Herpes simplex virus (HSV) infections are commonly regarded as being incurable. Yet ongoing studies have questioned this dire assumption. For many patients, the answer to herpes virus eradication appears to lie in activating a natural alternative cellular energy (ACE) pathway to fortify cells in their competition with the virus. This can be achieved by directing therapy at the site of reactivating skin lesions and by boosting the ACE pathway through an IDEA program comprising i) Intention to be cured; ii) Detoxification; iii) consumption of Enerceuticals and iv) physical Activation of the ACE pathway. The goal of therapy extends beyond the absence of further clinical recurrences to the actual disappearance of detectable anti-HSV antibodies. Pursuit of these studies holds enormous promise for the suppression of other viruses, including those that have undergone stealth adaptation.

Herpes Viruses

The presence of serum antibodies that can differentiate between HSV-1 and HSV-2 provides a means for assessing whether an individual has been previously infected with one or both of these viruses. Anti-HSV-1 antibodies are present in up to 90% of the adult human population. Anti-HSV-2 antibodies are present in approximately 20% of the adult population with a marked racial difference of 17% among whites and 48% among blacks.

Herpes viruses generally remain inactive (latent) in nerve ganglia for long periods of time. In some individuals, and for reasons not fully understood, the viruses may periodically replicate in the nerves and re-migrate back to the region of primary skin infection. The re-infecting virus can lead to localized areas of cell damage that provokes a rapid and intense anti-viral inflammatory reaction, followed by a healing process. These outbreaks are referred to as recurrent herpes and occur in fewer than 10% of seropositive individuals. Using very sensitive molecular based assays, periodic sub-clinical virus shedding from either the oral or genital mucosa can be demonstrated in the majority of seropositive individuals.

The clinically apparent skin lesions appear as one or more small swellings of intact skin (papules) that form fluid filled vesicles within one to three days. After several more days the vesicles becomes crusted. The crusts promptly shed and the underlying skin reforms without scarring. Periods of virus shedding can occur without the formation of obvious lesions, while in other patients the lesions can be annoyingly large, multiple and painful. The frequency of recurrences and of asymptomatic shedding, vary widely between individuals and even within the same patient. Skin lesions tend to become less common, especially over the first few years. Recurrent herpes can be socially embarrassing and in the case of genital infections can adversely affect sexual relationships. Even determining that an asymptomatic individual is seropositive for HSV-2 has been used to raise the possibility of sexual transmission of infection and to justify long term use of marginally effective drug therapy. Occasionally, HSV can lead to very severe illnesses including blindness from eye infection, encephalitis from brain infection and neonatal herpes from infection of the developing fetus. Genital HSV lesions can also facilitate the transmission of human immunodeficiency (HIV) virus and hasten the progression to AIDS.

HSV viruses belong to a large group of structurally related viruses that infect humans and animals. Additional human herpes viruses (HHV) include varicella zoster virus (HHV-3); Epstein-Barr virus (HHV-4); cytomegalovirus (HHV-5) and human herpes viruses, 6, 7 and 8. The virus genome comprises linear double stranded DNA compacted into a nuclear capsid surrounded by a collection of proteins comprising a tegument within an outer glycoprotein containing lipid envelop.

Herpes virus induced cell damage is best viewed as a competition between viral and cellular strategies. The virus needs to co-opt many cellular processes for its survival and replication. It also needs to disarm various mechanisms by which the body can suppress virus replication. Emotional stress is widely viewed as one of the triggering factors in virus reactivation, while the immune system is recognized as an important host defense mechanism. In reality, the immune system is quite effective in limiting virus induced damage to only localized areas of the skin and for periods of only several days. Indeed, studies on recurrent lesions have shown falling virus levels after the first day of a recurrent outbreak. Much of the remaining time consists of a tissue repair process.

