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.
HSV-1 has been proposed as a possible cause of Alzheimer's disease.[26][27] In the presence of a certain gene variation (APOE-epsilon4 allele carriers), HSV-1 appears to be particularly damaging to the nervous system and increases one's risk of developing Alzheimer's disease. The virus interacts with the components and receptors of lipoproteins, which may lead to its development.[28][29]
Recurrent outbreaks of genital herpes may happen, with some patients having four to six outbreaks in the span of a year. Compared to the first infection, subsequent recurrences are less painful and occur in shorter periods than the first infection. There are some patients, however, who don’t have another outbreak for many years or even once more during their lifetime.11
Following active infection, herpes viruses establish a latent infection in sensory and autonomic ganglia of the nervous system. The double-stranded DNA of the virus is incorporated into the cell physiology by infection of the nucleus of a nerve's cell body. HSV latency is static; no virus is produced; and is controlled by a number of viral genes, including latency-associated transcript.[70]
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Evidence is insufficient to support use of many of these compounds, including echinacea, eleuthero, L-lysine, zinc, monolaurin bee products, and aloe vera.[68] 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.[69]
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]
'Using condoms or dams can help to protect against STIs, but herpes can also be passed on by skin-to-skin contact with the affected area, so it’s strongly recommended that you don’t have sex during this time,' she adds. 'This includes direct genital contact or skin-to-skin contact with the affected area, and doesn’t have to be penetrative sex,' says O’Sullivan.
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