I do plan on dumping him, but I don't know how. I think I am still with him because I think if my test comes back positive for genital herpes he is the only guy who will ever want me if he did in fact give it to me or I have to stay with him because I may have given it to him. Somedays I feel like I can hand the idea of having herpes for the rest of my life but other days I am not so sure. I am so afraid. Its funny I use to say I never wanted to get married and have kids, but this situation has made me realize how much I want those things and now I may never get the chance. I guess thats life. Funny, as I write this I remember the first time I had sex with him he told me he used a condom but I don't think he did. I am such an idiot. I pray my blood test comes back negative. If it comes back positive life for me will be over.
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]
Only a health care provider can diagnose herpes by performing a physical exam and tests. A blood test can tell if you are infected with oral or genital herpes — even if you don't have symptoms. Health care providers can also confirm herpes infection by testing fluids taken from the sores. If you think you have herpes sores, get them checked out as soon as possible. Your local Planned Parenthood health center, many other health centers that test for sexually transmitted diseases, private health care providers, and health departments offer herpes tests and herpes treatments.

HSV-1 has been proposed as a possible cause of Alzheimer's disease.[26][27] In the presence of a certain gene variation (APOE-epsilon4 allele carriers), HSV-1 appears to be particularly damaging to the nervous system and increases one's risk of developing Alzheimer's disease. The virus interacts with the components and receptors of lipoproteins, which may lead to its development.[28][29]
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.
There’s herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2). “HSV-1 and HSV-2 are different but closely related viruses,” says Dr. Christine Johnston, MPH, who is the Associate Medical Director of the Virology Research Clinic at the University of Washington. Johnston explains that both are transmitted through close mucosal or skin contact with infected secretions. HSV-1 primarily causes oral outbreaks, also known as cold sores, and HSV-2 usually causes genital outbreaks. But HSV-1 can also cause genital outbreaks through oral-to-genital contact, according to the CDC. According to Johnston, genital HSV-1 is less likely to recur than HSV-2, and there’s less asymptomatic shedding (transmitting the virus without realizing it) with HSV-1 than with HSV-2.
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 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]
Many HSV-infected people experience recurrence within the first year of infection.[14] Prodrome precedes development of lesions. Prodromal symptoms include tingling (paresthesia), itching, and pain where lumbosacral nerves innervate the skin. Prodrome may occur as long as several days or as short as a few hours before lesions develop. Beginning antiviral treatment when prodrome is experienced can reduce the appearance and duration of lesions in some individuals. During recurrence, fewer lesions are likely to develop and are less painful and heal faster (within 5–10 days without antiviral treatment) than those occurring during the primary infection.[14] Subsequent outbreaks tend to be periodic or episodic, occurring on average four or five times a year when not using antiviral therapy.
Human herpes virus 3 (HHV3) is also called varicella-zoster virus. HHV3 causes chickenpox. It can also cause a recurrent virus infection of the skin, which is called herpes zoster or shingles. Shingles occurs when dormant varicella-zoster virus from an initial bout of chickenpox becomes reactivated. Like its close relative, HHV1, herpes zoster likes to infect skin cells and nerve cells. This virus may also recur along nerve fibre pathways, causing multiple sores where nerve fibres end on skin cells. Because an entire group of nerve cells is often affected, shingles is generally much more severe than a recurrence of herpes simplex. The lesions generally appear in a band-like or belt-like pattern occurring on one side of the body and are often accompanied by itching, tingling, or even severe pain. Healing usually occurs in 2 to 4 weeks, and scars may remain. Postherpetic neuralgia is a complication of shingles where the pain associated with the infection can persist for months and even years. Most people who experience shingles once do not experience it again.
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).
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]
There’s quite a variety, in short. And while genital herpes certainly can and does cause these signs of infection literally on the genitals (the penis or the vulva) it also can produce signs of infection nearby. Herpes sores on or between the buttocks are common (and sometimes slow to heal), as are lesions on the thigh. Herpes can bring about what feels like a tiny fissure around the anus, something easily confused with hemorrhoids. So remember: recurring signs and symptoms in the genital or anal area could well be herpes lesions.

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]
Herpes virus type 4 is also called Epstein-Barr virus. It typically causes infectious mononucleosis, a “kissing” disease. Symptoms include skin rash, fever, sore throat and swollen lymph glands. The virus can be involved in cancers like nasopharyngeal cancer. Herpes virus type 4 is contagious through bodily fluids, including saliva. Kissing, coughing, sneezing, or sharing utensils can make the infection spread.
These herpes viruses enter the body through small cuts, abrasions, or breaks in the skin or mucous membranes. The incubation period for herpes simplex infections is about three to six days. Transmission (spread) of the virus is person to person and more likely to occur if blisters or lesions are present. The majority enter after an uninfected person has direct contact with someone carrying the virus (either with or without noticeable lesions). Simply touching an infected person is often the way children get exposed. Adolescents and adults frequently get exposed by skin contact but may get their first exposure by kissing or sexual contact (oral and/or genital contact), especially for HSV-2. Statistical studies suggest that about 80%-90% of people in the U.S. have been exposed to HSV-1 and about 30% have been exposed to HSV-2. Usually, the contagious period continues until lesions heal. Some people (estimated from 30%-50%) occasionally shed herpes virus while having few or no associated symptoms or signs.
Genital herpes is an incurable disease. But, there are medications to relieve symptoms and prevent recurrent outbreaks. Prosurx is the best and most common treatment option for genital herpes. It can give your partner immediate relief and stop their outbreak before it starts. Prosurx can also reduce your partner’s risks of spreading the virus to you. So, ask your partner to apply Prosurx 2-3 times a day to get rid of genital herpes.

Genital herpes is an incurable disease. But, there are medications to relieve symptoms and prevent recurrent outbreaks. Prosurx is the best and most common treatment option for genital herpes. It can give your partner immediate relief and stop their outbreak before it starts. Prosurx can also reduce your partner’s risks of spreading the virus to you. So, ask your partner to apply Prosurx 2-3 times a day to get rid of genital herpes.
A 2004 study in the New England Journal of Medicine found that suppressive therapy decreases the risk of HSV-2 transmission from symptomatic, infected partners to uninfected partners by 48%. So “the risk of transmission is significantly reduced, but cannot be eliminated even with suppressive therapy,” Johnston explains, and she stresses that the virus can be passed along even without signs or symptoms.
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