Alternative Cellular Energy (ACE) and Stealth Adapted Viruses

While important, the immune system is not the only defense mechanism available to the body. Especially with recurrent lesions, the areas of outbreaks accumulate materials termed alternative cellular energy (ACE) pigments. These materials were initially identified in studies on herpes viruses, including cytomegaloviruses, which failed to activate a cellular immune inflammatory response. These viruses were termed stealth or stealth-adapted. Detailed studies on a stealth-adapted African green monkey simian cytomegalovirus (SCMV) isolated from a patient with a moderately severe, persisting, chronic fatigue syndrome (CFS), showed deletions or mutation of the three genes that correspond to those that code for the antigens that are targeted by over 90% of anti-human cytomegalovirus cytotoxic T cells. The virus presumably originated as a contaminant of a live polio vaccine, since these vaccines were routinely being produced using kidney cell cultures of SCMV infected African green monkeys. The prototype SCMV-derived stealth-adapted virus readily induced severe, non-inflammatory illness when inoculated into cats. The acute illness lasted 2-3 weeks and was followed by near complete recovery. Similarly, repair and recovery of tissue culture cells infected with stealth-adapted viruses will occur if ACE pigments are allowed to accumulate within the culture fluid. Virus reactivation rapidly occurs by simply replacing the tissue culture fluids and thereby removing ACE pigments. The reactivation process can be prevented by including ACE pigments in the replacing fluid.

ACE pigments display prominent energy based activities, including electrical charge separation, electron donating (reducing) activity, auto-fluorescence and occasionally ferromagnetism. They comprise both minerals and organic, (commonly aromatic), compounds and have the capacity to self assemble into discrete fibers and other particles. The fluorescence evoked by ultraviolet light can be enhanced by certain dyes including acridine orange, neutral red and saffranine.

Dye/Light Therapy of HSV

The application of neutral red dye to HSV lesions followed by light illumination was commonly practiced in the early 1970’s. The presumed principle of action was the neutral red mediated formation of oxygen free radicals, which were known to damage the lipid envelopes and nucleic acids of viruses, including HSV. In spite of early reports of success in recurrent, but not primary herpes skin lesions, subsequent controlled trials using regular light sources failed to establish efficacy. The incandescent light chosen for these controlled studies was based on it having a green light component that could activate the neutral red dye. Some of the earlier studies had used fluorescent lights that probably emitted ultraviolet light in addition to regular white light.. A concern expressed at the time of these studies was that partial damage to HSV could result in a virus with possible cancer causing capacity. This concern, along with the negative double blind studies and the advent of anti-HSV drugs such as Acyclovir led to an abandonment of light therapy for HSV.

In another study, light illuminated neutral red was tested in patients with persistent multiple genital warts caused by human papillomavirus (HPV). Although the treated warts resolved, the study was dismissed because resolution also occurred in the untreated warts on the same patient. The ineffectiveness of dye light therapy in primary HSV lesions and the regression of both treated and untreated HPV lesions are understandable in terms of the ACE pigment activation hypothesis.

Based on his own studies an optometrist, Dr. Jon Stoneburner, was convinced that neutral red was an effective therapy providing an ultraviolet light source was used and that this therapy dramatically reduced the rate of further recurrences. The procedure also required that the neutral red dye be freshly prepared and a small amount of chlorine be added to the neutral red solution. The possible role of the neutral red is to reduce oxygen quenching of the potential fluorescence of UV activated ACE pigments. This model is in keeping with a presumption that the ACE pathway probably preceded atmospheric oxygen and conventional photosynthesis. It is also in keeping with long term activity of anaerobically stored neutral red compared to the loss of fluorescence enhancing activity of aerobically stored neutral red. This proposition can be tested using other oxygen barrier methods.

Dr. Jon Stoneburner had used a similar approach in the therapy of shingles caused by herpes zoster virus (HZV) and genital warts caused HPV. An Institutional Review Board (IRB) approved clinical trial comparing neutral red with a food coloring dye confirmed these findings. The results of the trial were published in a peer reviewed medical journal ().

