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.

Consequently, you may already have the virus. A doctor can determine this with a blood test for Herpes 2 (Ig), a type-specific immunoglobulin. If you are already infected, you won’t be at risk for a new infection — you and your boyfriend already share the virus. But knowing your herpes status will tell you whether you are capable of infecting a future partner.
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]
After exposure to the virus, many people experience a so called primary infection which is typically associated with sores on or around the genitals or the anus. During a primary infection some people experience pain in the groins or a mild fever. Not all infected individuals experience a primary infection or show any symptoms at all, but they can still pass the disease on to other people.
Genital herpes is passed on by skin-to-skin contact during vaginal, oral or anal sex, or by sharing sex toys. You can get genital herpes even if there are no visible sores or blisters, and once you have the virus, there is no cure. 'Herpes is more likely to be passed on just before, during or straight after an outbreak, as herpes blisters and sores are highly infectious,' says O’Sullivan.
This content is accurate and true to the best of the author’s knowledge and does not substitute for diagnosis, prognosis, treatment, prescription, and/or dietary advice from a licensed health professional. Drugs, supplements, and natural remedies may have dangerous side effects. If pregnant or nursing, consult with a qualified provider on an individual basis. Seek immediate help if you are experiencing a medical emergency.
Herpes has been known for at least 2,000 years. Emperor Tiberius is said to have banned kissing in Rome for a time due to so many people having cold sores. In the 16th-century Romeo and Juliet, blisters "o'er ladies' lips" are mentioned. In the 18th century, it was so common among prostitutes that it was called "a vocational disease of women".[91] The term 'herpes simplex' appeared in Richard Boulton's A System of Rational and Practical Chirurgery in 1713, where the terms 'herpes miliaris' and 'herpes exedens' also appeared. Herpes was not found to be a virus until the 1940s.[91]
To reduce the chance of acquiring HSV-1, avoid touching saliva, skin, or mucous membranes of people who have HSV-1 lesions. Prevention of genital HSV may be accomplished by latex condoms, but protection is never 100%. Spermicides do not protect against HSV. Some clinicians recommend using dental dams (small latex squares) during oral sex, but like condoms, they are not 100% protective.
Herpes symptoms commonly show in or around the mouth. Sores may also occur at the back of the throat, causing the lymph nodes in the neck to swell. Mouth herpes is very common in children, as their parents or relatives can pass it on to them easily by a greeting or goodnight kiss. To get a better understanding of oral herpes, let us take a look at its causes.
Once a person is infected, there are no symptoms for anywhere between 2 days to 2 weeks. This is known as the incubation period and is the time during which the virus multiplies profusely. The first symptoms that are seen are the small fluid-filled blisters known as vesicles. This arises as the virus starts destroying cells at the site and causes intense localized inflammation. These small vesicles or sometimes the larger bullae may either burst resulting in ulcer or heal completely with no scarring. The virus may also travel from the site of infection and “hides” by the sensory dorsal root. Here it remains latent until is it is reactivated.

People who have had HSV-1 are less likely to contract HSV-2 than those who have not. Previous exposure to HSV-1 also decreases the severity of an HSV-2 outbreak. Reoccurrence of the virus is common, and the virus can be active yet asymptomatic. These infections are more likely to be contracted since the person isn’t aware the virus is active. Studies have shown that 50 percent of the cases of sexual transmission of the virus occurred during asymptomatic infections.
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.
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.
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.
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.

The cell this virus targets is the B lymphocyte. These cells mature in the bone marrow and are a type of mononuclear leukocyte cells - white blood cells with a one-lobed nucleus. The incubation period for the Epstein – Barr Virus (EBV) is about 30 to 50 days, and patients typically have enlarged lymph nodes and spleens. Some patients have signs of hepatitis.
Herpes, whether on the mouth or genitals, is caused by a family of over 70 related viruses. These viral infections cause small, fluid-filled blisters to develop on the skin and mucous membranes. There are actually eight different types of herpes simplex viruses that both children and adults can acquire, but two are by far the most common: HSV-1 and HSV-2.
HSV-2 is contracted through forms of sexual contact with a person who has HSV-2. An estimated 20 percent of sexually active adults in the United States are infected with HSV-2, according to the American Academy of Dermatology (AAD). HSV-2 infections are spread through contact with a herpes sore. In contrast, most people get HSV-1 from an infected person who is asymptomatic, or does not have sores.
Genital herpes is contracted through sexual activity, and may show symptoms around the genital area (anus, buttocks, thigh, penis, vulva, etc.). Additionally, people with HIV can experience significantly worse symptoms of herpes.  See a doctor if your partner has herpes, or if you notice any unusual sores on your body.  How do you know if you have herpes?  Read more in our Diagnosing Herpes section here.  
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]
Antibodies that develop following an initial infection with a type of HSV prevents reinfection with the same virus type—a person with a history of orofacial infection caused by HSV-1 cannot contract herpes whitlow or a genital infection caused by HSV-1.[citation needed] In a monogamous couple, a seronegative female runs a greater than 30% per year risk of contracting an HSV infection from a seropositive male partner.[37] If an oral HSV-1 infection is contracted first, seroconversion will have occurred after 6 weeks to provide protective antibodies against a future genital HSV-1 infection.[citation needed] Herpes simplex is a double-stranded DNA virus.[38]
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