If one looks back into the medical literature, many different treatment recommendations can be found for herpes infections (HI) going back many decades. Prior to the arrival of effective anti-viral compounds, treatment options included such diverse concepts as topical application of deoxyglucose or the surgical removal of infected areas. The former ultimately was proved to be ineffective, and the latter resulted in individuals having viral recurrences along the surgical scar. Neither, of course, are recommended by anyone today.

The message, though, is that desperate people who are suffering will often jump at offers of "cures" from various medical and quasi-medical solutions which have not been substantially examined by peer-reviewed research. The results of these "solutions" in fact may include increased suffering by the victim and a worsened public health outcome both for the victim and the victim’s consorts.

The author respectfully requests that the reader take a few minutes and review this paper. The reader will find a broad, readable discussion about the current recommended treatments for HI. After reading this discussion, hopefully the appropriate treatment(s) for the condition will become apparent.

Herpes is a virus that infects the nervous system, modifying the DNA of the nerve cells supplying the skin through which the virus entered. The infection is permanent. Most patients suffer from recurrences that may vary in frequency from once in a lifetime to non-stop infections that never go away. The average rate of recurrences is about four times per year, plus or minus one or two, with some variation of recurrence rate by gender. Recurrences typically take about a week or so to heal. This means that the average untreated person with HI spends about a month out of the year with lesions.

Another fact about having an infected nerve cell is that the cell may be making viral particles at any time, perhaps most of the time. The signs of recurrence on the skin apparently are related to the production of a large amount of viral particles. Probably when the nerve cell makes fewer viral particles, the skin may not show signs. Put another way, the nerve cell may be actively producing viral particles even though the skin has no rash or redness. This condition is called "asymptomatic viral shedding". The general consensus is that any person with HI who does not have any symptoms currently in fact is shedding virus about 4% of the time. Put another way, an asymptomatic person with HI has a 1 in 25 chance of being contagious at any given time. This is true assuming of course that the person is not on medications (see below). Current research in female patients puts the asymptomatic viral shedding rate in genital Herpes infections (GHI) even higher in one published study.

The problem with HI, therefore, is that a piece of viral DNA resides permanently in a nerve cell . This viral DNA is periodically copied and turned into viral particles that may generate contagious viral shedding or cause a contagious rash. It is through interfering with the process of the formation of viral particles where the opportunity comes to "treat" the problem and prevent the spread of these particles to non-infected patients.

The mainstay of treatment is in the identification of the illness and forming a rational plan to manage the condition. Evidence exists that patients "auto-inoculate" themselves. In this condition, the patient makes him/herself worse, either through the spreading of the infection on the skin to adjacent skin areas OR actual spread from nerve cell to nerve cell in the area where the nerve cell lives beside the spinal cord (called the ganglion). The former occurs in part when the untreated rash is allowed to remain undrained and uncleaned. The latter probably occurs at various time, including when the patient has symptoms and does not take medication to terminate the symptoms.

The first point of care then is that a person with symptoms needs a diagnosis. Any person with an oral or genital/rectal rash, especially associated with blisters, pain, or pain referred into the buttocks or legs, should be seen and evaluated by a physician or other trained medical professional skilled in the evaluation and management of HI. A viral culture should be taken of a lesion at some point in the person’s medical history to attempt to identify the organism. The patient’s consort should be counseled and possibly evaluated along with the patient.

Blood tests to establish diagnosis of HI are not always very helpful. The only REAL way to document that a patient has suddenly developed HI from a blood test is to draw blood quickly after the onset of symptoms and to document that the patient’s blood test is negative. Then 4 to 6 weeks later a second blood test is drawn to document that the patient has suddenly developed antibody against the virus. Even then, these tests are not completely reliable and often do not give clear and concise answers.

Smart living prevents infections. It is clear from various studies that educated patients and educated consorts can drastically reduce the transmission of infections. While it has been shown in earlier studies that consorts do often become infected, it is also clear that the use of anti-viral medications (see below) decreases both recurrence frequency and viral shedding. Medication combined with smart living and use of condoms can drastically lower disease transmission. This is not a guarantee, of course, but it does offer some reassurance that in the symptom-free patient who is taking medications as directed and using a latex condom, the risk of transmission is very, very low, possibly as low as one chance in a thousand per exposure.

