“Herpes simplex virus infection has long been a major epidemic problem throughout the world. Up to 10% of the US population has genital herpes and more than a half million new cases are reported each year. The number of people that have oral herpes is vastly higher.
The herpes virus is almost always transmitted through skin to skin contact (sexual or nonsexual) and results in periodic flare-ups of painful or itching blisters and sores around the mouth, face and genital regions. These are sometimes accompanied by fever and other symptoms of infection, particularly during the initial exposure. Most physicians and scientists say that herpes is incurable because they have not yet found a vaccine or other treatment that effectively controls or destroys the virus. The best that they can offer has been complicated, difficult-to follow diets that help keep the virus in its latent (inactive) state, ointments that merely ease some of the symptoms, and a new generation of toxic, marginally effective acyclovir-like drugs that interfere with DNA transcription (both viral and human).” Steven Fowkes www.ceri.com
The Viral Infection Process
“When any kind of herpes-like virus is transmitted from one person to another, the virus particles penetrate the skin, bind to cells near the surface, and inject their DNA or RNA into the cell. This DNA or RNA “hijacks” the DNA-copying and protein-making machinery of the cells. DNA (deoxyribonucleic acid) is the molecule of human inheritance that encodes all the “instructions” and “machinery” necessary to create the structure and coordinate the function of the human body. DNA is like a computer code that translates into words in an encyclopedia. The DNA “words” are called genes, each of which produces a specific protein or enzyme when it is translated. The DNA “volumes” of the encyclopedia are called chromosomes. The human “encyclopedia,” called the genome, consists of 23 volumes (chromosomes). Other animals have different numbers of chromosomes. The DNA in chromosomes is extremely long. A typical human chromosome contains 50 to 300 million nucleic acids strung together in a chain. It takes three nucleotides to code for each “letter,” and a dozen-to-thousands of letters to code for each “word.” Still, that’s a lot of words. This extremely long strand of DNA strand is wound around a protein core called a histone very much like the way thread is wound around a spool. Viral DNA is much smaller. Viral genomes are only 5-50 thousand nucleotides long. They are extremely small because much of the biochemical machinery that they need in order to replicate is provided by the host cell. They only need to carry the “extra” stuff not present in their host. When virus DNA inserts itself into the cell, it is copied (transcribed, translated) repeatedly into RNA, like a Zerox machine making multiple photocopies. These RNA “copies” are then repeatedly translated (transcribed) into proteins. RNA viruses carry an extra protein called reverse transcriptase, which repeatedly copies the RNA into DNA (the reverse of the normal cellular process). This DNA is then repeatedly copied back into RNA the same way that DNA viruses are copied. These DNA-to-RNA and RNA-to-protein processes are the exact same steps by which human DNA is translated into human proteins. Only with viral DNA, you get viral proteins. A virus “assembly line” is created that manufactures new viruses. Some viruses “bud” out through the cell membrane as they are produced, taking a coating of the membrane with them as a lipid envelope. Other viruses simply accumulate in the infected cell to the point where the cell eventually ruptures and is destroyed, spewing forth thousands to millions of new viruses into the blood stream where they travel to infect new cells. If this viral life cycle continues unchecked, the virus will multiply until it either causes serious organ pathology or it kills enough cells to kill its host. Fortunately, the immune system counteracts this process by detecting the virus proteins and destroying infected cells and free viruses.” Steven Fowkes
“In the case of herpes, the immune system has a difficult time getting at the virus because of a lipid (fatty) coating that camouflages most of its proteins. Scientists call herpes a lipid-enveloped virus because of the fat (lipid) found in the outer shell or coat. To the immune system, lipid-enveloped viruses look more like tiny fat droplets than an infectious organism. Not all viruses are lipid enveloped. For example, poliomyelitis (polio) virus, hepatitis A and the common cold virus (rhinovirus) have no lipid covering their outer protein shell. There is not yet any clear evidence yet that suggests that BHT has an effect on non-lipid viruses. However, there has been medical reporting over many decades that antibiotic use seems to result in beneficial effects in viral disease, even though there is no known mechanism (!) why this would be the case (except for the metabolic hypothesis…
