Many HSV-infected people experience recurrence within the first year of infection.[14] Prodrome precedes development of lesions. Prodromal symptoms include tingling (paresthesia), itching, and pain where lumbosacral nerves innervate the skin. Prodrome may occur as long as several days or as short as a few hours before lesions develop. Beginning antiviral treatment when prodrome is experienced can reduce the appearance and duration of lesions in some individuals. During recurrence, fewer lesions are likely to develop and are less painful and heal faster (within 5–10 days without antiviral treatment) than those occurring during the primary infection.[14] Subsequent outbreaks tend to be periodic or episodic, occurring on average four or five times a year when not using antiviral therapy.
Consider designating a special, brightly colored bracelet or visual designator that you will wear only during active viral periods: this will serve as a visual cue, reminding you each time that you eat or drink that food and/or beverage sharing is not an option during this time: this subtle cue will remind you to not engage in a high-risk behavior during an active viral period.

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]
In infants for whom the condition is quickly diagnosed and controlled by antiviral medication, prognosis is good. However, in untreated and undiagnosed infants, the virus can attack the body’s organs systems, causing serious and potentially life-threatening complications, including seizures and Encephalitis, which can cause brain and/or spinal damage.

Recurrent outbreaks of genital herpes may happen, with some patients having four to six outbreaks in the span of a year. Compared to the first infection, subsequent recurrences are less painful and occur in shorter periods than the first infection. There are some patients, however, who don’t have another outbreak for many years or even once more during their lifetime.11


At the other end of the spectrum, there is a possibility of a herpetic flare up taking a sinister turn and leading to herpetic encephalitis. It is estimated to affect at least 1 in 500,000 individuals per year. The mechanism of this is not fully understood, but it is believed that the infection occurs through direct transmission of the virus via nerves from other parts of the body to the brain. In such cases, a person may complain of fever, headache, and lethargy, followed by confusion or delirium. In some cases, some people even develop seizures. This requires immediate medical attention and treatment.
As with almost all sexually transmitted infections, women are more susceptible to acquiring genital HSV-2 than men.[41] On an annual basis, without the use of antivirals or condoms, the transmission risk of HSV-2 from infected male to female is about 8–11%.[37][42] This is believed to be due to the increased exposure of mucosal tissue to potential infection sites. Transmission risk from infected female to male is around 4–5% annually.[42] Suppressive antiviral therapy reduces these risks by 50%.[43] Antivirals also help prevent the development of symptomatic HSV in infection scenarios, meaning the infected partner will be seropositive but symptom-free by about 50%. Condom use also reduces the transmission risk significantly.[44][45] Condom use is much more effective at preventing male-to-female transmission than vice versa.[44] Previous HSV-1 infection may reduce the risk for acquisition of HSV-2 infection among women by a factor of three, although the one study that states this has a small sample size of 14 transmissions out of 214 couples.[46]
Herpes viruses typically infect the oral or genital mucosa. When herpes affects the mouth, it causes the typical "cold sores," which are painful sores or blisters that form on the lips, mouth, or gums. Prior to the development of the blisters, there may be a prodrome (early symptoms indicating onset of a particular disease) consisting of an itching, burning, or tingling sensation in the affected area. The virus remains dormant in the nervous system throughout life, and this is the reason that cold sores often recur in the same location.
Cullins explains that even if you’ve never had an outbreak, if you’ve been exposed to herpes, it lies dormant in your body. A blood test could reveal antibodies for HSV-1 and/or HSV-2, which means that you have been exposed to the infection in your past, you have been infected, and you have developed antibodies because your body has or is fighting the infection.
As with almost all sexually transmitted infections, women are more susceptible to acquiring genital HSV-2 than men.[41] On an annual basis, without the use of antivirals or condoms, the transmission risk of HSV-2 from infected male to female is about 8–11%.[37][42] This is believed to be due to the increased exposure of mucosal tissue to potential infection sites. Transmission risk from infected female to male is around 4–5% annually.[42] Suppressive antiviral therapy reduces these risks by 50%.[43] Antivirals also help prevent the development of symptomatic HSV in infection scenarios, meaning the infected partner will be seropositive but symptom-free by about 50%. Condom use also reduces the transmission risk significantly.[44][45] Condom use is much more effective at preventing male-to-female transmission than vice versa.[44] Previous HSV-1 infection may reduce the risk for acquisition of HSV-2 infection among women by a factor of three, although the one study that states this has a small sample size of 14 transmissions out of 214 couples.[46]
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.
The frequency and severity of recurrent outbreaks vary greatly between people. Some individuals' outbreaks can be quite debilitating, with large, painful lesions persisting for several weeks, while others experience only minor itching or burning for a few days. Some evidence indicates genetics play a role in the frequency of cold sore outbreaks. An area of human chromosome 21 that includes six genes has been linked to frequent oral herpes outbreaks. An immunity to the virus is built over time. Most infected individuals experience fewer outbreaks and outbreak symptoms often become less severe. After several years, some people become perpetually asymptomatic and no longer experience outbreaks, though they may still be contagious to others. Immunocompromised individuals may experience longer, more frequent, and more severe episodes. Antiviral medication has been proven to shorten the frequency and duration of outbreaks.[79] Outbreaks may occur at the original site of the infection or in proximity to nerve endings that reach out from the infected ganglia. In the case of a genital infection, sores can appear at the original site of infection or near the base of the spine, the buttocks, or the back of the thighs. HSV-2-infected individuals are at higher risk for acquiring HIV when practicing unprotected sex with HIV-positive persons, in particular during an outbreak with active lesions.[80]
Both HSV-1 and HSV-2 infections are acquired from direct contact with someone who carries the virus. The infectious secretions that pass on HSV-1 or HSV-2 live on oral, genital or anal mucosal surfaces. They’re passed through skin-to-skin transmission, and any form of direct contact with sores on the mouth, buttocks or genitals can cause the virus to be passed.
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'.
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]
Although the cause is unknown, outbreaks are often associated with periods of weakened immune systems, skin wounds, menstruation, fever, nerve damage, tissue damage from surgery, or exposure to extreme climate situations. A genital herpes outbreak or episode occurs when the HSV-1 or HSV-2 virus is reactivated from its dormant stage. Genital herpes is an incurable disease, and once you contract it, you may experience outbreaks throughout your lifetime. Those who are experiencing their first herpes episode of genital herpes can expect to have several (typically four or five) outbreaks within a year. Over time these recurrences usually decrease in frequency and severity. The first outbreak of herpes is often the longest outbreak experienced. After that, short and inconsistent episodes can be managed and treated with antiviral medication.
I am so scared. My boyfriend is the only person I have ever had unprotected sex with 4 times. We had a herpes scare. He got tested. They swabbed him and gave him a blood test and his results for Herpes 1 and 2 came back negative. I went to the doctor but the lumps on my vagina healed and they said come back when you have a lesion. I told my BF but he still wanted to have sex, I told him what the doctor said and I told him we should not have sex or use a condom. He said it does not matter because if he did not have herpes I did not have Herpes. He said ok and put the condom on but  when we were done he started to laugh and said he took the condom off. Since then we have had sex twice. I went to the doctor and they gave me a blood test. They said if something was wrong they would send a letter to the house. Since they never sent the letter to the house I thought I was fine and I never had any other lumps since then and my boy friend never had any symptoms I thought I was fine.Today something told me to go to the doctor. I went and they said they never ordered the test. I AM So ANGRY. What Should I do? If I do have it shouldn't it have been in his blood from me? I am so scared that I may have it? I am also worried that one day he may get symptoms because his test was wrong and think I gave it to him when he was the one who may have given it to me if my blood test comes back positive. I have only had sex once with a condom before him. What should I do? He has had other a few partners. What is the likely hood that I may have given him herpes?
“Someone having HSV doesn't mean that they were reckless or irresponsible with their sex life,” says Sara, age 30. “I used condoms with all my partners, and I still caught it.” For Jamie, who contracted herpes from her husband three years into their monogamous relationship, he was her first and only sexual partner. And she says that he contracted it from one of his very first sexual encounters. No matter how and why someone contracted the virus, it doesn't erase their humanity and right to respect.

