Jamie*, 29, is HSV-positive and contracted herpes from her husband. But, she explains, “He only had one outbreak when he was young and that was it. So he didn't realize what it was.” Jamie was infected three years into their relationship simply because he had outbreaks that infrequently. She says, “I was worried he had cheated on me, but then found similar stories online, and our outbreak patterns underscore that what happened is very possible.”
Oral herpes, commonly referred to as mouth herpes, is a viral infection of the mouth and gums primarily by the Herpes simplex virus type 1 (HSV-1) but may also be due to the genital variant (HSV-2). It is also known as recurrent herpetic stomatitis or acute herpetic gingivostomatitis. The infection of the mouth typically causes small fluid-filled blisters known as vesicles on the roof of the mouth (palate), inside of the cheeks (buccal muscosa), tongue, gums and even the lips (herpes labialis). It may also occur on the skin around the mouth and extend to the nose and into the nasal cavity.
Until the 1980s serological tests for antibodies to HSV were rarely useful to diagnosis and not routinely used in clinical practice. The older IgM serologic assay could not differentiate between antibodies generated in response to HSV-1 or HSV-2 infection. However, a glycoprotein G-specific (IgG) HSV test introduced in the 1980s is more than 98% specific at discriminating HSV-1 from HSV-2.
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."
Pain, itching and the appearance of sores called lesions are common symptoms of genital herpes. Lesions may appear inside or outside the vagina, and on or around the penis. In both women and men, these sores may appear in and around the anus.6 Lesions typically appear from two days to two weeks after you first get infected with the virus, and will take seven to 14 days or more to heal.7
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.
Evidence is insufficient to support use of many of these compounds, including echinacea, eleuthero, L-lysine, zinc, monolaurin bee products, and aloe vera. While a number of small studies show possible benefit from monolaurin, L-lysine, aspirin, lemon balm, topical zinc, or licorice root cream in treatment, these preliminary studies have not been confirmed by higher-quality randomized controlled studies.
No method eradicates herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks. Analgesics such as ibuprofen and paracetamol (acetaminophen) can reduce pain and fever. Topical anesthetic treatments such as prilocaine, lidocaine, benzocaine, or tetracaine can also relieve itching and pain.
According to Cullins, there are no standardized guidelines from the CDC for suppressive therapy through medication, but it is an option that people with HSV should talk to their healthcare providers about. “If a person knows they have had herpes in the past that has affected their genitals, they can take suppressive therapy — for example, 500 mg of valacyclovir daily.” While it won’t prevent outbreaks, it will prevent asymptomatic virus shedding. Preventing exposure to the virus through both medication and a physical barrier can be very effective.