots of 1.0 ml at -80 ° C. Monocyte-macrophage monolayers were infected at a MOI of 0.1. Compounds to be evaluated in the monolayers were infected at a MOI of 0.1. Compounds to be evaluated in the onocito-macrophage assay were added to the monolayers shortly before infection in order to maximize the potential to identify active compounds. Two days after infection, the medium is decanted and the cultures are washed twice with complete medium in order to remove the excess virus. Fresh medium alone or medium containing the appropriate concentration of drugs are added and incubation continues for an additional 5 days. XTT-tetrazolium or trypan blue exclusion assays for cell viability and HIV p24 ELISA assays for production of p24 core antigen were performed on day 7 post-infection. ELISA kits were purchased from Coulter. Control curves were generated in each assay to accurately quantify the amount of protein capsid in each sample. Data were obtained by spectrophotometric analysis at 450 nm, using a plate reader from Molecular Devices Vmax. Concentrations p24 are calculated from the optical density values by use of the Soft Max software package from Molecular Device.

TABLE 27 MACROFAGO ASSAY FOR VIRACEA 1 Activity pg / mL P-24 o Os TABLE 28 MACROFAGO ASSAY FOR VIRACEA 2 Activity pg / mL P-24 o • i fifteen TABLE 29 MACROFAGO ASSAY FOR VIRACEA 1 Activity pg / mL P-24 o 00 fifteen twenty TABLE 30 MACROFAGO ASSAY FOR V1RACEA 2 Toxicity Studies Absorbance o sO !5 TABLE 31 ANTI-HIV MACROPHASE ASSAY (P24) For VIRACEA # 2-4 15 twenty TABLE 33 ANTI-HIV MACROPHASE TEST (P24) For VIRACEA # 2-5 TABLE 34 VIRACEA # 2-5 fifteen twenty • TABLE 35 ANTI-HIV IN VITRO MACROPHASE ASSAY For VIRACEA 1 TABLE 36 VIRACEA 1 fifteen twenty • • TABLE 37 ANTI-HIV IN VITRO MACROPHASE TEST For VIRACEA 2 15 EXAMPLES 79-90 Fusion Inhibition and Binding Assays These assays use galactosidase-HeLa-CD4-LTR-β cells that employ a tat protein-induced transactivation of the β-galactosidase gene driven by the long-terminal repeat (LTR) promoter HIV-1. The assay is used to quantify both the binding of infectious virions to cells and the cell-cell fusion events. Infected syncytial cells can be easily counted microscopically after incubation with X-gal. The HIV binding inhibition assay involves plating 1 x 10"HeLa-CD4-LTR-B-cells-galactosidase in 200 μl in 96-well flat-bottom microtiter plates.The cells were incubated overnight, the medium was removed and replaced with 100 μl of various concentrations of ISIS 5320 or control compound. One hour later, 100 μl of virus-containing medium is added to each well. Cells were incubated for an additional hour and the monolayer washed extensively to remove unbound and extracellular compound. At 48 hours, the cells were fixed and stained with X-gal. Blue multinucleated cells were then counted under an inverted microscope. The cell-cell fusion inhibition assay was also performed in 96-well flat bottom microtiter plates. HeLa-CD4-LTR-β-galactosidase cells (5 x 103) were added to each well and incubated with the test compound for 1 hour before the addition of 5 x 10 3 HL2 / 3 cells (28). The cells were incubated for an additional 48 hours and fixed and stained with X-gal. Blue syncytia were counted microscopically. Staining of the cells is done by fixing the cells with a solution of 1% formaldehyde and 0.2% glutaraldehyde and staining the fixed cells with 4 μM with potassium ferrocyanide, 4 μM potassium ferricyanide, 2 μM MgCl2 and 0.4 μM. % of X-gal in PBS. The trans-activation of β-galactosidase expression is also verified by ELISA. Cell extracts were prepared by freeze-thawing and assayed for β-galactosidase activity according to the manufacturer's recommendations. The ELISA results were quantified spectrophotometrically at 405 nm using a microtiter plate reader V ax from Molecular Devices.

