The causes of reactivation are uncertain, but several potential triggers have been documented. A 2009 study showed the protein VP16 plays a key role in reactivation of the dormant virus.[71] Changes in the immune system during menstruation may play a role in HSV-1 reactivation.[72][73] Concurrent infections, such as viral upper respiratory tract infection or other febrile diseases, can cause outbreaks. Reactivation due to other infections is the likely source of the historic terms 'cold sore' and 'fever blister'.
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Genital herpes is so common. It’s affecting more than 3 million Americans each year. And 1 out of 5 people is estimated to have this disease at some point in their lives. Your partner can also have the chances of contracting genital herpes. Many people may be shocked and disappointed when their partners have this disease. But, remember that people with genital herpes really need acceptance and support. Here’s what you should do when you find out your partner has genital herpes.
Herpes sores usually appear as one or more blisters on or around the genitals, rectum or mouth. The blisters break and leave painful sores that may take a week or more to heal. These symptoms are sometimes called “having an outbreak.” The first time someone has an outbreak they may also have flu-like symptoms such as fever, body aches, or swollen glands.
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.

At least 80 to 90 percent of people in the U.S. have already been exposed to the HSV-1 virus.sup style="font-size: 10px;">21 Meanwhile, around 3.7 billion HSV-1 infections were recorded in 2012 all over the world, according to the World Health Organization. Africa was home to the highest number of cases, with 87 percent of occurrences coming from this continent.22
To reduce the chance of acquiring HSV-1, avoid touching saliva, skin, or mucous membranes of people who have HSV-1 lesions. Prevention of genital HSV may be accomplished by latex condoms, but protection is never 100%. Spermicides do not protect against HSV. Some clinicians recommend using dental dams (small latex squares) during oral sex, but like condoms, they are not 100% protective.
However, asymptomatic carriers of the HSV-2 virus are still contagious. In many infections, the first symptom people will have of their own infections is the horizontal transmission to a sexual partner or the vertical transmission of neonatal herpes to a newborn at term. Since most asymptomatic individuals are unaware of their infection, they are considered at high risk for spreading HSV.[47]

The most effective method of avoiding genital infections is by avoiding vaginal, oral, and anal sex.[1] Condom use decreases the risk.[1] Daily antiviral medication taken by someone who has the infection can also reduce spread.[1] There is no available vaccine[1] and once infected, there is no cure.[1] Paracetamol (acetaminophen) and topical lidocaine may be used to help with the symptoms.[2] Treatments with antiviral medication such as aciclovir or valaciclovir can lessen the severity of symptomatic episodes.[1][2]
Oral herpes (HSV-1) infection (or exposure without noticeable infection) is common. About 65% of the U.S. population has detectable antibodies to HSV-1 by age 40. This article will focus on HSV-1, or oral herpes, not on HSV-2, also commonly known as genital herpes. Genital herpes is considered to be a sexually transmitted disease (STD). In addition, HSV-2 virus should not be confused with human papillomavirus (HPV), the cause of genital warts, and some cervical and other cancer types.
Pain, sore lips, burning sensation, tingling, or itching occurs at the infection site before the sores appear. These are the early symptoms (prodrome). Sometimes these symptoms happen prior to the appearance of sores, bumps, pimple-like lesions, or blisters (herpes or herpetic stomatitis). Thereafter, clusters or groups of painful blisters (also termed fever blisters) or vesicles erupt or ooze with a clear to yellowish fluid that may develop into a yellowish crust. These blisters break down rapidly and appear as tiny, shallow gray ulcers on a red base. Fever blisters are smaller than canker sores. A few days later, they become crusted or scabbed and appear drier and more yellow.
Human herpes virus 3 (HHV3) is also called varicella-zoster virus. HHV3 causes chickenpox. It can also cause a recurrent virus infection of the skin, which is called herpes zoster or shingles. Shingles occurs when dormant varicella-zoster virus from an initial bout of chickenpox becomes reactivated. Like its close relative, HHV1, herpes zoster likes to infect skin cells and nerve cells. This virus may also recur along nerve fibre pathways, causing multiple sores where nerve fibres end on skin cells. Because an entire group of nerve cells is often affected, shingles is generally much more severe than a recurrence of herpes simplex. The lesions generally appear in a band-like or belt-like pattern occurring on one side of the body and are often accompanied by itching, tingling, or even severe pain. Healing usually occurs in 2 to 4 weeks, and scars may remain. Postherpetic neuralgia is a complication of shingles where the pain associated with the infection can persist for months and even years. Most people who experience shingles once do not experience it again.

