Herpes simplex type 1, which is transmitted through oral secretions or sores on the skin, can be spread through kissing or sharing objects such as toothbrushes or eating utensils. In general, a person can only get herpes type 2 infection during sexual contact with someone who has a genital HSV-2 infection. It is important to know that both HSV-1 and HSV-2 can be spread even if sores are not present.
Primary orofacial herpes is readily identified by examination of persons with no previous history of lesions and contact with an individual with known HSV infection. The appearance and distribution of sores is typically presents as multiple, round, superficial oral ulcers, accompanied by acute gingivitis.[39] Adults with atypical presentation are more difficult to diagnose. Prodromal symptoms that occur before the appearance of herpetic lesions help differentiate HSV symptoms from the similar symptoms of other disorders, such as allergic stomatitis. When lesions do not appear inside the mouth, primary orofacial herpes is sometimes mistaken for impetigo, a bacterial infection. Common mouth ulcers (aphthous ulcer) also resemble intraoral herpes, but do not present a vesicular stage.[39]
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]
Oral herpes is a viral infection mainly of the mouth area and lips caused by a specific type of the herpes simplex virus. Oral herpes is also termed HSV-1, type 1 herpes simplex virus, or herpes labialis. The virus causes painful sores on the upper and lower lips, gums, tongue, roof of the mouth, inside the cheeks or nose, and sometimes on the face, chin, and neck. Infrequently, it may cause genital lesions. It also can cause symptoms such as swollen lymph nodes, fever, and muscle aches. People commonly refer to the infection as "cold sores."
The most common reason that people develop cold sores on their mouths is due to becoming infected with HSV-1. (4) HSV-1 usually causes cold sore breakouts around the lips or mouth, or what some people describe as “fever blisters.” Someone can become infected with HSV-1 starting as a child, and then the virus can lay dormant in the body until the immune system is weakened, at which point symptoms can surface.
If you have herpes, you should talk to your sex partner(s) and let him or her know that you do and the risk involved. Using condoms may help lower this risk but it will not get rid of the risk completely. Having sores or other symptoms of herpes can increase your risk of spreading the disease. Even if you do not have any symptoms, you can still infect your sex partners.
HSV-2 is contracted through forms of sexual contact with a person who has HSV-2. An estimated 20 percent of sexually active adults in the United States are infected with HSV-2, according to the American Academy of Dermatology (AAD). HSV-2 infections are spread through contact with a herpes sore. In contrast, most people get HSV-1 from an infected person who is asymptomatic, or does not have sores.
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