Do everything possible to prevent spreading it to other people. The virus cannot live long when it is not in contact with the skin, so door handles and towels are not likely to spread it. Do not share your personal belongings, like toothbrushes and combs.  Wash your hands with soap and water often, and immediately if you touch the sores.  This is important so as to minimize the chance of getting ocular herpes (herpes infection of the eye) which is a serious infection. Be especially careful around infants because their immune systems may not be fully developed. Little children often express affection with sloppy wet kisses. This is a common way to spread the herpes virus within the family.
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.
The most common reason that people develop cold sores on their mouths is due to becoming infected with HSV-1. (4) HSV-1 usually causes cold sore breakouts around the lips or mouth, or what some people describe as “fever blisters.” Someone can become infected with HSV-1 starting as a child, and then the virus can lay dormant in the body until the immune system is weakened, at which point symptoms can surface.

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.
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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'.

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). 
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.
There’s herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2). “HSV-1 and HSV-2 are different but closely related viruses,” says Dr. Christine Johnston, MPH, who is the Associate Medical Director of the Virology Research Clinic at the University of Washington. Johnston explains that both are transmitted through close mucosal or skin contact with infected secretions. HSV-1 primarily causes oral outbreaks, also known as cold sores, and HSV-2 usually causes genital outbreaks. But HSV-1 can also cause genital outbreaks through oral-to-genital contact, according to the CDC. According to Johnston, genital HSV-1 is less likely to recur than HSV-2, and there’s less asymptomatic shedding (transmitting the virus without realizing it) with HSV-1 than with HSV-2.
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.
Herpesviral encephalitis and herpesviral meningitis Herpes simplex encephalitis (HSE) is a rare life-threatening condition that is thought to be caused by the transmission of HSV-1 either from the nasal cavity to the brain's temporal lobe or from a peripheral site on the face, along the trigeminal nerve axon, to the brainstem.[16][17][18][19] Despite its low incidence, HSE is the most common sporadic fatal encephalitis worldwide. HSV-2 is the most common cause of Mollaret's meningitis, a type of recurrent viral meningitis.
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You should stop having sexual contact as soon as you feel warning signs of an outbreak. Warning signs may include a burning, itching, or tingling feeling on the genitals or around the mouth. Do not have vaginal, anal, or oral sex — even with a condom — until seven days after the warning signs stop or the sore heals. The virus can spread from sores not covered by the condom. It can also spread in sweat or vaginal fluids to places the condom doesn't cover.

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.


The annual incidence in Canada of genital herpes due to HSV-1 and HSV-2 infection is not known (for a review of HSV-1/HSV-2 prevalence and incidence studies worldwide, see Smith and Robinson 2002). As many as one in seven Canadians aged 14 to 59 may be infected with herpes simplex type 2 virus[85] and more than 90 per cent of them may be unaware of their status, a new study suggests.[86] In the United States, it is estimated that about 1,640,000 HSV-2 seroconversions occur yearly (730,000 men and 910,000 women, or 8.4 per 1,000 persons).[87]
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.
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."
Herpetic whitlow and herpes gladiatorum Herpes whitlow is a painful infection that typically affects the fingers or thumbs. On occasion, infection occurs on the toes or on the nail cuticle. Individuals who participate in contact sports such as wrestling, rugby, and football (soccer), sometimes acquire a condition caused by HSV-1 known as herpes gladiatorum, scrumpox, wrestler's herpes, or mat herpes, which presents as skin ulceration on the face, ears, and neck. Symptoms include fever, headache, sore throat, and swollen glands. It occasionally affects the eyes or eyelids.
In all cases, HSV is never removed from the body by the immune system. Following a primary infection, the virus enters the nerves at the site of primary infection, migrates to the cell body of the neuron, and becomes latent in the ganglion.[14] As a result of primary infection, the body produces antibodies to the particular type of HSV involved, preventing a subsequent infection of that type at a different site. In HSV-1-infected individuals, seroconversion after an oral infection prevents additional HSV-1 infections such as whitlow, genital herpes, and herpes of the eye. Prior HSV-1 seroconversion seems to reduce the symptoms of a later HSV-2 infection, although HSV-2 can still be contracted.
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]

Canker sores are sometimes thought to be caused by HSV, but this is not true. Canker sores occur only inside the mouth, on the tongue, and on the soft palate (roof of mouth), not on skin surfaces. Although they reoccur, they are not contagious, usually are self-limiting, and have almost no complications. Canker sores are caused by substances that irritate the lining of the mouth.
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]
According to Cullins, there are no standardized guidelines from the CDC for suppressive therapy through medication, but it is an option that people with HSV should talk to their healthcare providers about. “If a person knows they have had herpes in the past that has affected their genitals, they can take suppressive therapy — for example, 500 mg of valacyclovir daily.” While it won’t prevent outbreaks, it will prevent asymptomatic virus shedding. Preventing exposure to the virus through both medication and a physical barrier can be very effective.
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