Human herpes virus 1 (HHV1) is also known as herpes simplex virus 1 (HSV1). It is typically the cause of cold sores around the mouth. HHV1 can also lead to infection in the genital area causing genital herpes usually through oral-genital contact, such as during oral sex. HHV1 infections are contagious and are usually spread from skin-to-skin contact with an infected person through small breaks in the skin or mucous membrane. The HHV1 virus is more likely to be spread through things like sharing eating utensils, razors, and towels from a person who has an active lesion.

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.


Avoid touching any sores you have. If you do, wash your hands with soap and water. You should avoid sex while you have sores, and use a male or female condom or dental dam with your partner if sex occurs despite intentions to not have sex. Herpes is most contagious during an outbreak, but it’s also possible to spread herpes when no symptoms are present.
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]

There are two types of herpes simplex viruses (HSV), they are termed HSV-1 and HSV-2. These two viruses have distinctly different DNA, and both cause oral and genital lesions. However, HSV-1 causes about 80% of all oral lesions and only about 20% of genital lesions while HSV-2 causes the reverse (about 80% genital and 20% oral). Studies also suggest that in adolescents, up to 40% of genital herpes is caused by HSV-1 because of reported increased oral/genital contact (transmission by oral sex).

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.

Antibodies that develop following an initial infection with a type of HSV prevents reinfection with the same virus type—a person with a history of orofacial infection caused by HSV-1 cannot contract herpes whitlow or a genital infection caused by HSV-1.[citation needed] In a monogamous couple, a seronegative female runs a greater than 30% per year risk of contracting an HSV infection from a seropositive male partner.[37] If an oral HSV-1 infection is contracted first, seroconversion will have occurred after 6 weeks to provide protective antibodies against a future genital HSV-1 infection.[citation needed] Herpes simplex is a double-stranded DNA virus.[38]
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.

While some people realize that they have genital herpes, many do not. It is estimated that one in five persons in the United States has genital herpes; however, as many as 90 percent are unaware that they have the virus. This is because many people have very mild symptoms that go unrecognized or are mistaken for another condition or no symptoms at all.


Some people have recurrent outbreaks with the so-called “classic” blister-like herpes lesions that crust over, or with painful sores. In recurrent herpes, however, this process usually takes about half the time it does in first episodes. In addition, many people have very subtle forms of recurrent herpes that heal up in a matter of days. And lastly, herpes is capable of reactivating without producing any visible lesions (asymptomatic reactivation).
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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.

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]


“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.

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.

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.
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]

Patients with genital herpes have reported that outbreaks or episodes typically diminish through the years. Early prodromal symptoms, or warning signals, that are followed by outbreaks. These prodromal symptoms often include mild tingling or shooting pains in the legs, hips and buttocks, and can last from 2 hours to 2 days. After the prodromal symptoms occur the blisters develop into painful red spots, which then evolve into yellowish, clear fluid-filled blisters after a day or two. These blisters burst or break and leave ulcers that usually heal in about 10 days. In women, blisters can develop inside the vagina and cause painful urination.
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.
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