The Food and Drug Administration (FDA) was notified of the results. FDA insisted that the neutral red by classified as a drug and that further testing be placed under the primary jurisdiction of the Center for Drug Evaluation and Research (CDER), rather than the Center for Devices and Radiological Health (CDRH). This change required formal submission and approval of Investigational New Drug (IND) applications that would cover every phase of further studies that could lead to eventual consideration of licensure. The FDA ombudsman did not respond to a reported FDA employee’s statement that because the therapy was challenging an 18 billion dollar industry, that the application process would be purposely held up. Nevertheless, an initial IND application for a study on 8 HSV infected patients was submitted to the FDA and approval was obtained.

Pharmaceutical Based Therapy of HSV Skin Lesions

Acyclovir is a guanine nucleoside analog that is selectively phosphorylated by a kinase enzyme coded by HSV. Its discovery contributed to the awarding of the 1988 Nobel Prize in Medicine and became the single most profitable drug for Burroughs Wellcome. In most patients, it reduces the duration of HSV lesions by several days and long term use can reduce, but rarely eliminates the reoccurrence of active lesions. Having come off patent, the drug cost is approximately $10.00 for a month’s supply. In contrast, a prodrug of acylovir, valacylovir (Valtrex), is still on patent and markets in the United States at nearly $200.00 for a month’s supply. Both acylovir and valacylovir have been associated with severe neurological and/or renal damage in a small number of recipients. Multiple additional adverse effects can occasionally occur. Although treated animals have not shown an increased incidence of cancers, in vitro tests have clearly shown the potential of these drugs to cause genetic damage. Some HSV isolates are lacking the gene for the specific kinase and are, therefore, resistant to acyclovir and its prodrug.

Complimentary/Alternative Medicine (CAM) Protocols

While still lacking formal validation in controlled clinical trials, a number of naturopathic healthcare practitioners have claimed success using a wide variety of herbal formulations in conjunction with lifestyle and dietary changes. A striking feature garnered from interviewing such patients is the extent to which the intention to get well appears to have played a major role in the patient’s recovery. This realization has led to the exciting possibility that the brain may help function in the activation of ACE pigments. This notion extends a basic assumption of several branches of non-orthodox medicine, including neural therapy, chiropractic and oriental healing.

Consuming more whole foods, including uncooked raw vegetables, also appear to have benefited these patients. One potential explanation is that such diets help minimize intake of pesticides while at the same time providing materials that may assist in the elimination of toxins. Indeed some CAM practitioners largely focus their efforts on detoxifying their patients even before resorting to the use of various herbs. A class of dietary supplements has been termed “enerceuticals™” since they appear to provide a dietary source of ACE. Included in these products are water extracted terpenes/terpenoids and organically bound minerals such as humic/fulvic acids. Certainly some patients have attributed these protocols to a complete freedom from future outbreaks of herpetic lesions. An important observation in some of these patients is the actual disappearance of anti-HSV antibodies; a finding that is consistent with the complete eradication of infectious HSV. Such a conclusion has helped alleviate much of the anguish of HSV infected individuals concerning possible transmission of infection to sexual partners, and in the case of pregnant women, to their fetus or newborn child.

The IDEA Program

A comprehensive non-pharmacological approach to treating recurrent herpes infections is being formulated by the Institute of Progressive Medicine and undergoing evaluation for optimization. It combines the goal of achieving an Intention to get well with effective Detoxification methods followed by the use of Enerceuticals™. ACE pigments are “Activated” using an ultraviolet light or alternative energy source. The light mediated activation will commonly need to be triggered by contact with a freshly prepared neutral red dye. ACE pigment activation is easier with active lesions, but recent studies have confirmed the retrieval of ACE materials from skin and hair. This approach is a work in progress with the end points being not only a cessation of recurrent herpes but the seroconversion from HSV positive to negative status.

Summary