TABLE 39 Beta-gal Fusion Assay: Viracea # 1 / SKI twenty TABLE 41 Beta-gal Fusion Test: Viracea # 2 / SKl TABLE 42 Fusion Test Beta-gal-Viracea # 2 / SK2 fifteen twenty TABLE 43 Beta-gal Fusion Assay: Viracea # 1 twenty TABLE 45 Beta-gal Fusion Assay: Viracea # 2 15 twenty Topic Microbicide Assay MEI 180 cervical epithelial cells were coated on the inner walls of a 96-well flat bottom microtiter plate at a density of 5 x 10 cells per well and incubated overnight. Chronically infected H9 cells were treated with 200 μg / ml itomycin C in complete medium for one hour, washed extensively and resuspended at 4 x lo5 per ml. The concentration of mitomycin C used resulted in the extermination of chronically infected cells within 48 hours of treatment, allowing sufficient time for cell-cell transmission of virus to the ME-180 cells while ensuring that the endpoint quantification of virus it will not include a contribution from chronically infected cells. Antiviral compounds and chronically infected cells (2 x 10") were added to each well containing ME180 of cells and incubated for 6 hours.After co-cultivation, the monolayer is washed extensively and fresh medium is added. medium and fresh medium is added 24 and 48 hours after infection to remove dead lymphocytes .. On day 6 post-infection, supernatant samples were removed and analyzed for virus content by p24 ELISA CD4 Expression assay Quantification of the effect of Viracea in CD4 expression is performed using standard flow cytometric techniques.The cells were treated with Viracea for one hour at 37 ° C in tissue culture medium.Briefly, 105 CEM-SS cells were incubated with or without compound for 60 minutes at temperature environment Anti-CD4 monoclonal antibodies (20 μl, 4 μg / ml) (Becton-Dickinson, San Jos, CA) were added and the cells were incubated at 4 ° C for 40 minutes. s times with PBS, resuspended in 1 ° C of paraformaldehyde and analyzed using a FACSort flow cytometer from Becton-Dickinson. Macromolecular synthesis CEM-SS cells were cultured in triplicate in the presence or absence of the compound 24 hours at 37 ° C in a humidified C02 incubator. At 24 hours, 1 μC1 of [ethyl-3H] -thymidine, [5-3H] -uridine or [3, 4, 5-3H] -leucine is added to the culture and the incubation is continued for an additional 8 hours. The cells were transferred to glass fiber filter papers by use of Skatron cell harvester. The glass fibers were washed with distilled water, placed in a flash ampule and the amount of radioactivity incorporated was quantified in a Packard Tri-Carb flash counter. HIV Test Results Viracea-1 and Viracea-2 were evaluated in an anti-HIV microtiter assay that quantifies the ability of a test compound to inhibit HIV replication and destruction of HIV-induced cells. The two compounds were determined active against the RF strain of HIV-1 in CEM-SS cells. Cytopathic effects induced by HIV, induced by Viracea-1 (IC30) at a dilution of 1: 400, while Viracea-2 exhibits an IC25 at a dilution of 1,900 and does not reach a 50% inhibitory value. Both Viracea-1 and Viracea-2 exhibit toxicity (TC30) to CEM-SS cells at dilutions of approximately 1:20 and 1: 250 respectively. The positive control compound, ddC, exhibits the expected level of activity against the RF virus. Viracea-1 and Viracea-2 were evaluated for activity in fresh human PBMCs infected with the clinical HIV isolate RED. This low-pass isolate has been defined as a virus isolate that induces drug-sensitive syncytium (AZT, ddC, nevirapine). Neither Viracea-1 or Viracea-2 inhibited the replication of this isolate at non-toxic concentrations. Further evaluation of the compounds in PMBCs infected with RED were performed using IL2 stimulation of PBMCs instead of the PHA blastogenesis. Again, no activity was detected below concentrations that inhibit the growth of PBMCs. AZT exhibits the expected level of activity in these trials.

