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, keratitis, in immunocompromised (transplant) patients, or disseminated herpes zoster. The original compounds used were 5-iodo-2'-deoxyuridine, AKA idoxuridine, IUdR, or(IDU) and 1-β-D-arabinofuranosylcytosine or ara-C, later marketed under the name cytosar or cytarabine. The usage expanded to include topical treatment of herpes simplex, zoster, and varicella. Some trials combined different antivirals with differing results. 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, trifluorothymidine (TFT), Ribivarin, interferon, Virazole, and 5-methoxymethyl-2'-deoxyuridine (MMUdR). The introduction of 9-(2-hydroxyethoxymethyl)guanine, AKA aciclovir, in the late 1970s raised antiviral treatment another notch and led to vidarabine vs. aciclovir trials in the late 1980s. 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. 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. However, aciclovir seems to inhibit antibody response, and newborns on aciclovir antiviral treatment experienced a slower rise in antibody titer than those on vidarabine.
Although there is no cure for herpes, treatments can relieve the symptoms. Medication can decrease the pain related to an outbreak and can shorten healing time. They can also decrease the total number of outbreaks. Drugs including Famvir, Zovirax, and Valtrex are among the drugs used to treat the symptoms of herpes. Warm baths may relieve the pain associated with genital sores.
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.
Cullins explains that the first, or initial, outbreak is usually the worst, and “over time when you have recurrent episodes, you may not have systemic symptoms” or frequent symptoms. But everyone’s body and immune system reacts to the virus differently; while some people may never have many outbreaks, other people may be more chronically symptomatic. The National Institutes of Health indicate that infrequent outbreaks, around one or two per year, are not uncommon.
If not treated immediately, it has potential spread to other parts of the body. Being highly contagious in nature it gets readily transmitted by sharing utensils, clothes, and toothbrush. Maintaining sexual contact, kissing and touching also leads to the spread of virus. It is likely to spread more when the virus is present with physical outbursts. It is less contagious if the virus is present without any outward physical signs.
“I kind of can't stand when people tell me how ‘brave’ I am for talking about it,” says Lachrista Greco, 30, who was diagnosed with herpes almost two year ago. That kind of narrative can actually perpetuate the stigma around the virus. By insinuating that talking about something makes someone brave, the implication is that that thing shouldn’t be talked about at all.
Consider designating a special, brightly colored bracelet or visual designator that you will wear only during active viral periods: this will serve as a visual cue, reminding you each time that you eat or drink that food and/or beverage sharing is not an option during this time: this subtle cue will remind you to not engage in a high-risk behavior during an active viral period.
Herpes type 2 (HSV-2) can cause genital herpes. This is one of the most common sexually transmitted infections (STIs) in the US. It causes sores or painful blisters on the penis, vagina, scrotum, anus and buttocks. Along with blisters, people with HSV-2 may experience tingling, itching or pain. Like HSV-1, HSV-2 infections are highly contagious. They can be spread easily through skin-to-skin contact. Sexual intercourse is the main route of transmission.
Herpes of the mouth is a viral infection. The virus HSV-1 may be transmitted by droplet spread – direct contact with saliva or even respiratory droplets. These droplets must make contact with broken skin or the mucous membranes in order to infect a person. The method of spread can involve kissing an infected person or even through touch. It can also be spread through the use of contaminated kitchen utensils. Sexual contact accounts for a small number of cases of HSV-1. Nevertheless it is a consideration when genital lesions are present. HSV-2 on the other hand is usually transmitted through sexual contact.
While some people realize that they have genital herpes, many do not. It is estimated that one in five persons in the United States has genital herpes; however, as many as 90 percent are unaware that they have the virus. This is because many people have very mild symptoms that go unrecognized or are mistaken for another condition or no symptoms at all.