There is currently no cure that can eradicate herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks. Antiviral drugs also reduce asymptomatic shedding; it is believed asymptomatic Genital HSV-2 viral shedding occurs on 20% of days per year in patients not undergoing antiviral treatment, versus 10% of days while on antiviral therapy.
Antiviral medications used against herpes viruses work by interfering with viral replication, effectively slowing the replication rate of the virus and providing a greater opportunity for the immune response to intervene. All drugs in this class depend on the activity of the viral enzyme thymidine kinase to convert the drug sequentially from its prodrug form to monophosphate (with one phosphate group), diphosphate (with two phosphate groups), and finally to the triphosphate (with three phosphate groups) form which interferes with viral DNA replication.
There are several prescription antiviral medications for controlling herpes simplex outbreaks, including aciclovir (Zovirax), valaciclovir (Valtrex), famciclovir (Famvir), and penciclovir. Acyclovir was the original, and prototypical, member of this drug class; it is now available in generic brands at a greatly reduced cost. Valaciclovir and famciclovir—prodrugs of aciclovir and penciclovir, respectively—have improved solubility in water and better bioavailability when taken orally.
The use of valaciclovir and famciclovir, while potentially improving treatment compliance and efficacy, are still undergoing safety evaluation in this context.
Several studies in humans and mice provide evidence that early treatment with famciclovir soon after the first infection with herpes can significantly lower the chance of future outbreaks of herpes. Early use of famciclovir has been shown to reduce the amount of latent virus in the neural ganglia. A review of human subjects treated for five days with famciclovir 250 mg three times daily during their first herpes episode found that only 4.2 percent experienced a recurrence within six months after the first outbreak, a fivefold decrease compared to the 19 percent recurrence in acyclovir-treated patients. Despite these promising results, early famciclovir treatment for herpes in this or similar dosage regimes has yet to find mainstream adoption. As a result, some doctors and patients have opted for off-label use. One suggested regime is famciclovir at 10–20 mg/kg per day for 5–10 days, with treatment to commence as soon as possible after the first herpes infection(not the first symptoms or outbreak), and the most effective time for initiating treatment to be five days or less after the first herpes infection. However, the window of opportunity for this treatment is only a few months after first infection with the virus, following this the potential effect on latency drops to zero.
Antiviral medications are also available as topical creams for treating recurrent outbreaks on the lips, although their effectiveness is disputed.
Penciclovir cream has a 7-17 hour longer cellular half-life than aciclovir cream, increasing its effectiveness relative to aciclovir when topically applied.
Docosanol, used in many cosmetics as an emollient and barrier ingredient, is also available as an over-the-counter (OTC) drug formula for the treatment of oral herpes simplex outbreaks. It was thought to prevent HSV from fusing to cell membranes, but this has not been proven and it is known that docosanol also enters the cytoplasm of cells. The OTC drug formulation of docosanol is marketed by Avanir Pharmaceuticals under the name Abreva. Abreva was approved for use after clinical trials by the FDA in July 2000.
Abreva was the first over-the-counter antiviral drug approved for sale in the United States and Canada. Research leading to the licensing of Abreva showed that the OTC formula shortened recovery time to a moderate degree. Avanir Pharmaceuticals and GlaxoSmithKline Consumer Healthcare were the subject of a U.S. nationwide class-action suit in March due to the misleading claim that it cut recovery times in half.
Tromantadine is available as a gel that inhibits the entry and spread of the virus by altering the surface composition of skin cells and inhibiting release of viral genetic material. Zilactin is a topical analgesic barrier treatment, which forms a "shield" at the area of application to prevent a sore from increasing in size, and decrease viral spreading during the healing process.
Lipactin by Novartis is another over-the-counter topical gel which has been clinically shown to reduce symptoms and healing duration of a Herpes Simplex infection.
There is some limited research that has shown that tea tree oil may have topical anti-viral activity, especially with the Herpes virus Upon first feeling tingling or soreness in the area (i.e when one bites their lip), prior to any physical manifestation, apply tea tree oil constantly for several hours. If caught early enough a cold sore will not form.
Cimetidine, a common component of heartburn medication, and probenecid have been shown to reduce the renal clearance of aciclovir. These compounds also reduce the rate, but not the extent, at which valaciclovir is converted into aciclovir.
Limited evidence suggests that low dose aspirin (125 mg daily) might be beneficial in patients with recurrent HSV infections. Aspirin (acetylsalicylic acid) is an non-steroidal anti-inflammatory drug which reduces the level of prostaglandins—naturally occurring lipid compounds—that are essential in creating inflammation. A recent study in animals showed inhibition of thermal (heat) stress induced viral shedding of HSV-1 in the eye by aspirin, and a possible benefit in reducing the frequency of recurrences.