Worldwide rates of either HSV-1 or HSV-2 are between 60% and 95% in adults.[4] HSV-1 is usually acquired during childhood.[1] Rates of both increase as people age.[4] 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.[4] 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.[10] Most people with HSV-2 do not realize that they are infected.[1] The name is from Greek: ἕρπης herpēs which means "to creep", referring to spreading blisters.[11] The name does not refer to latency.[12]


Herpes sores follow a similar cyclical pattern and appear first like pimples that turn into small vesicles.  Then, the skin becomes crusty, and eventually a scab is formed.  It can take up to several weeks for the lesions to heal, during which time there may be one outbreak followed by another.  Certain risk factors may increase the likelihood of an outbreak, such as: asthma medication, lack of sleep, stress, decreased immunity and ultraviolet rays.
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]
An important source of support is the National Herpes Resource Center which arose from the work of the American Sexual Health Association (ASHA).[113] The ASHA was created in 1914 to in response to the increase in sexually transmitted diseases that had spread during World War I.[114] During the 1970s, there was an increase in sexually transmitted diseases. One of the diseases that increased dramatically was genital herpes. In response, ASHA created the National Herpes Resource Center in 1979. The HRC was designed to meet the growing need for education and awareness about the virus. One of the projects of The Herpes Resource Center (HRC) was to create a network of local support (HELP) groups. The goal of these HELP groups was to provide a safe, confidential environment where participants can get accurate information and share experiences, fears, and feelings with others who are concerned about herpes.[115][116]

What is herpes gladiatorum? Herpes gladiatorum is a virus similar to that which causes the common cold. It is spread through skin-to-skin contact. The symptoms vary between people, but they include a fever and skin sores. If the virus affects the eyes, it can be dangerous. Find out about the symptoms, risks, treatment, and prevention options. Read now
Most people with genital herpes have no symptoms, have very mild symptoms that go unnoticed, or have symptoms but do not recognize them as a sign of infection. Genital herpes symptoms include blisters, sharp pain or burning feelings if urine flows over sores, an inability to urinate if severe swelling of sores blocks the urethra (tube from the bladder to outside the vagina), itching, open sores, and pain in the infected area.

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.
There’s quite a variety, in short. And while genital herpes certainly can and does cause these signs of infection literally on the genitals (the penis or the vulva) it also can produce signs of infection nearby. Herpes sores on or between the buttocks are common (and sometimes slow to heal), as are lesions on the thigh. Herpes can bring about what feels like a tiny fissure around the anus, something easily confused with hemorrhoids. So remember: recurring signs and symptoms in the genital or anal area could well be herpes lesions.
If not treated immediately, it has potential  spread to other parts of the body. Being highly contagious in nature it gets readily transmitted by sharing utensils, clothes, and toothbrush. Maintaining sexual contact, kissing and touching also leads to the spread of virus. It is likely to spread more when the virus is present with physical outbursts. It is less contagious if the virus is present without any outward physical signs.
Research has gone into vaccines for both prevention and treatment of herpes infections. Unsuccessful clinical trials have been conducted for some glycoprotein subunit vaccines.[citation needed] As of 2017, the future pipeline includes several promising replication-incompetent vaccine proposals while two replication-competent (live-attenuated) HSV vaccine are undergoing human testing.[citation needed]

Transmission of HSV-1 occurs by direct exposure to saliva or droplets formed in the breath of infected individuals. In addition, skin contact with the lesions on an infected individual can spread the disease to another individual. Although close personal contact is usually required for transmission of the virus, it is possible to transmit HSV-1 when people share toothbrushes, drinking glasses, or eating utensils.
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.

We usually do this for short durations of time. Not something that can be taken as lifelong therapy. I know it might not make sense to some of you. You’re probably asking why it is that we can’t just take the suppressive antiviral medications for the rest of our lives and with that, have no flares of herpes? Well basically, we know that having a high viral load is not the definitive factor in determining a herpetic flare. It is how the body is coping with the virus. So ultimately, you can be taking medications for months on end with your body in good shape to contain the virus so that there are no breakouts but that does not mean that the virus is eliminated from your body.
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]

If you are pregnant and have genital herpes, it is very important for you to go to prenatal care visits. Tell your doctor if you have ever had symptoms of, or have been diagnosed with, genital herpes. Also tell your doctor if you have ever been exposed to genital herpes. There is some research that suggests that genital herpes infection may lead to miscarriage, or could make it more likely for you to deliver your baby too early.


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]
A doctor will base a presumptive diagnosis on information provided by the patient and on the physical examination. The characteristic appearance of the herpes sores leaves little doubt about the diagnosis, so the typical appearance of the sores is key to the diagnosis. This appearance helps distinguish oral herpes from oral thrush, shingles, gonorrhea, and syphilis. In addition, chapped or sunburned lips can resemble oral herpes, but the tissue stain (Tzanck smear, see below) shows no virus-induced cell changes. Further testing is usually not necessary but is sometimes done.
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