Your healthcare provider may diagnose genital herpes by simply looking at your symptoms. Providers can also take a sample from the sore(s) and test it. In certain situations, a blood test may be used to look for herpes antibodies. Have an honest and open talk with your health care provider and ask whether you should be tested for herpes or other STDs.

Herpes “triggers” (determining exactly what leads to an outbreak) are highly individual, but with time, many people learn to recognize, and sometimes avoid, factors that seem to reactivate HSV in their own bodies. Illness, poor diet, emotional or physical stress, friction in the genital area, prolonged exposure to ultraviolet light (commonly for oral herpes, such as a beach trip or skiing weekend), surgical trauma, and steroidal medication (such as asthma treatment) may trigger a herpes outbreak.
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The herpes virus is probably the most well-known virus after influenza (the flu) or the common cold. What most people don’t know is that this nasty little virus can take several different forms, eight to be exact. The most common form of the herpes virus is chicken pox, which is called varicella-zoster. Herpes simplex is the sexually transmitted version of the virus.
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

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 “triggers” (determining exactly what leads to an outbreak) are highly individual, but with time, many people learn to recognize, and sometimes avoid, factors that seem to reactivate HSV in their own bodies. Illness, poor diet, emotional or physical stress, friction in the genital area, prolonged exposure to ultraviolet light (commonly for oral herpes, such as a beach trip or skiing weekend), surgical trauma, and steroidal medication (such as asthma treatment) may trigger a herpes outbreak.
Herpes of the mouth is a viral infection. The virus HSV-1 may be transmitted by droplet spread – direct contact with saliva or even respiratory droplets. These droplets must make contact with broken skin or the mucous membranes in order to infect a person. The method of spread can involve kissing an infected person or even through touch. It can also be spread through the use of contaminated kitchen utensils. Sexual contact accounts for a small number of cases of HSV-1. Nevertheless it is a consideration when genital lesions are present. HSV-2 on the other hand is usually transmitted through sexual contact.
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]
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.
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.
Herpes is contracted through direct contact with an active lesion or body fluid of an infected person.[31] Herpes transmission occurs between discordant partners; a person with a history of infection (HSV seropositive) can pass the virus to an HSV seronegative person. Herpes simplex virus 2 is typically contracted through direct skin-to-skin contact with an infected individual, but can also be contracted by exposure to infected saliva, semen, vaginal fluid, or the fluid from herpetic blisters.[32] To infect a new individual, HSV travels through tiny breaks in the skin or mucous membranes in the mouth or genital areas. Even microscopic abrasions on mucous membranes are sufficient to allow viral entry.
Varicella-zoster is transmitted though the mucosa of the respiratory system, specifically the upper respiratory tract, or the conjunctiva of the eye. Initial replication takes place in the regional lymph nodes, and then the virus spreads and replication begins in the liver and spleen. The virus is then transported to the skin where the rash develops. The incubation period of varicella is about 10 to 21 days.
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]

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.


Although it’s not caused by either the HSV-1 or HSV-2 virus, herpes zoster falls under the umbrella of herpes diseases. Also known as shingles, it’s an infection caused by the varicella-zoster virus, and is characterized by the development of painful skin rashes on one side of the face or body.23 These rashes are red patches of fluid-filled blisters that tend to crack easily.24,25
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