Another treatment is the use of petroleum jelly. Healing of cold sores is sped by barring water or saliva from reaching the sore.
The National Institutes of Health (NIH) in the United States is currently conducting phase III trials of Herpevac, a vaccine against HSV-2.
The vaccine has only been shown to be effective for women who have never been exposed to HSV-1. Overall, the vaccine is approximately 48% effective in preventing HSV-2 seropositivity and about 78% effective in preventing symptomatic HSV-2. During initial trials, the vaccine did not exhibit any evidence of preventing HSV-2 in males.
More importantly, a breakthrough was made by Harvard Medical School's Higgins Professor of Microbiology, David Knipe. His laboratory developed dl5-29, a replication-defective mutant virus that has proved successful both in preventing HSV-2/HSV-1 infections, and in combating the virus in already infected hosts, in animal models. Specifically, Knipe's lab has already shown that the replication defective vaccine induces strong HSV-2-specific antibody and T-cell responses; protects against challenge with a wild-type HSV-2 virus; greatly reduces the severity of recurrent disease; provides cross-protection against HSV-1, and renders the virus unable to revert to a virulent state or to become latent. His vaccine is now being researched and developed by Accambis, and is due to be applied as an Investigational New Drug in 2009.
Additionally, another solution may be found with regards to curing the infection. A cross anti-viral drug called Bavituximab has already proved successful in effectively treating mice and guinea pigs infected with various enveloped viruses. Herpes viruses fall within this category, and it is thought that the virus might be eradicated from the body using this drug. The drug works by binding onto infected cells, including cancer cells, and signaling to the immune system to come and destroy the problem cells. This is a novel technique in medicine and is eagerly anticipated since it is believed that cross-protection against latent viruses such as herpes simplex, Epstein-Barr, &c., will make an important contribution to improving public health.
Another possibility to eradicate the HSV-1 variant is being pursued by Prof Bryan Cullen and his team. By figuring out how to switch the virus from latency to its active stage, it is thought that conventional over the counter drugs can kill the virus, since it can no longer hide in the nerve cells. One class of drugs called antagomir could serve this purpose. These are chemically engineered oligonucleotides or short segments of RNA, that can be made to mirror their target genetic material, namely herpes microRNAs. They could be engineered to attach and thus 'silence' the microRNA, thus rendering the virus incapable to keep latent in their host. Prof Cullen believes a drug could be developed to block the microRNA whose job it is to suppress HSV-1 into latency.
Certain dietary adjustments, dietary supplements, and alternative remedies are believed to be beneficial in the treatment of herpes, either alone, or in conjunction with prescribed antiviral therapy. There is currently insufficient scientific and clinical evidence to support the effective use of many of these compounds to treat herpes in humans.
Lysine supplementation has been used for the prophylaxis and treatment of herpes simplex. Lysine shows greater effect against HSV-1 but may not be active against all virus variants. Dosage is critical with less than 1 gram (1000 mg) per day ineffective and more than 8 grams (8000 mg) gaining no additional benefit. Lysine is most effective if corn based products (which contain high amounts of Arginine) such as popcorn are avoided during an outbreak. Lysine treatment is somewhat body mass sensitive with higher dosage required for effective treatment as body mass increases. It should be taken as 3 or more doses in a 24 hour period and should be started when first outbreak symptoms, such as skin numbness or itching, are detected.
Aloe vera, available as a cream or gel, makes an affected area heal faster and may prevent recurrences.
Lemon balm (Melissa officinalis) has antiviral activity against HSV-2 in cell culture and may reduce HSV symptoms in herpes infected people.
There is conflicting evidence on a possible benefit from extracts from the plant echinacea in treating oral, but not genital, herpes.
Resveratrol, a compound naturally produced by plants and a component of red wine, prevents HSV replication in cultured cells and reduces cutaneous HSV lesion formation in mice. It is not considered potent enough to be an effective treatment on its own.
Extracts from garlic have shown antiviral activity against HSV in cell culture experiments, although the extremely high concentrations of the extracts required to produce an antiviral effect was also toxic to the cells.
The plant Prunella vulgaris, commonly known as ''selfheal'', also prevents expression of both type 1 and type 2 herpes in cultured cells.
Lactoferrin, a component of whey protein, has been shown to have a synergistic effect with aciclovir against HSV in vitro.
Some dietary supplements have been suggested to positively treat herpes. These include vitamin C, vitamin A, vitamin E, and zinc.
Butylated hydroxytoluene (BHT), commonly available as a food preservative, has been shown in cell culture and animal studies to inactivate herpes virus. However, BHT has not been clinically tested and approved to treat herpes infections in humans.
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