HSV infection causes several distinct medical disorders. Common infection of the skin or mucosa may affect the face and mouth (orofacial herpes), genitalia (genital herpes), or hands (herpetic whitlow). More serious disorders occur when the virus infects and damages the eye (herpes keratitis), or invades the central nervous system, damaging the brain (herpes encephalitis). People with immature or suppressed immune systems, such as newborns, transplant recipients, or people with AIDS, are prone to severe complications from HSV infections. HSV infection has also been associated with cognitive deficits of bipolar disorder,[13] and Alzheimer's disease, although this is often dependent on the genetics of the infected person.

^ Xu, Fujie; Fujie Xu; Maya R. Sternberg; Benny J. Kottiri; Geraldine M. McQuillan; Francis K. Lee; Andre J. Nahmias; Stuart M. Berman; Lauri E. Markowitz (2006-10-23). "Trends in Herpes Simplex Virus Type 1 and Type 2 Seroprevalence in the United States". JAMA. 296 (8): 964–73. doi:10.1001/jama.296.8.964. PMID 16926356. Archived from the original on 2010-04-24.
The HSV viruses multiply in the human cell by overtaking and utilizing most of the human cells functions. One of the HSV steps in multiplication is to take control of the human cell's nucleus and alter its structure. The altered nucleus (enlarged and lobulated or multinucleated) is what actually is used to help diagnose herpes simplex infections by microscopic examination. The reason sores appear is because as they mature the many HSV particles rupture the human cell's membrane as they break out of the cell.

Human herpes virus 2 (HHV2) is also called herpes simplex virus 2 (HSV2). It typically causes genital herpes, a sexually transmitted infection. However, it can also cause cold sores in the facial area. Like HHV1, the HHV2 infection is contagious and is spread by skin-to-skin contact. The main route of transmission is through sexual contact, as the virus does not survive very long outside the body.
Following active infection, herpes viruses establish a latent infection in sensory and autonomic ganglia of the nervous system. The double-stranded DNA of the virus is incorporated into the cell physiology by infection of the nucleus of a nerve's cell body. HSV latency is static; no virus is produced; and is controlled by a number of viral genes, including latency-associated transcript.[70]
'Using condoms or dams can help to protect against STIs, but herpes can also be passed on by skin-to-skin contact with the affected area, so it’s strongly recommended that you don’t have sex during this time,' she adds. 'This includes direct genital contact or skin-to-skin contact with the affected area, and doesn’t have to be penetrative sex,' says O’Sullivan.
Some people experience very mild genital herpes symptoms or no symptoms at all. Frequently, people infected with the virus don't even know they have it. However, when it causes symptoms, it can be described as extremely painful. This is especially true for the first outbreak, which is often the worst. Outbreaks are described as aches or pains in or around the genital area or burning, pain, or difficulty urinating. Some people experience discharge from the vagina or penis.
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'.
Condoms offer moderate protection against HSV-2 in both men and women, with consistent condom users having a 30%-lower risk of HSV-2 acquisition compared with those who never use condoms.[49] A female condom can provide greater protection than the male condom, as it covers the labia.[50] The virus cannot pass through a synthetic condom, but a male condom's effectiveness is limited[51] because herpes ulcers may appear on areas not covered by it. Neither type of condom prevents contact with the scrotum, anus, buttocks, or upper thighs, areas that may come in contact with ulcers or genital secretions during sexual activity. Protection against herpes simplex depends on the site of the ulcer; therefore, if ulcers appear on areas not covered by condoms, abstaining from sexual activity until the ulcers are fully healed is one way to limit risk of transmission.[52] The risk is not eliminated, however, as viral shedding capable of transmitting infection may still occur while the infected partner is asymptomatic.[53] The use of condoms or dental dams also limits the transmission of herpes from the genitals of one partner to the mouth of the other (or vice versa) during oral sex. When one partner has a herpes simplex infection and the other does not, the use of antiviral medication, such as valaciclovir, in conjunction with a condom, further decreases the chances of transmission to the uninfected partner.[14] Topical microbicides that contain chemicals that directly inactivate the virus and block viral entry are being investigated.[14]
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]

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.


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.
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.

Herpes infection can be passed from you to your unborn child before birth but is more commonly passed to your infant during delivery. This can lead to a potentially deadly infection in your baby (called neonatal herpes). It is important that you avoid getting herpes during pregnancy. If you are pregnant and have genital herpes, you may be offered anti-herpes medicine towards the end of your pregnancy. This medicine may reduce your risk of having signs or symptoms of genital herpes at the time of delivery. At the time of delivery, your doctor should carefully examine you for herpes sores. If you have herpes symptoms at delivery, a ‘C-section’ is usually performed.
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