For mild infections, self-care may be adequate for treatment. Other treatments termed "home remedies" are not considered cures but can ease or hasten recovery. These remedies include aloe vera gel, cornstarch paste, and tea or mint leaves. A cool compress may reduce pain. There is no cure for the infection. People with severe infection symptoms, especially children, should be evaluated by a medical caregiver.
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]
As with almost all sexually transmitted infections, women are more susceptible to acquiring genital HSV-2 than men.[41] On an annual basis, without the use of antivirals or condoms, the transmission risk of HSV-2 from infected male to female is about 8–11%.[37][42] This is believed to be due to the increased exposure of mucosal tissue to potential infection sites. Transmission risk from infected female to male is around 4–5% annually.[42] Suppressive antiviral therapy reduces these risks by 50%.[43] Antivirals also help prevent the development of symptomatic HSV in infection scenarios, meaning the infected partner will be seropositive but symptom-free by about 50%. Condom use also reduces the transmission risk significantly.[44][45] Condom use is much more effective at preventing male-to-female transmission than vice versa.[44] Previous HSV-1 infection may reduce the risk for acquisition of HSV-2 infection among women by a factor of three, although the one study that states this has a small sample size of 14 transmissions out of 214 couples.[46]

Doctors prescribe suppressive treatment if a person experiences more than six recurrences in a year. In some cases, a doctor my recommend that the individual takes daily antiviral treatment indefinitely. The aim here is to prevent further recurrences. Although suppressive treatment significantly reduces the risk of passing HSV to a partner, there is still a risk.

Until the 1980s serological tests for antibodies to HSV were rarely useful to diagnosis and not routinely used in clinical practice.[39] The older IgM serologic assay could not differentiate between antibodies generated in response to HSV-1 or HSV-2 infection. However, a glycoprotein G-specific (IgG) HSV test introduced in the 1980s is more than 98% specific at discriminating HSV-1 from HSV-2.[40]

Doctors prescribe suppressive treatment if a person experiences more than six recurrences in a year. In some cases, a doctor my recommend that the individual takes daily antiviral treatment indefinitely. The aim here is to prevent further recurrences. Although suppressive treatment significantly reduces the risk of passing HSV to a partner, there is still a risk.
^ Nasser M, Fedorowicz Z, Khoshnevisan MH, Shahiri Tabarestani M (October 2008). "Acyclovir for treating primary herpetic gingivostomatitis". The Cochrane Database of Systematic Reviews (4): CD006700. doi:10.1002/14651858.CD006700.pub2. PMID 18843726. (Retracted, see doi:10.1002/14651858.cd006700.pub3. If this is an intentional citation to a retracted paper, please replace {{Retracted}} with {{Retracted|intentional=yes}}.)
Prodrome: Early in the phase of reactivation (also called an outbreak), many people experience an itching, tingling, or painful feeling in the area where their recurrent lesions will develop. This sort of warning symptom – called a “prodrome” – often comes a day or two before lesions appear. To be on the safe side, it’s best to assume virus is active (and, therefore, can be spread through direct skin-to-skin contact) during these times.
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]
Stage 3 -- Recurrence: When people encounter certain stresses (also termed triggers), emotional or physical, the virus may reactivate and cause new sores and symptoms. The following factors may contribute to or trigger recurrence: stress, illness, ultraviolet light (UV rays including sunshine), fever, fatigue, hormonal changes (for example, menstruation), immune depression, and trauma to a site or a nerve region where previous HSV infection occurred.
In infants for whom the condition is quickly diagnosed and controlled by antiviral medication, prognosis is good. However, in untreated and undiagnosed infants, the virus can attack the body’s organs systems, causing serious and potentially life-threatening complications, including seizures and Encephalitis, which can cause brain and/or spinal damage.

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]
^ Nasser M, Fedorowicz Z, Khoshnevisan MH, Shahiri Tabarestani M (October 2008). "Acyclovir for treating primary herpetic gingivostomatitis". The Cochrane Database of Systematic Reviews (4): CD006700. doi:10.1002/14651858.CD006700.pub2. PMID 18843726. (Retracted, see doi:10.1002/14651858.cd006700.pub3. If this is an intentional citation to a retracted paper, please replace {{Retracted}} with {{Retracted|intentional=yes}}.)
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.
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]
Herpes viruses typically infect the oral or genital mucosa. When herpes affects the mouth, it causes the typical "cold sores," which are painful sores or blisters that form on the lips, mouth, or gums. Prior to the development of the blisters, there may be a prodrome (early symptoms indicating onset of a particular disease) consisting of an itching, burning, or tingling sensation in the affected area. The virus remains dormant in the nervous system throughout life, and this is the reason that cold sores often recur in the same location.
In infants for whom the condition is quickly diagnosed and controlled by antiviral medication, prognosis is good. However, in untreated and undiagnosed infants, the virus can attack the body’s organs systems, causing serious and potentially life-threatening complications, including seizures and Encephalitis, which can cause brain and/or spinal damage.

Although there is no cure for herpes, treatments can relieve the symptoms. Medication can decrease the pain related to an outbreak and can shorten healing time. They can also decrease the total number of outbreaks. Drugs including Famvir, Zovirax, and Valtrex are among the drugs used to treat the symptoms of herpes. Warm baths may relieve the pain associated with genital sores.
Cullins explains that the first, or initial, outbreak is usually the worst, and “over time when you have recurrent episodes, you may not have systemic symptoms” or frequent symptoms. But everyone’s body and immune system reacts to the virus differently; while some people may never have many outbreaks, other people may be more chronically symptomatic. The National Institutes of Health indicate that infrequent outbreaks, around one or two per year, are not uncommon.
This means they cannot function independently outside the living cell. Once inside, however, they provide a far different picture. They are parasitic. This means they live off the host at the host’s expense. Unless you have already been exposed to a particular virus, your body is essentially unable temporarily to prevent viral multiplication inside your body.
Herpes virus type 5 is also known as cytomegalovirus. It is the major cause of mononucleosis. Mononucleosis causes symptoms similar to infectious mononucleosis. It is spread via blood transfusion, breast-feeding, organ transplants, and sexual contact. The virus causes diarrhea, or severe vision problems and even leads to AIDS. People with weakened immune systems are more susceptible to these diseases.
If you are pregnant and have genital herpes, it is very important for you to go to prenatal care visits. Tell your doctor if you have ever had symptoms of, or have been diagnosed with, genital herpes. Also tell your doctor if you have ever been exposed to genital herpes. There is some research that suggests that genital herpes infection may lead to miscarriage, or could make it more likely for you to deliver your baby too early.
Although there is no cure for herpes, treatments can relieve the symptoms. Medication can decrease the pain related to an outbreak and can shorten healing time. They can also decrease the total number of outbreaks. Drugs including Famvir, Zovirax, and Valtrex are among the drugs used to treat the symptoms of herpes. Warm baths may relieve the pain associated with genital sores.
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