You may have concerns about how genital herpes will impact your overall health, sex life, and relationships. It is best for you to talk to a health care provider about those concerns, but it also is important to recognize that while herpes is not curable, it can be managed with medication. Daily suppressive therapy (i.e., daily use of antiviral medication) for herpes can also lower your risk of spreading genital herpes to your sex partner. Be sure to discuss treatment options with your healthcare provider. Since a genital herpes diagnosis may affect how you will feel about current or future sexual relationships, it is important to understand how to talk to sexual partners about STDsExternal.

During these periods, it is especially important to abstain from kissing and any form of physical contact with the blistering area, saliva, or sexual discharge. If you are infected, be sure to wash your hands after touching an infected area on either the oral or genital regions. Herpes medications can also help reduce your risk of transmitting the virus to another individual.


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]
With the first outbreak of herpes virus infection, an individual may also experience nonspecific flu-like symptoms like fever, swollen lymph nodes, headache, and muscle aches. It is also possible to have herpes virus infection without having any symptoms or signs, or having signs and symptoms that are so mild that the infection is mistaken for another condition.
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.
Worldwide rates of either HSV-1 or HSV-2 are between 60% and 95% in adults.[4] HSV-1 is usually acquired during childhood.[1] Rates of both increase as people age.[4] Rates of HSV-1 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 worldwide (16% of the population) were infected with HSV-2 as of 2003 with greater rates among women and those in the developing world.[10] Most people with HSV-2 do not realize that they are infected.[1] The name is from Greek: ἕρπης herpēs which means "to creep", referring to spreading blisters.[11] The name does not refer to latency.[12]
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]
The good news is that the first cold sores you experience from either HSV virus will most likely be the worst, and then you can expect immunity against the virus to usually improve over time. You can speed up this tolerance to the virus through making lifestyle changes, as well as becoming educated about safe sex and limiting the risk of transmitting the virus. So if you want to get rid of herpes symptoms, you can do it naturally.
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.
Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.
That being said, if on paper the HSV titres are high, indicating a high viral load in the body, this can be an indicator of an impending flare. Knowing this, we can prescribe antiviral medications with the aim of suppressing the virus activity. The idea is that we reduce the viral load of HSV, therefore helping the body’s immunity better contain the virus.
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.

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]
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
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]
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).

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]
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]
Human herpes virus 8 (HHV8) was recently discovered in the tumours called Kaposi's Sarcoma (KS). These tumours are found in people with AIDS and are otherwise very rare. KS forms purplish tumours in the skin and other tissues of some people with AIDS. It is very difficult to treat with medication. HHV8 may also cause other cancers, including certain lymphomas (lymph node cancers) associated with AIDS. The fact that these cancers are caused by a virus may explain why they tend to occur in people with AIDS when their immune systems begin to fail. The discovery also provides new hope that specific treatments for these tumours will be developed that target the virus.
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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