The combination of smart living with anti-viral medications (in patients for whom these medications work) can potentially create a vast public health improvement affecting literally millions of individuals.

Anti-Viral Medications

About twenty years ago it was noticed that certain viral infections could be treated through the use of chemicals that are part of DNA. Specifically, modified "bases" could be applied topically (on the outside of the body) in the setting of virus infections in the eye, for example, that could improve the infection. Soon to follow was the use of a modified "guanosine", called acyclovir, as a cream to be applied onto HI lesions, which produced some modest improvement in symptoms. The rash would clear up a couple of days quicker than if no cream were used. Recurrence frequency was not affected.

About 15 years ago acyclovir became available for oral use. Studies rapidly appeared indicating that the medication was not only safe but highly effective. When taken as directed, patients’ symptoms of both acute infections and recurrences rapidly improved. When the medication was taken ONLY for recurrences, little influence was found upon recurrence frequency.

About 10 years ago it was found that acyclovir, when taken on a daily basis, could decrease recurrence frequency to about once per year. Also, it was found that when a recurrence DID occur, it was milder and of shorter duration. Further, recent studies have indicated that asymptomatic viral shedding was reduced as much as 80% in patients who took acyclovir regularly.

How does Acyclovir work? Its actual effect in killing virus has not been definitely proved. Acyclovir has several actions in the test tube. It inhibits the enzymes that copy viral DNA, and it also inhibits the replication of virus. Also, again in the test tube, acyclovir is taken up into the growing chains of viral DNA, causing termination of these chains. Acyclovir seems to be "selectively" taken up by infected cells. Acyclovir is much less toxic for normal cells because less is drug is taken up, less is converted to active form, and normal cell enzymes are less sensitive to the chemical (to paraphrase the PDR online).

The problem with acyclovir is this: It doesn't stay in the body very long, and when taken by mouth, its blood levels are fairly low. A modification of the acyclovir molecule, called valacyclovir, gives higher blood levels. As a matter of fact, valacyclovir is able to achieve blood levels almost equivalent to the intravenous administration of acyclovir.

The use of any anti-infective chemical can be associated with increasing the occurrence of resistant organisms. Certainly this is also true in the case of acyclovir for HI. Resistant organisms have occurred, in some cases requiring multiple anti-viral medications to control symptoms. Interestingly, one study suggested that allowing break periods in the administration of acyclovir allowed sensitivity to the drug to return. This technique is speculative and not currently recommended.

That being said, however, HI resistance to acyclovir and the other antiviral medications is relatively rare. Specifically, the percentage of cases of acyclovir resistance seems to be stable at about 0.3% of all persons with herpes infections. This means that 99.7% of people with herpes infections carry viruses that are sensitive to acyclovir, and this is great news for almost everyone that has a herpes infection. If outbreaks occur, then if acyclovir is taken (or the other antivirals such as famciclovir or valacyclovir), almost certainly the outbreak will come under control.

Almost all patients can control symptoms through Smart Living concepts along with medication. The medication is very well tolerated and has few side effects.

How much medication is enough? For acute episodes the recommended dosage of acyclovir is 200 mg taken five times per day for approximately ten days, possibly longer. This author’s clinical experience indicates that 400 mg taken two or three times daily is probably equally effective.

The dosage of valacyclovir is 500 to 1000 mg daily for outbreaks. This medication can be taken once or twice daily, which is more convenient for most people. The duration of the therapy is the same as for acyclovir. The cost of the brand product of valacyclovir is much higher than generic acyclovir, so the consumer will have to weigh if an additional benefit is brought by the additional cost.

Therapy for recurrences can be performed in two ways: Episodic therapy, and chronic suppressive therapy. In the first, the patient takes about 400 mg of acyclovir two or three times per day (whichever level it takes to reduce symptoms) for about a week or ten days. The dosage of valacyclovir is 500 to 1000 mg once or twice daily, depending on the responsiveness of the patient. Most patients will promptly clear their symptoms on this level of medication. Depending on the patient’s "disease level", either the condition will go away for an indefinite period OR the patient will then have another recurrence once off the medication.