Standard vaccination approaches for lipid-viral diseases become difficult-to-impossible because they are based on the immune system’s response to proteins. Lipid-enveloped viral diseases are among the most difficult diseases to treat. Currently identified lipid viruses include all herpes strains, Epstein-Barr virus, human immunodeficiency virus (HIV, all strains), cytomegalovirus (CMV), hepatitis viris (B and C), rubella virus (German measles), varicella virus (chicken pox), Newcastle disease virus, swine fever virus, SARS virus, West Nile virus, and influenza virus (all strains, including bird flu virus).” Steven Fowkes
Herpes Associates with Nerve Ganglia
“Herpes viruses have a special affinity for the human nervous system. Virus that successfully evades the immune system retreats through nerve fibers to nerve clusters (ganglia) near the brain or spinal cord, where they go into a latent state. Sometimes, the virus will remain in this state for life, causing no apparent harm. In many cases however, it is awakened periodically by changes in body chemistry due to stress, diet, illness, weakened immune system, menstruation, overexposure to sunlight, or other causes. Even sexual activity can trigger the dormant virus to become active. The virus then travels from the ganglia, through the nerve fibers, back to the same area that it first affected and the victim has another episode of sores and blisters. These eventually subside as the virus retreats once more to its hiding place in the ganglia, where it remains until it is triggered again into its active state.” Steven Fowkes
What is BHT?
“BHT (butylated hydroxytoluene) is a synthetic food preservative that is widely used in the US to prevent rancidity in fat-containing foods, such as breakfast cereals, baked goods, potato chips, pork sausage, peanut butter, instant potatoes, and other commercially prepared foods. Even foods labeled “no preservatives” or “no preservatives added” may and often do contain BHT which was present in the ingredients used in making the food.” Steven Fowkes
Mechanisms of BHT’s Action
“In test-tube experiments, scientists have identified two specific ways in which BHT inactivates lipid-containing viruses. First, it disrupts the virus’s lipid envelope, leaving it naked and vulnerable to attack by the immune system. Second, it removes binding proteins that viruses need to bind to and penetrate cell membranes. Without these binding proteins, viruses are non-infective. Whether or not these mechanisms are applicable to living animals has not been determined. In fact, it may be near to impossible to make that determination. In test-tube experiments, scientists can utilize viral preparations that are 100% whole (i.e., they have been purified to remove all viral fragments). They can then study whether whole viruses disintegrate in response to an antiviral agent. This is not the case with lab animals suffering from a viral infection. The viral replication process (the assembly line) is not particularly efficient. There are many more viral parts produced that there are fully assembled viruses. Massive numbers of viral fragments are released when an infected cell ruptures. Scientists cannot easily distinguish between viral fragments that are a natural product of inefficient viral replication and viral fragments that are produced by BHT disruption of intact viruses. So in real-life, we haven’t yet figured out how BHT works. Despite these unanswered questions, researchers have found that BHT does interfere in the course of lipid-enveloped viral diseases. Animals given BHT resolve their lipid-enveloped viral diseases much faster than otherwise. And people using BHT do experience relief from their herpes infections. Empirically, it works.
…Topical application of BHT maximizes skin concentrations of BHT which can be especially important with skin-active viral diseases like herpes and shingles.”
BHT is not a cure for herpes. Once infected, the herpes virus inserts itself into our DNA and becomes, essentially, a part of our genes. BHT does not change that. No known technology can yet change that. However, BHT does have antiviral activity against the “active” viruses that cause symptoms and infect new cells. BHT may even be able to block herpes infection in the first place—and reinfection in people already infected—if used prophylactically.” Steven Fowkes
Below are scientific cites regarding BHT:
A Comparison of Herpes Simplex Virus Plaque Development After Viral Treatment With Anti-DNA or AntiLipid Agents, Thomas P. Coohill, Michael Babich, William D. Taylor, and Wallace Snipes, Biophysics Program, Western Kentucky University, Bowling Green, Kentucky 42101, and Department of Biochemistry and Biophysics, Pennsylvania State University, University Park, Pennsylvania, 16802 U.S.A.
