Canker sores are sometimes thought to be caused by HSV, but this is not true. Canker sores occur only inside the mouth, on the tongue, and on the soft palate (roof of mouth), not on skin surfaces. Although they reoccur, they are not contagious, usually are self-limiting, and have almost no complications. Canker sores are caused by substances that irritate the lining of the mouth.
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“Someone having HSV doesn't mean that they were reckless or irresponsible with their sex life,” says Sara, age 30. “I used condoms with all my partners, and I still caught it.” For Jamie, who contracted herpes from her husband three years into their monogamous relationship, he was her first and only sexual partner. And she says that he contracted it from one of his very first sexual encounters. No matter how and why someone contracted the virus, it doesn't erase their humanity and right to respect.
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.

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.
I am looking at this at a totally different angle. Are you 100% sure you saw on paper his negative test results for HSV1 and 2? I am going to speculate here. What if this guy has it and knows he gave it to you since you had lumps and will play the card that you gave it to him when he gets his next outbreak? Just seems kind of odd for someone to take off a condom when you're screaming STD's at him. Something just isn't right and you know what Judge Judy says about things that don't sound right. I would ask your boyfriend for the written results of his HSV tests first and go from there.
Traditionally, it was assumed that HSV-1 strictly caused oral sores and blisters, whereas HSV-2 caused genital and/or rectal sores and blisters. However, the virus- or perhaps just our understanding of the virus itself- has evolved in such a way that doctors now recognize that either HSV-1 or HSV-2 can cause genital and/or rectal sores, albeit with HSV-2 causing the majority of sores in the genital or rectal areas.
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.
An important source of support is the National Herpes Resource Center which arose from the work of the American Sexual Health Association (ASHA).[113] The ASHA was created in 1914 to in response to the increase in sexually transmitted diseases that had spread during World War I.[114] During the 1970s, there was an increase in sexually transmitted diseases. One of the diseases that increased dramatically was genital herpes. In response, ASHA created the National Herpes Resource Center in 1979. The HRC was designed to meet the growing need for education and awareness about the virus. One of the projects of The Herpes Resource Center (HRC) was to create a network of local support (HELP) groups. The goal of these HELP groups was to provide a safe, confidential environment where participants can get accurate information and share experiences, fears, and feelings with others who are concerned about herpes.[115][116]
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]
According to Cullins, there are no standardized guidelines from the CDC for suppressive therapy through medication, but it is an option that people with HSV should talk to their healthcare providers about. “If a person knows they have had herpes in the past that has affected their genitals, they can take suppressive therapy — for example, 500 mg of valacyclovir daily.” While it won’t prevent outbreaks, it will prevent asymptomatic virus shedding. Preventing exposure to the virus through both medication and a physical barrier can be very effective.
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