Herpes type 2 (HSV-2) can cause genital herpes. This is one of the most common sexually transmitted infections (STIs) in the US. It causes sores or painful blisters on the penis, vagina, scrotum, anus and buttocks. Along with blisters, people with HSV-2 may experience tingling, itching or pain. Like HSV-1, HSV-2 infections are highly contagious. They can be spread easily through skin-to-skin contact. Sexual intercourse is the main route of transmission.
In order to diagnose herpes, a health care provider can swab an area of visibly active herpes infection or, if symptoms aren’t active, a blood test can be given that measures the number of herpes antibodies present in the body. The antibodies don’t indicate herpes itself, but rather show the immune system’s response to the presence of the virus in the body. It’s important to note that sometimes a swab can give false negative results since herpes lesions need to be large enough to yield enough detectable virus and if the outbreak is already healing it also may not be detected in a swab. (6)
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. 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.
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.
According to Gina*, 21, “A herpes diagnosis is very shaking and it gives you the opportunity to look inward and really find what you love about yourself.” Gina says she has even better self-esteem than prior to finding out she had HSV. She explains, “You learn not to lower your standards, because you start to pick out who it is worth disclosing to and who isn't.”
These herpes viruses enter the body through small cuts, abrasions, or breaks in the skin or mucous membranes. The incubation period for herpes simplex infections is about three to six days. Transmission (spread) of the virus is person to person and more likely to occur if blisters or lesions are present. The majority enter after an uninfected person has direct contact with someone carrying the virus (either with or without noticeable lesions). Simply touching an infected person is often the way children get exposed. Adolescents and adults frequently get exposed by skin contact but may get their first exposure by kissing or sexual contact (oral and/or genital contact), especially for HSV-2. Statistical studies suggest that about 80%-90% of people in the U.S. have been exposed to HSV-1 and about 30% have been exposed to HSV-2. Usually, the contagious period continues until lesions heal. Some people (estimated from 30%-50%) occasionally shed herpes virus while having few or no associated symptoms or signs.
Worldwide rates of either HSV-1 or HSV-2 are between 60% and 95% in adults. HSV-1 is usually acquired during childhood. Rates of both increase as people age. Rates of HSV-1 are between 70% and 80% in populations of low socioeconomic status and 40% to 60% in populations of improved socioeconomic status. An estimated 536 million people worldwide (16% of the population) were infected with HSV-2 as of 2003 with greater rates among women and those in the developing world. Most people with HSV-2 do not realize that they are infected. The name is from Greek: ἕρπης herpēs which means "to creep", referring to spreading blisters. The name does not refer to latency.
Although herpes treatment is helpful, there is no cure. However, in most cases, outbreaks become fewer, less painful, and weaker over the course of a few years. If you have herpes, you can take certain medications to help manage the infection. Using herpes treatments is usually very effective in speeding up the healing of sores and preventing them from returning frequently.
A 2004 study in the New England Journal of Medicine found that suppressive therapy decreases the risk of HSV-2 transmission from symptomatic, infected partners to uninfected partners by 48%. So “the risk of transmission is significantly reduced, but cannot be eliminated even with suppressive therapy,” Johnston explains, and she stresses that the virus can be passed along even without signs or symptoms.