Viracea-1 and Viracea-2 were evaluated in human fresh monocytes-macrophages infected with low-pass clinical isolated ADA. In these trials, both compounds exhibited high levels of activity with Viracea-2 which is clearly superior. The 50% effective concentration of Viracea-1 and Viracea-2 was 1: 4000 and 1: 1000, respectively. No monocyte-macrophage monolayer toxicity was detected by morphological examination or staining of XTT-Tetrazolium. AZT exhibited the expected level of activity in these trials. Viracea-1 and Viracea-2 were found to inhibit the connection of infectious virus to HeLa-CD4-LTR-β-galactosidase CD4 expression cells. The inhibition of virus binding to the target cells is detected at dilutions of about 1: 1000 to 1: 3200 for both compounds. No compound had an antiviral effect on the fusion of HL2 / 3 cells expressing envelope with HeLa-LTR-β-galatosidase cells. Toxicity was noted for both compounds in the fusion assay where the compound is present for the full duration of the assay, as well as with Viracea-2 in the binding assay where the compound was only present for 2 hours. Chicago Sky Blue, a sulfonated dye exhibited the expected level of activity in each of these trials. Viracea-2 prevented the transmission of the virus from chronically infected lymphocytes to the cervical epithelial cell line ME180 at a dilution of approximately 1: 500 (IC30). No toxicity was detected in this assay to ME180 cells. In this trial, the drug is present during the time of infection alone (4 hours). Dextran sulfate (positive control, sulfated polysaccharide) and dextran (negative control) exhibited the expected level of activity in these assays. Viracea-2 had no effect on the expression of CD4 on the cell surface. Inhibition of thymidine incorporation (DNA), uridine (RNA) or leucine (protein) in high molecular weight macromolecules is observed at dilutions greater than 1: 320. The inhibition of the synthesis of macromolecules was parallel to the toxicity of the compounds in CEM-SS cells. Summary of HIV Test Results Viracea-1 and Viracea-2 inhibit HIV infection in established T-cells with a narrow therapeutic index. Viracea-1 and Viracea-2 potentially inhibit another replication of HIV in monocyte-macrophage. Viracea-l and Viracea-2 inhibit the connection of viruses to target cells but do not prevent the fusion of infected and uninfected cells. Viracea-2 inhibits the transmission of viruses in a topical microbicide assay and may be useful to prevent sexual transmission of HIV. Viracea-2 has no effect on the expression of CD4 on the cell surface. PREVENTION AND TREATMENT The antimicrobial compound provides a microbicide and medicine that can (1) help prevent the sexual transmission of HIV; (2) control viral load of HIV and other viruses; (3) Eradicate HIV; (4) extend the latency periods of the autoimmune deficiency syndrome (AIDS - AIDS) in patients who have contracted HIV; (5) decreases the pain and suffering of HIV patients; (6) reduces the infectious dispersion of HIV; and (7) provides better and more successful treatment of patients with HIV. Medical treatment can also resolve the physical symptoms of an infectious outbreak of HIV, herpes simplex, virus 1 or 2 (HSV 1 or HSV 2) or other infectious microbial diseases. The foregoing can be achieved by systemic application or injection of the above-described preferred antimicrobial compound (medicine) with a syringe in the rectal channel (rectum, rectal tissue, anus or anal tissue) or the vagina (vaginal tissue) of a patient infected with HIV or another infectious microbial disease 8 to 12 times a day, preferably 10 times a day at intervals of every two hours, for a period of 10-18 consecutive days, preferably 14 consecutive days (two weeks) for better results. The dose, concentration and amount of the antimicrobial compound (medicine) can be varied depending on the severity and extent of the disease as well as the age, sex, weight, race and health of the patient. Conveniently, the infected area is rinsed (washed) and dried to remove soap or debris in the infected area before the antimicrobial compound (medicine) is applied. For the treatment of herpes simplex virus 1 or 2, the antimicrobial compound can be applied in the infected area such as for 19-24 hours. Preferably, the vesicular eruption of the herpes virus resolves in 19-24 hours and consequently the herpes lesions are healed. Among the many advantages of medical treatment and medicine (compositions) of the invention are: 1. Superior treatment and prevention of HIV and other infectious diseases. 2. Superior results to end the pain of HIV, viral infections of herpes simplex and other microbial infections without toxicity. 3. Outstanding performance to quickly resolve outbreaks of HIV, herpes simplex virus and other microbial diseases. 4. Save the lives of newborns, children, adults and animals.