The plaque development of Herpes simplex virus type 1 (HSV) is slower for viruses treated with two anti-DNA agents: ultraviolet radiation (UV) or n-acetoxy-2-acetyl-aminofluorene. For HSV treated with three anti-membrane agents -butylated hydroxytoluene, acridine plus near UV radiation, or ether-the plaque development time is the same as for untreated viruses. These differences hold even for viruses that survived treatment that lowered viability below the 1% level. Gamma ray inactivation of HSV produces no change in plaque development even though this agent is believed to preferentially affect viral DNA. All rights reserved.
Inactivation of the Lipid-Containing Bacteriophage PM2 by Butylated Hydroxytoluene, James cup, Paul Wanda, Alec Keith,* and Wallace Snipes, Department of Biophysics, The Pennsylvania State University, University Park, Pennsylvania 16802, Received for publication 9 July 1975, Antimicrobial Agents and Chemotherapy, Dec. 1975, p. 698-706 Copyright C) 1975 American Society for Microbiology Vol. 8, No. 6 Printed in U.S.A.
Several factors have been investigated which are of significance in the inactivation of PM2, a lipid-containing bacterial virus, by butylated Hydroxytoluene (BHT). Studies of the time dependence of inactivation during exposure to BHT showed that virus killing occurs rapidly, with the majority of the effect taking place in the first 5 min. The degree of inactivation is dependent upon the initial virus titer, the solvent from which BHT is added, and the presence of a variety of protective agents, including surfactants, bovine serum albumin, and bacterial cells. Sucrose gradient analysis of 32P-labeled, BHT-treated virus was used to determine the degree to which the virion is disrupted by BHT. These experiments show that the 32P-labeled molecules are converted into very slowly sedimentable material by BHT treatment, indicating complete destruction of the virus particle. All rights reserved.
Inactivation of the Enveloped Bacteriophage φ6 by Butylated Hydroxytoluene and Butylated Hydroxyanisole, Paul Wanda, James Cupp, Wallace Snipe,* Alec Keith, Tom Rucinsky, Louis Polish, and Jeffrey Sands, Antimicrobial Agents and Chemotherapy, July 1976, p. 96-101 Copyright 0 1976 American Society for Microbiology, Vol. 10, No. 1, Printed in U.S.A. Biophysics Laboratory, Department of Biochemistry and Biophysics, The Pennsylvania State University, University Park, Pennsylvania 16802,* and Physics Department and Molecular Biology Program, Lehigh University, Bethlehem, Pennsylvania 18015 Received for publication 5 April 1976
Butylated hydroxytoluene (BHT) is a potent in activator of the enveloped bacterial virus φ6 at concentrations as low as 3 x 10-5 M. The viral envelope is not removed by BHT treatment, in contrast to the effects of exposure to the detergent Triton X-100. BHT-treated viruses are morphologically indistinguishable from controls but are defective in their ability to attach to the host cell. Temperature at the time of exposure was found to .be a crucial factor in the effectiveness of BHT against φ6. A precipitous drop in the degree of inactivation by 3 x 10-5 M BHT occurred when the temperature was lowered from 20 to 15 C. Calcium ions were found to potentiate the effect of BHT, particularly at lower temperatures where BHT alone was relatively ineffective. Barium and strontium, but not magnesium, were also effective in enhancing the activity of BHT. A structurally related molecule, butylated hydroxyanisole (BHA), was also found to inactivate φ6 virus, but higher concentrations were required than with BHT. Both BHT and BHA are commonly used as food additives, have apparent low toxicity to humans and other animals, and are potentially useful as antiviral agents. All rights reserved.
