I am so scared. My boyfriend is the only person I have ever had unprotected sex with 4 times. We had a herpes scare. He got tested. They swabbed him and gave him a blood test and his results for Herpes 1 and 2 came back negative. I went to the doctor but the lumps on my vagina healed and they said come back when you have a lesion. I told my BF but he still wanted to have sex, I told him what the doctor said and I told him we should not have sex or use a condom. He said it does not matter because if he did not have herpes I did not have Herpes. He said ok and put the condom on but  when we were done he started to laugh and said he took the condom off. Since then we have had sex twice. I went to the doctor and they gave me a blood test. They said if something was wrong they would send a letter to the house. Since they never sent the letter to the house I thought I was fine and I never had any other lumps since then and my boy friend never had any symptoms I thought I was fine.Today something told me to go to the doctor. I went and they said they never ordered the test. I AM So ANGRY. What Should I do? If I do have it shouldn't it have been in his blood from me? I am so scared that I may have it? I am also worried that one day he may get symptoms because his test was wrong and think I gave it to him when he was the one who may have given it to me if my blood test comes back positive. I have only had sex once with a condom before him. What should I do? He has had other a few partners. What is the likely hood that I may have given him herpes?
Primary orofacial herpes is readily identified by examination of persons with no previous history of lesions and contact with an individual with known HSV infection. The appearance and distribution of sores is typically presents as multiple, round, superficial oral ulcers, accompanied by acute gingivitis.[39] Adults with atypical presentation are more difficult to diagnose. Prodromal symptoms that occur before the appearance of herpetic lesions help differentiate HSV symptoms from the similar symptoms of other disorders, such as allergic stomatitis. When lesions do not appear inside the mouth, primary orofacial herpes is sometimes mistaken for impetigo, a bacterial infection. Common mouth ulcers (aphthous ulcer) also resemble intraoral herpes, but do not present a vesicular stage.[39]
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]
Evidence is insufficient to support use of many of these compounds, including echinacea, eleuthero, L-lysine, zinc, monolaurin bee products, and aloe vera.[68] While a number of small studies show possible benefit from monolaurin, L-lysine, aspirin, lemon balm, topical zinc, or licorice root cream in treatment, these preliminary studies have not been confirmed by higher-quality randomized controlled studies.[69]
For mild infections, self-care may be adequate for treatment. Other treatments termed "home remedies" are not considered cures but can ease or hasten recovery. These remedies include aloe vera gel, cornstarch paste, and tea or mint leaves. A cool compress may reduce pain. There is no cure for the infection. People with severe infection symptoms, especially children, should be evaluated by a medical caregiver.
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.
That being said, if on paper the HSV titres are high, indicating a high viral load in the body, this can be an indicator of an impending flare. Knowing this, we can prescribe antiviral medications with the aim of suppressing the virus activity. The idea is that we reduce the viral load of HSV, therefore helping the body’s immunity better contain the virus.
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