. Reduce global economic losses from HIV, herpes and other microbial diseases. 6. It solves a lot of the serious mental and emotional anguish of those affected by HIV and herpes. 7. Easily available materials (ingredients). 8. Economic. 9. Security 10. Ease of use. 11. Reliable 12. Effective. Although modalities and examples of the invention have been shown and described, it will be understood that various modifications and substitutions as well as rearrangements of component parts and process steps, methods and treatments can be performed by those skilled in the art without departing from the spirit and scope. novelty of this invention.

Claims (20)

1. CLAIMS 1. A composition comprising a nutrient and a plant, characterized in that the nutrient comprises folic acid, the plant comprises a herbaceous botanical product of the genus Echinacea and the Echinacea comprises Echinacea purpurea.
2. 2. A composition according to claim 1, characterized in that the composition further includes a second plant comprising a botanical herbaceous product of the genus Commiphora.
3. 3. A composition according to claim 2, characterized in that the Commiphora comprises a species consisting of Commiphora myrrha, Commiphora molmol or Commiphora erythraea.
4. 4. A composition according to any of the preceding claims 2-3, characterized in that the Commiphora comprises Commiphora myrrh.
5. 5. A composition according to any of the preceding claims, characterized in that the composition comprises by weight: from about 2% to about 12% folic acid; from about 40% to about 60% of Echinacea purpurea and Commiphora myrrha; and from about 20% to about 60% water.
6. 6. A composition according to any of the preceding claims 3-5, characterized in that the ratio of Commiphora myrrha to Echinacea purpurea is in the range of about 1: 2 to about 1: 4.
7. A composition according to any of the preceding claims, characterized in that the composition further includes from about 0.02% to less than 0.26% by weight of a quaternary ammonium salt surfactant.
8. 8. A composition according to claim 7, characterized in that the quaternary ammonium salt surfactant comprises benzalkonium chloride.
9. 9. The use of a composition according to any of claims 1-8, in the preparation of a product in the treatment or prevention of sexual transmission of the human immunodeficiency virus (HIV).
10. 10. The use of a composition according to any of claims 1-8, in the preparation of a product in the treatment of herpes simplex virus 1.
11. 11. The use of a composition according to any of claims 1-8. , in the preparation of a product in the treatment of herpes simplex virus 2.
12. 12. The use of a composition according to any of claims 1-8, in the preparation of a product in the treatment of varicella zoster virus (herpes zoster).
13. 13. The use of a composition according to any of claims 1-8, in the preparation of a product in the treatment of cytomegalovirus.
14. 14. The use of a composition according to any of claims 1-8, in the preparation of a product in the treatment of Epstein Barr.
15. 15. The use of a composition according to any of claims 1-8, in the preparation of a product in the treatment of papilloma virus.
16. 16. The use of a composition according to any of claims 1-8, in the preparation of a product in the treatment of influenza.
17. 17. The use of a composition according to any of claims 1-8, in the preparation of a product in the treatment of a virus comprising adenovirus, arbovirus, arenavirus, picornavirus, coronavirus, syncytial virus or cellulitis.
18. 18. The use of a composition according to any of claims 1-8, in the preparation of a product in the treatment of a bacterial infection comprising staphylococci, mycobacterial streptococci or anaerobic bacilli.
19. 19. The use of a composition according to any of claims 1-8, in the preparation of a product in the treatment of encephalitis comprising viral encephalitis or bacterial encephalitis.
20. 20. The use of a composition according to any of claims 1-8, in the preparation of a product in the treatment of meningitis comprising viral meningitis or bacterial meningitis.