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.


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No method eradicates herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks. Analgesics such as ibuprofen and paracetamol (acetaminophen) can reduce pain and fever. Topical anesthetic treatments such as prilocaine, lidocaine, benzocaine, or tetracaine can also relieve itching and pain.[58][59][60]
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.
Genital herpes is not usually accommodated by symptoms. Two-thirds of genital herpes cases are asymptomatic. Getting tested for both HSV-1 and HSV-2 is the only sure way to know if you have genital herpes. Blisters or sores in the genital area, fever, body aches, swollen lymph nodes, headaches, tiredness and painful urination call all be symptoms of genital herpes.
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]
Condoms offer moderate protection against HSV-2 in both men and women, with consistent condom users having a 30%-lower risk of HSV-2 acquisition compared with those who never use condoms.[49] A female condom can provide greater protection than the male condom, as it covers the labia.[50] The virus cannot pass through a synthetic condom, but a male condom's effectiveness is limited[51] because herpes ulcers may appear on areas not covered by it. Neither type of condom prevents contact with the scrotum, anus, buttocks, or upper thighs, areas that may come in contact with ulcers or genital secretions during sexual activity. Protection against herpes simplex depends on the site of the ulcer; therefore, if ulcers appear on areas not covered by condoms, abstaining from sexual activity until the ulcers are fully healed is one way to limit risk of transmission.[52] The risk is not eliminated, however, as viral shedding capable of transmitting infection may still occur while the infected partner is asymptomatic.[53] The use of condoms or dental dams also limits the transmission of herpes from the genitals of one partner to the mouth of the other (or vice versa) during oral sex. When one partner has a herpes simplex infection and the other does not, the use of antiviral medication, such as valaciclovir, in conjunction with a condom, further decreases the chances of transmission to the uninfected partner.[14] Topical microbicides that contain chemicals that directly inactivate the virus and block viral entry are being investigated.[14]
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.

But I was wrong, on so many levels. I did find love again. And I wasn’t alone — very far from it, in fact. Herpes is extremely common, with statistics showing that as many as one in six people ages 14 to 49 in the U.S. has herpes caused by the herpes simplex-2 virus (and since herpes simplex-1 virus also causes herpes, that number is likely even higher).


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.
Herpes simplex type 1, which is transmitted through oral secretions or sores on the skin, can be spread through kissing or sharing objects such as toothbrushes or eating utensils. In general, a person can only get herpes type 2 infection during sexual contact with someone who has a genital HSV-2 infection. It is important to know that both HSV-1 and HSV-2 can be spread even if sores are not present.
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]
Diagnosing herpes is made much easier if you present to your clinician at the time that the rash is present and if possible, we can take a sample from that to be sent for Herpes PCR (Polymerase Chain Reaction) studies to confirm the diagnosis. Advanced medical investigative techniques such as this will allow us to differentiate type one from type two herpes regardless of the nature and distribution of the rash.
Worldwide rates of either HSV-1 and/or HSV-2 are between 60 and 95% in adults.[4] HSV-1 is more common than HSV-2, with rates of both increasing as people age.[4] HSV-1 rates 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 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.[10] Rates of infection are determined by the presence of antibodies against either viral species.[81]

When we say, “herpes” many of us are thinking about genital herpes, famously known as an incurable inconvenience. But there is more to it than being just a sexually transmitted infection. There are multiple ways that herpes can transmit but genital herpes is usually picked up from sexual contact. Apart from that, herpes can be transmitted when sharing an environment with someone who has the infection as well.
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]
Neonatal herpes simplex is a HSV infection in an infant. It is a rare but serious condition, usually caused by vertical transmission of HSV-1 or -2) from mother to newborn. During immunodeficiency, herpes simplex can cause unusual lesions in the skin. One of the most striking is the appearance of clean linear erosions in skin creases, with the appearance of a knife cut.[20] Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicles.[21]:369 Eczema herpeticum is an infection with herpesvirus in patients with chronic atopic dermatitis may result in spread of herpes simples throughout the eczematous areas.[21]:373

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Laboratory testing is often used to confirm a diagnosis of genital herpes. Laboratory tests include culture of the virus, direct fluorescent antibody (DFA) studies to detect virus, skin biopsy, and polymerase chain reaction to test for presence of viral DNA. Although these procedures produce highly sensitive and specific diagnoses, their high costs and time constraints discourage their regular use in clinical practice.[39]
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.
It should not be confused with conditions caused by other viruses in the herpesviridae family such as herpes zoster, which is caused by varicella zoster virus. The differential diagnosis includes hand, foot and mouth disease due to similar lesions on the skin. Lymphangioma circumscriptum and dermatitis herpetiformis may also have a similar appearance.
HSV-2 is commonly referred to as genital herpes because it usually causes cold sores to erupt around the genitalia. In fact, genital herpes is the No. 1 cause of genital ulcers worldwide, according to the Centers for Disease Control and Prevention (CDC), and affects up to 1 in 3 adults (although most who are infected don’t even know it). (5) Both types of herpes viruses are highly contagious, and both can cause cold sores in either area of the body (or sometimes both). 

HSV asymptomatic shedding occurs at some time in most individuals infected with herpes. It can occur more than a week before or after a symptomatic recurrence in 50% of cases.[33] Virus enters into susceptible cells by entry receptors[34] such as nectin-1, HVEM and 3-O sulfated heparan sulfate.[35] Infected people who show no visible symptoms may still shed and transmit viruses through their skin; asymptomatic shedding may represent the most common form of HSV-2 transmission.[33] Asymptomatic shedding is more frequent within the first 12 months of acquiring HSV. Concurrent infection with HIV increases the frequency and duration of asymptomatic shedding.[36] Some individuals may have much lower patterns of shedding, but evidence supporting this is not fully verified; no significant differences are seen in the frequency of asymptomatic shedding when comparing persons with one to 12 annual recurrences to those with no recurrences.[33]
According to a study in the New England Journal of Medicine, more than 30% of pregnant women in the United States have genital HSV. During pregnancy, people are immunocompromised so that their body doesn’t fight the fetus as a foreign invader. And when a person’s immune system is weakened, they are more likely to have herpes outbreaks. According to Cullins, “Pregnancy is the time period when [a provider] really wants to know whether or not the person has had herpes in the past,” so they can protect the pregnant person and their infant from a herpes infection.
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