Herpes antiviral therapy began in the early 1960s with the experimental use of medications that interfered with viral replication called deoxyribonucleic acid (DNA) inhibitors. The original use was against normally fatal or debilitating illnesses such as adult encephalitis,[92] keratitis,[93] in immunocompromised (transplant) patients,[94] or disseminated herpes zoster.[95] The original compounds used were 5-iodo-2'-deoxyuridine, AKA idoxuridine, IUdR, or(IDU) and 1-β-D-arabinofuranosylcytosine or ara-C,[96] later marketed under the name cytosar or cytarabine. The usage expanded to include topical treatment of herpes simplex,[97] zoster, and varicella.[98] Some trials combined different antivirals with differing results.[92] The introduction of 9-β-D-arabinofuranosyladenine, (ara-A or vidarabine), considerably less toxic than ara-C, in the mid-1970s, heralded the way for the beginning of regular neonatal antiviral treatment. Vidarabine was the first systemically administered antiviral medication with activity against HSV for which therapeutic efficacy outweighed toxicity for the management of life-threatening HSV disease. Intravenous vidarabine was licensed for use by the U.S. Food and Drug Administration in 1977. Other experimental antivirals of that period included: heparin,[99] trifluorothymidine (TFT),[100] Ribivarin,[101] interferon,[102] Virazole,[103] and 5-methoxymethyl-2'-deoxyuridine (MMUdR).[104] The introduction of 9-(2-hydroxyethoxymethyl)guanine, AKA aciclovir, in the late 1970s[105] raised antiviral treatment another notch and led to vidarabine vs. aciclovir trials in the late 1980s.[106] The lower toxicity and ease of administration over vidarabine has led to aciclovir becoming the drug of choice for herpes treatment after it was licensed by the FDA in 1998.[107] Another advantage in the treatment of neonatal herpes included greater reductions in mortality and morbidity with increased dosages, which did not occur when compared with increased dosages of vidarabine.[107] However, aciclovir seems to inhibit antibody response, and newborns on aciclovir antiviral treatment experienced a slower rise in antibody titer than those on vidarabine.[107]
Genital herpes is so common. It’s affecting more than 3 million Americans each year. And 1 out of 5 people is estimated to have this disease at some point in their lives. Your partner can also have the chances of contracting genital herpes. Many people may be shocked and disappointed when their partners have this disease. But, remember that people with genital herpes really need acceptance and support. Here’s what you should do when you find out your partner has genital herpes.
Herpes sores follow a similar cyclical pattern and appear first like pimples that turn into small vesicles.  Then, the skin becomes crusty, and eventually a scab is formed.  It can take up to several weeks for the lesions to heal, during which time there may be one outbreak followed by another.  Certain risk factors may increase the likelihood of an outbreak, such as: asthma medication, lack of sleep, stress, decreased immunity and ultraviolet rays.
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The frequency and severity of recurrent outbreaks vary greatly between people. Some individuals' outbreaks can be quite debilitating, with large, painful lesions persisting for several weeks, while others experience only minor itching or burning for a few days. Some evidence indicates genetics play a role in the frequency of cold sore outbreaks. An area of human chromosome 21 that includes six genes has been linked to frequent oral herpes outbreaks. An immunity to the virus is built over time. Most infected individuals experience fewer outbreaks and outbreak symptoms often become less severe. After several years, some people become perpetually asymptomatic and no longer experience outbreaks, though they may still be contagious to others. Immunocompromised individuals may experience longer, more frequent, and more severe episodes. Antiviral medication has been proven to shorten the frequency and duration of outbreaks.[79] Outbreaks may occur at the original site of the infection or in proximity to nerve endings that reach out from the infected ganglia. In the case of a genital infection, sores can appear at the original site of infection or near the base of the spine, the buttocks, or the back of the thighs. HSV-2-infected individuals are at higher risk for acquiring HIV when practicing unprotected sex with HIV-positive persons, in particular during an outbreak with active lesions.[80]
Herpes simplex viruses -- more commonly known as herpes -- are categorized into two types: herpes type 1 (HSV-1, or oral herpes) and herpes type 2 (HSV-2, or genital herpes). Most commonly, herpes type 1 causes sores around the mouth and lips (sometimes called fever blisters or cold sores). HSV-1 can cause genital herpes, but most cases of genital herpes are caused by herpes type 2. In HSV-2, the infected person may have sores around the genitals or rectum. Although HSV-2 sores may occur in other locations, these sores usually are found below the waist.
The herpes virus can be shed from an infected person even when there are no lesions visible. So caution is important. Some may wish to take the daily prophylactic oral drug Valtrex (an antiviral oral medication) to help cut down on shedding. Herpes can also be transmitted on any skin: fingers, lips, etc. Depending on sexual practices, herpes simplex can be transferred to genitals and or buttocks from the lips of someone who has fever blisters. Honesty between partners is very important so these issues can be discussed openly.
A 2004 study in the New England Journal of Medicine found that suppressive therapy decreases the risk of HSV-2 transmission from symptomatic, infected partners to uninfected partners by 48%. So “the risk of transmission is significantly reduced, but cannot be eliminated even with suppressive therapy,” Johnston explains, and she stresses that the virus can be passed along even without signs or symptoms.
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