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.
Some people have recurrent outbreaks with the so-called “classic” blister-like herpes lesions that crust over, or with painful sores. In recurrent herpes, however, this process usually takes about half the time it does in first episodes. In addition, many people have very subtle forms of recurrent herpes that heal up in a matter of days. And lastly, herpes is capable of reactivating without producing any visible lesions (asymptomatic reactivation).
To reduce the chance of acquiring HSV-1, avoid touching saliva, skin, or mucous membranes of people who have HSV-1 lesions. Prevention of genital HSV may be accomplished by latex condoms, but protection is never 100%. Spermicides do not protect against HSV. Some clinicians recommend using dental dams (small latex squares) during oral sex, but like condoms, they are not 100% protective.
Although herpes treatment is helpful, there is no cure. However, in most cases, outbreaks become fewer, less painful, and weaker over the course of a few years. If you have herpes, you can take certain medications to help manage the infection. Using herpes treatments is usually very effective in speeding up the healing of sores and preventing them from returning frequently.
Herpes is transmitted via skin-to-skin contact, not through blood or saliva. Cullins explains that someone with HSV can be shedding the herpes virus without having an outbreak (known as asymptomatic virus shedding), and infect somebody that way. Suppressive antiviral medications, like acyclovir or valacyclovir, inhibit HSV replication, which decreases shedding but does not completely eliminate it, says Johnston.
Genital herpes is contracted through sexual activity, and may show symptoms around the genital area (anus, buttocks, thigh, penis, vulva, etc.). Additionally, people with HIV can experience significantly worse symptoms of herpes. See a doctor if your partner has herpes, or if you notice any unusual sores on your body. How do you know if you have herpes? Read more in our Diagnosing Herpes section here.
Avoid physical contact with anyone who has visible blisters and sores, and don't share towels or anything that may have come into contact with the sores. "It is also important that before you have any intimate contact with anyone you ask them about their sexual health, whether they have a herpes infection or have ever had any other sexually transmitted infection," Michael advises. "This is because statistically, people who have had an STI are more likely to be infected with the herpes virus. Using condoms and dental dams can also help reduce your risk of catching oral herpes."
With the first outbreak of herpes virus infection, an individual may also experience nonspecific flu-like symptoms like fever, swollen lymph nodes, headache, and muscle aches. It is also possible to have herpes virus infection without having any symptoms or signs, or having signs and symptoms that are so mild that the infection is mistaken for another condition.
A doctor will base a presumptive diagnosis on information provided by the patient and on the physical examination. The characteristic appearance of the herpes sores leaves little doubt about the diagnosis, so the typical appearance of the sores is key to the diagnosis. This appearance helps distinguish oral herpes from oral thrush, shingles, gonorrhea, and syphilis. In addition, chapped or sunburned lips can resemble oral herpes, but the tissue stain (Tzanck smear, see below) shows no virus-induced cell changes. Further testing is usually not necessary but is sometimes done.