Dennis H. Bamford. Lipid-containing bacterial viruses: Disruption studies on φ6. Prog Clin Biol Res 64: 477-89, 1981.
Neal DeLuca, Alec Keith and Wallace Snipes. Studies with a hydrophobic, spin-labeled virucidal agent. Antimicrob Agents Chemother 17(1): 63-70, Jan 1980.
S. Eletr, M.A. Williams, T. Watkins and A. Keith. Perturbations of the dynamics of lipid alkyl chains in membrane systems: Effect on the activity of membrane bound enzymes. Biochim Biophys Acta 339: 190-201, 1974.
Bulylated Hydroxytoluene Inactivates Lipid – Containing Viruses, W. Snipes, S. Person, A. Keith, and J. Cupp, Science, Vol. 187, p. 64-66.
Inactivation of Lipid – Containing Bacteriophage PM2 by Butylated Hydroxytoluene, James Cupp, Paul Wanda, Alec Keith, and Wallace Snipes; Antimicrobial Agents and Chemotherapy, Vol. 8, Num. 6, p. 698-706, Dec. 1975.
Butylated Hydroxytoluene in Sarcoma – Prone Dogs, Robert Alan Franklyn; The Lancet, p. 1296, 12 June 1976.
Butylated Hydroxytoluene Protects Chickens Exposed to Newcastle Disease Virus, Max Brugh, Jr., Science, Vol. 197, p. 1291-2, Sept. 1977.
Inactivation of Cytomegalovirus and Semliki Forest Virus, by Brugh M. Butylated hydroxytoluene protects chickens exposed to Newcastle disease virus. Science 197, p 1291-1292, 1977.
Coohill TP, Ferrell BR, Carson D, and Elliott LP. Orally administered butylated hydroxytoluene inhibits herpes simplex virus (type I) infection in rabbits. Presented at the Eighty- third Annual Meeting of the American Society for Microbiology, New Orleans, LA (abstract number S41) March 6-11, 1983.
Denz FA and Llaurado, JG. Some effects of phenolic anti- oxidants on sodium and potassium balance in the rabbit. British Journal of Experimental Pathology, Vol 38(5), p 515- 552, 1957.
Fisherman EW and Cohen G. Chemical intolerance to butylated- hydroxyanisole (BHA) and butylated-hydroxytoluene (BHT) and vascular response as an indicator and monitor of drug intolerance. Ann Allergy 31(3), p 126-133, March 1973.
Franklyn RA. Butylated hydroxytoluene in sarcoma-prone dogs. The Lancet, p 1296, June 12, 1976.
Freeman DJ, Wenerstrom G and Spruance SL. Treatment of recurrent herpes simplex labialis with topical butylated hydroxytoluene. Clinical Pharmacology and Therapeutics 38, p 56-59, 1985.
Ito N., Fukushima S. and Tsuda H. Carcinogenicity and modification of the carcinogenic response by BHA, BHT, and other antioxidants. Critical Reviews In Toxicology 15(2) p 109-150, 1985.
Keith AD, Arruda D., Snipes W. and Frost P. The antiviral effectiveness of butylated hydroxytoluene on herpes cutaneous infections in hairless mice. Proceedings of the Society for Experimental Biology and Medicine 170, p 237-244, 1982. Kim KS., Moon HM., Sapienza V., Carp RI. and Pullarkat R. Inactivation of cytomegalovirus and Semliki Forest virus by butylated hydroxytoluene. The Journal of Infectious Diseases 138(1), p 91-94, July 1978.
Kim KS., Moon HM., Sapienza V., Carp RI. and Pullarkat R. Inactivation of cytomegalovirus and Semliki Forest virus by butylated hydroxytoluene. The Journal of Infectious Diseases 138(1), p 91-94, July 1978.
Llaurado JG. The saga of BHT and BHA in life extension myths. Journal of the American College of Nutrition 4, p 481-484, 1985.
Mann JA. and Fowkes, SW. Wipe Out Herpes With BHT. Megahealth Society, P.O. Box 1684, Manhattan Beach, CA, 1983.
