The “classic” symptoms that most people associate with genital herpes are sores, vesicles, or ulcers – all of which can also be called “lesions.” (The scientific literature on herpes uses the term “lesion” to describe any break or irregularity in the skin.) These classic lesions of genital herpes often resemble small pimples or blisters that eventually crust over and finally scab like a small cut. These lesions may take anywhere from two to four weeks to heal fully.
Doctors prescribe suppressive treatment if a person experiences more than six recurrences in a year. In some cases, a doctor my recommend that the individual takes daily antiviral treatment indefinitely. The aim here is to prevent further recurrences. Although suppressive treatment significantly reduces the risk of passing HSV to a partner, there is still a risk.
Consequently, you may already have the virus. A doctor can determine this with a blood test for Herpes 2 (Ig), a type-specific immunoglobulin. If you are already infected, you won’t be at risk for a new infection — you and your boyfriend already share the virus. But knowing your herpes status will tell you whether you are capable of infecting a future partner.
Some people experience negative feelings related to the condition following diagnosis, in particular if they have acquired the genital form of the disease. Feelings can include depression, fear of rejection, feelings of isolation, fear of being found out, and self-destructive feelings.[108] Herpes support groups have been formed in the United States and the UK, providing information about herpes and running message forums and dating websites for sufferers. People with the herpes virus are often hesitant to divulge to other people, including friends and family, that they are infected. This is especially true of new or potential sexual partners whom they consider casual.[109]
If you think you have or have been exposed to herpes you should see your primary care provider for follow up, screening, and possible treatment. Many providers today will not test unless you have symptoms of an outbreak, as often tests come back as false positive and the CDC has concluded that false positives cause psychological trauma to those tested. There is much debate on if you should test without symptoms or not, others say it is unethical to not be aware of your current STD status and risk infecting other people.
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]
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]
^ Nasser M, Fedorowicz Z, Khoshnevisan MH, Shahiri Tabarestani M (October 2008). "Acyclovir for treating primary herpetic gingivostomatitis". The Cochrane Database of Systematic Reviews (4): CD006700. doi:10.1002/14651858.CD006700.pub2. PMID 18843726. (Retracted, see doi:10.1002/14651858.cd006700.pub3. If this is an intentional citation to a retracted paper, please replace {{Retracted}} with {{Retracted|intentional=yes}}.)
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