As of 2017, there is not currently a herpes vaccine available to prevent HSV-1 or HSV-2. (There is a vaccine available for another virus, herpes zoster; however, despite the similar name, it actually refers to the shingles virus. And, in fact, shingles occurs due to the reactivation of yet another virus, varicella zoster, which causes chicken pox.)


When a herpes outbreak occurs, you can expect cold sores to take about 10–14 days to heal on average. During this time period, the virus is considered to be active, and you should be very careful to avoid direct contact between a sore and someone else. If after trying the natural remedies for herpes described above you still experience frequent recurrences, talk to your doctor for how to get rid of herpes symptoms. Sometimes immunity is suppressed due to another infection or virus, or even as a side effect of taking some medications, so be sure to rule these causes out.
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.
OK, so the majority of people have it. Just this year, the World Health Organization released a study that estimates two thirds of people in the world (67%) have the HSV-1 strain of the herpes simplex virus — that’s approximately 3.7 billion people worldwide. While HSV-1 typically refers to oral herpes infections, it also includes some genital infections. The new report estimates that half of the HSV-1 infections in people between the ages of 15–49 are actually genital infections transmitted via oral-to-genital contact. The Center For Disease Control (CDC) estimates that 1 in 6 people have genital herpes.

The herpes simplex virus is probably the most well-known virus of the herpes family, and it is just as contagious. Herpes simplex infects epithelial cells and remains latent in neurons. HSV-1 causes recurrent oropharyngeal lesions, commonly known as “fever blisters" or "cold sores.” It is also the primary cause of sporadic encephalitis (inflammation of the brain), gingivostomatitis (inflammation of the gums and mucous lining of the mouth), and keratoconjunctivitis (severe dryness of the eye that involves the cornea) and dendritic corneal ulcers (also called HSV keratitis) in which the cornea becomes affected by herpetic lesions that look like the dendrites of neurons in the brain.
Prodrome: Early in the phase of reactivation (also called an outbreak), many people experience an itching, tingling, or painful feeling in the area where their recurrent lesions will develop. This sort of warning symptom – called a “prodrome” – often comes a day or two before lesions appear. To be on the safe side, it’s best to assume virus is active (and, therefore, can be spread through direct skin-to-skin contact) during these times.
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.
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