You may have concerns about how genital herpes will impact your overall health, sex life, and relationships. It is best for you to talk to a health care provider about those concerns, but it also is important to recognize that while herpes is not curable, it can be managed with medication. Daily suppressive therapy (i.e., daily use of antiviral medication) for herpes can also lower your risk of spreading genital herpes to your sex partner. Be sure to discuss treatment options with your healthcare provider. Since a genital herpes diagnosis may affect how you will feel about current or future sexual relationships, it is important to understand how to talk to sexual partners about STDsExternal.
Although it’s not caused by either the HSV-1 or HSV-2 virus, herpes zoster falls under the umbrella of herpes diseases. Also known as shingles, it’s an infection caused by the varicella-zoster virus, and is characterized by the development of painful skin rashes on one side of the face or body.23 These rashes are red patches of fluid-filled blisters that tend to crack easily.24,25
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
So, if you have unprotected sex with your partner, you could be infected, too. Any form of sexual contact (oral, vaginal and anal sex) can put you at risks” the doctor said. Even when you use condoms or dental dams during sex, you can possibly contract HSV. In fact, condoms cannot provide 100 percent protection against genital herpes. Directly touching your partner’s genitals can also make you become infected. This happens when your partner develops visible herpes sores on their genitals.
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.