Patients who seem to have regular recurrences in spite of Smart Living and/or in spite of episodic therapy are candidates for chronic suppressive therapy. In this treatment method, the patient will take a daily dosage of acyclovir or valacyclovir either once or twice daily. The dosage per pill will be 200 mg to 800 mg for acyclovir and 500 mg to 1000 mg for valacyclovir. The minimal dosage that will control symptoms is the dosage that should be taken. Given this treatment method, recurrences in almost all patients can be reduced to once or twice per year, and the recurrences that occur will be milder. One should also remember that asymptomatic shedding will be substantially reduced on chronic suppressive therapy, which should reduce how contagious a person with GHI will be.

Famvir, a drug similar to acyclovir (penciclovir), theoretically, would seem to offer some advantage for therapy because of the increased presence of the medication within the cell, due to the manner in which the medication is phosphorylated. One would think that a medication which is more rapidly absorbed AND which persists longer inside the target area would in fact give a substantially improved effect. At this point, this does not seem to be the case based upon readily available patient treatment data.

How long can a patient safely be on acyclovir or other antivirals.? Two papers (Baker from Stony Brook and Goldberg from Baylor, possibly reporting the same data) report a study going out five years. No side effects were reported in the abstracts, and viral resistance to acyclovir was "not observed". Recurrences were diminished from a mean of about 13 recurrences per year to less than one, a reduction of 92%. They found that the recurrence frequency continued to be reduced into the third year on medication, and beyond that no further reduction in recurrence frequency was noted. In this study the dose of acyclovir was 400mg twice daily. The reader is referred to the quoted New England Journal article above suggesting that the patient should tailor the dosage to the minimum needed to "control symptoms".

Studies going out nearly a decade of patients on continuous acyclovir therapy continue to reveal the safety of antiviral medications for herpes infections when taken daily for many years. No toxicity was reported in these studies, nor was there an increase in viral resistance to the medication.

How should a patient actually take the medication when on suppressive therapy? This author suggests placing the dosage alongside a patient’s daily vitamins: Vitamins C, E, B complex, selenium (for males), and tomato juice (especially for males because of the lycopene) are suggested. (One might also consider taking dosages of atragalus, echinacea, and possibly red marine algae. These three have had various articles suggesting immune system benefits that could possibly reduce recurrence frequency, though the results of these studies are less clear). In this manner the prescription medication will not be forgotten.

What should a person on suppressive therapy do if an outbreak occurs? First, the patient should not panic. This happens, and this almost always does not mean that the patient is developing viral resistance. It simply means, apparently, that whatever trigger in the nerve cell is at work to initiate viral DNA transcription and replication is suddenly overwhelming the amount of Valtrex or acyclovir that is on board. One need only increase the dose of valacyclovir to 1000 mg daily (or 500 mg twice daily) or acyclovir to probably 400 mg three times daily (or, 200 mg five times daily), and the recurrence should begin to subside relatively soon, anywhere from one to a few days. The recurrence while on medication is typically milder and of shorter duration. After the lesions have formed dry scabs and the skin redness has subsided, the patient can usually go back to the original suppressive dosage once or twice daily.

A brief word would be in order about the development of viral resistance. A number of strains of HSV which are resistant to acyclovir, valacyclovir, and Famvir have been discovered. In the overall population resistant strains are relatively rare, though in immunocompromised patients, such as those in the later stages of HIV infection, resistant strains are somewhat more common.

Where does viral resistance come from, given that the viral DNA information is apparently incorporated into human DNA? Resistance, apparently, comes when virus particles are released from infected cells that no longer have the enzyme necessary to activate acyclovir. The virus particles, interestingly, have to convert the acyclovir to a chemical that kills themselves. Apparently they get smart and learn how to do without the enzyme that converts acyclovir into something that kills the virus. Again, the development of a recurrence while on suppressive therapy does NOT mean that the patient is harboring a resistant strain. Consistent inability to suppress acute infections with acyclovir is worrisome, however, and should be further evaluated. Tests for viral resistance ARE available but are generally found in centers that do research on such subjects.

