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.
Genital herpes is passed on by skin-to-skin contact during vaginal, oral or anal sex, or by sharing sex toys. You can get genital herpes even if there are no visible sores or blisters, and once you have the virus, there is no cure. 'Herpes is more likely to be passed on just before, during or straight after an outbreak, as herpes blisters and sores are highly infectious,' says O’Sullivan.
According to Melissa King, a psychotherapist who runs a support group for women with herpes in New York City, when someone finds out they’ve gotten herpes from a partner, there’s often immediately an assumption that the partner knew that they had it and lied, or that they were cheating. “But the reality is that in a lot of cases, people don’t know that they have it,” King tells BuzzFeed.
“Herpes is caused by sexual intimacy and contact with a person who is actively shedding the herpes virus,” says Cullins. If you have HSV-1, that shedding could happen through the mouth or a cold sore, which means that the virus can be transmitted through kissing, or just sharing a drink. If you have herpes that affects the genitals, it can be transmitted from sharing sex toys, grinding, or even mutual masturbation — any activity where the virus can be transmitted from one person to another through skin-to-skin or mucosal contact.
The broader issue is whether, if you do get infected, herpes will ultimately harm your health. Although I don’t want to trivialize this infection, in your general scheme of health, it probably will not. The major concern is that if you are pregnant and develop a new outbreak of herpes, the virus can be transmitted to the fetus, especially during vaginal delivery. What’s more, people with genital herpes have a much greater risk of acquiring HIV if they are exposed. (It’s theorized that the lesion causes microscopic breaks in the skin, allowing HIV to enter the body.)
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."
With the first outbreak of herpes virus infection, an individual may also experience nonspecific flu-like symptoms like fever, swollen lymph nodes, headache, and muscle aches. It is also possible to have herpes virus infection without having any symptoms or signs, or having signs and symptoms that are so mild that the infection is mistaken for another condition.
Worldwide rates of either HSV-1 and/or HSV-2 are between 60 and 95% in adults. HSV-1 is more common than HSV-2, with rates of both increasing as people age. HSV-1 rates 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 or 16% of the population worldwide were infected with HSV-2 as of 2003 with greater rates among women and in those in the developing world. Rates of infection are determined by the presence of antibodies against either viral species.
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.
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.
"Oral herpes is an infection found in the mouth, or on and around the lips, caused by the Herpes Simplex Virus (HSV)," Michael explains. "There are two types or strains of this virus called HSV1 and HSV2. Usually, the HSV1 strain infects the mouth and lips, and the HSV2 strain infects the genitals. It is however possible for HSV2 to infect your mouth and lips."