Pearson D. and Shaw S. The herpes epidemic: a possible solution. In The Life Extension Companion, Warner Books, New York, NY, 1984.
Richards JT., Katz ME. and Kern, ER. Topical butylated hydroxytoluene treatment of genital herpes simplex virus infections of guinea pigs. Antiviral Research 5, pages 281- 290, 1985.
Shlian DM. and Goldstone J. Toxicity of butylated hydroxytoluene. New England Journal of Medicine, p 648-649, March 6, 1986.
Snipes W., Person S., Keith A. and Cupp J. Butylated hydroxytoluene inactivates lipid-coated viruses. Science 188, p 64-66, April 4, 1975.
Tsuda H., Fukushima S., Imaida K., Sakata T. and Ito N. Modification of carcinogenesis by antioxidants and other compounds. Acta Pharmacol Toxicol 55 (Supplement 2), p 125- 143, 1984.
Winston VD., Bolen JB. and Consigli RA. Effect of butylated hydroxytoluene on Newcastle Disease virus. American Journal of Veterinary Research 41(3), p 391-394, 1980.
Witschi HP. Enhancement of lung tumor formation in mice. Carcinogenesis 8, page 147-158, 1985. Hydroxytoluene, K.S. Kim, H.M. Moon, V. Sapienza, R.I. Carp, and R. Pullarkat; Journal of Infectious Disease, Vol. 138, Num. 1, p. 91-4, July 1978.
Studies with a Hydrophobic, Spin – Labeled Virucidal Agent, Neal De Luca, Alec Keith, and Wallace Snipes; Antimicrobial Agents and Chemotherapy, Vol. 17, Num. 1, p. 63 -70, Jan. 1980.
Effects of Butylated Hydroxytoluene on Newcasle Disease Virus; Vern D. Winston, Joseph B. Bolen and Richard A. Consigili; American Journal of Veterinary Research, Vol. 41, Num. 3, p. 391 -4, 1980.
Lipid – Containing Bacterial Viruses: Disruption Studies on φ6, Dennis H. Bamford, Prog. Clin. Biol. Res. 64:477 – 89, 1981.
The Antiviral Effectiveness of Butylated Hydroxytoluene on Herpes Cutaneous Infections in Hairless Mice, Alec D. Keith, Dorris Arruda, Wallace Snipes, and Phillip Frost; Proceedings of the Society for Experimental Biology and Medicine, Vol. 170, p. 237 – 44, 1982.
Inactivation of Lipid – Containing Viruses with Butylated Hydroxytoluene, U.S. Patent No. 4350707, Sept. 1982.
Wipe Out Herpes with BHT by John A. Mann and Steven Wm. Fowkes, Published by the Mega Health Society.
Free Radical Theory of Aging: Free Radical Reactions in Serum, D. Harman and L.H. Piette, J. Gerontol. 21: 560, 1966.
Free Radical Theory of Aging: Effects of Free Radical Reaction Inhibitors on Mortality Rate of Male LAFI Mice, D. Harman, J. Gerontol. 23: 476 – 82, 1968.
Free Radical Theory of Aging: Effects of Free Radical Inhibitors on the Life Span of Male LAFI Mice, Second Experiment, Denham Harman, Gerontologist 8:13, 1968.
Free Radical Theory of Aging: Dietary Implications, Derham Harman, Am. J. Clin. Nutr. 25:8, 839 – 43, Aug. 1972.
Brugh M. Butylated hydroxytoluene protects chickens exposed to Newcastle disease virus. Science 197, p 1291-1292, 1977.
Butylated Hydroxytoluene Inactivates Lipid – Containing Viruses, W. Snipes, S. Person, A. Keith, and J. Cupp, Science, Vol. 187, p. 64-66. Freeman DJ, Wenerstrom G and Spruance SL. Treatment of recurrent herpes simplex labialis with topical butylated hydroxytoluene. Clinical Pharmacology and Therapeutics 38, p 56-59, 1985.