“Herpes is caused by sexual intimacy and contact with a person who is actively shedding the herpes virus,” says Cullins. If you have HSV-1, that shedding could happen through the mouth or a cold sore, which means that the virus can be transmitted through kissing, or just sharing a drink. If you have herpes that affects the genitals, it can be transmitted from sharing sex toys, grinding, or even mutual masturbation — any activity where the virus can be transmitted from one person to another through skin-to-skin or mucosal contact.
Because the herpes virus is so common most people who have either genital or oral herpes do not know that they have it.   Additionally, the symptoms of HSV1 or 2 may be mild or at time, may not appear for days, weeks, or even years and sometimes no symptoms of herpes are present at all.  It is important to note that symptoms do not have to be present in order to contract this virus, so it is important that you prevent transmission through proper hygiene and awareness.
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]
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.

The herpes simplex virus is probably the most well-known virus of the herpes family, and it is just as contagious. Herpes simplex infects epithelial cells and remains latent in neurons. HSV-1 causes recurrent oropharyngeal lesions, commonly known as “fever blisters" or "cold sores.” It is also the primary cause of sporadic encephalitis (inflammation of the brain), gingivostomatitis (inflammation of the gums and mucous lining of the mouth), and keratoconjunctivitis (severe dryness of the eye that involves the cornea) and dendritic corneal ulcers (also called HSV keratitis) in which the cornea becomes affected by herpetic lesions that look like the dendrites of neurons in the brain.
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.

Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications.

As of 2017, there is not currently a herpes vaccine available to prevent HSV-1 or HSV-2. (There is a vaccine available for another virus, herpes zoster; however, despite the similar name, it actually refers to the shingles virus. And, in fact, shingles occurs due to the reactivation of yet another virus, varicella zoster, which causes chicken pox.)

Cullins explains that even if you’ve never had an outbreak, if you’ve been exposed to herpes, it lies dormant in your body. A blood test could reveal antibodies for HSV-1 and/or HSV-2, which means that you have been exposed to the infection in your past, you have been infected, and you have developed antibodies because your body has or is fighting the infection.

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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