Let us leave the discussion of acyclovir and the other antiviral medications on a positive note. Utilizing once or twice daily suppressive therapy, almost all victims of this illness can dramatically decrease the incidence and severity of recurrences. Also, the patients and their consorts can take comfort in knowing that the incidence of aymptomatic viral shedding is likely reduced as well. This does not decrease the need to take appropriate precautions (see Smart Living). However, at least the risk of transmission is apparently substantially reduced. Also, regular use of the medication has been shown in the literature to CONTINUE to reduce the incidence of recurrences through the first three years of therapy, as mentioned above, a benefit that has also been shown to persist for at least two or three more years of therapy.

Medical therapy for GHI and to some degree OHI can dramatically improve the enjoyment of disease-free intervals, at the same time reducing the risk of shedding the virus and probably making disease transmission less likely. This dramatic improvement of symptoms through the use of a now inexpensive and essentially non-toxic chemical, when used as directed along with appropriate Smart Living techniques, promises to offer a major improvement of life enjoyment for the Herpes sufferer and his/her consort and improvement of the general public health as well for many years to come.

Non-prescription Therapies for Herpes Infections:

I have read extensively about possibilities that may come about with the use of Opuntia cactus. If a reader of this paper is interested in the use of Opuntia for the treatment of herpes, I would ask that reader to please contact me at the website and let me know so that I can assist in helping the reader find a source of it.

Interestingly, one recent paper indicated that the application of red wine to the lesion (topically, not consumed) actually will assist in aborting an outbreak.

I found another interesting series of papers recently on the use of Tagamet (generically it is called "cimetidine") for the treatment of herpes infections in animals. It turns out that cimetidine has "immunomodulation" effects, meaning specifically that it depresses the activity of "T suppressor cells" which may be inhibiting the body's natural cellular mediated immunity which is known to fight off recurrences. The interested reader can to go The National Library of Medicine and perform a search on "herpes" and "cimetidine" to read these articles. The reader might print these off and take them to the private physician for discussion. I do NOT recommend this therapy to anyone until more research is performed in this area. Someone who is immunosupressed already, such as with HIV or cancer, would want to particularly avoid such a treatment.

Future Medical Therapies for Herpes Infections:

New antiviral medications are constantly being researched. A recent Japanese paper reviewed research on dozens of new chemicals which suppress Herpes virus formation, including resistant viruses. Periodically new chemicals are produced that offer new approaches to treating recurrent disease. Some chemicals, like cidofovir, can be toxic to certain human cells, such as the kidneys, though are very effective at controlling herpes virus infection. The reader must remember, though, that it takes many years from the time of the identification of a chemical that seems to work until the release of the drug on the market that has been exhaustively determined to be "safe and effective".

The reader should review the adjacent paper on the current status and the future of herpes vaccines. At some future time the use of the body’s immune system MAY in fact be the most "safe and effective" method to control infection. Literally hundreds of published articles concerning many human and animal studies indicate that already methods exist to modestly, and sometimes substantially, alter the course of disease and offer prevention in some cases. However, the safety and efficacy of such vaccines have not been clearly proved in the world’s literature at this time.

This author was previously excited about the concepts of the "disabled infectious single cycle" vaccines and the DNA vaccine technology that might have offered exciting prospects for confronting both GHI and OHI and both controlling the spread of these diseases as well as controlling symptoms in infected patients. Sadly, the research did not indicate a positive benefit for all participants in the trial.

Another exciting area is in that of an evolving therapy for women that may both treat women as well as possibly offer protection for intimate partners. This falls into the area of "Intravaginal Release" of medications. European research is ongoing in this area, and we may soon see a new route of prevention and treatment available in this manner.

The cells that are infected can be localized. This is obviously true because of the skin location where recurrences occur. The infected cells transmit viral particles to the skin. This means that the skin identifies the infected cells. This WOULD be a conduit directly to the infected neurons, were there to be some medication that would permanently affect the involved cells and render then non-infectious or even dormant. A risk would be generated, of course, in killing the infected cells. These nerve cells are involved with sensation to the skin and possibly important reflex arcs and other important nervous system functions. Current research is ongoing in this area, with the possibility of direct DNA therapy to the infected cells being explored (see CytoGenix's work HERE. Clearly though this concept remains an area for future treatment considerations.