Although the exact cause of Bell's palsy—a type of facial paralysis—is unknown, it may be related to reactivation of HSV-1.[23] This theory has been contested, however, since HSV is detected in large numbers of individuals having never experienced facial paralysis, and higher levels of antibodies for HSV are not found in HSV-infected individuals with Bell's palsy compared to those without.[24] Antivirals may improve the condition slightly when used together with corticosteroids in those with severe disease.[25]
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.
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.

Jamie*, 29, is HSV-positive and contracted herpes from her husband. But, she explains, “He only had one outbreak when he was young and that was it. So he didn't realize what it was.” Jamie was infected three years into their relationship simply because he had outbreaks that infrequently. She says, “I was worried he had cheated on me, but then found similar stories online, and our outbreak patterns underscore that what happened is very possible.”


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Varicella-zoster is transmitted though the mucosa of the respiratory system, specifically the upper respiratory tract, or the conjunctiva of the eye. Initial replication takes place in the regional lymph nodes, and then the virus spreads and replication begins in the liver and spleen. The virus is then transported to the skin where the rash develops. The incubation period of varicella is about 10 to 21 days.
Doctors prescribe suppressive treatment if a person experiences more than six recurrences in a year. In some cases, a doctor my recommend that the individual takes daily antiviral treatment indefinitely. The aim here is to prevent further recurrences. Although suppressive treatment significantly reduces the risk of passing HSV to a partner, there is still a risk.
Stage 3 -- Recurrence: When people encounter certain stresses (also termed triggers), emotional or physical, the virus may reactivate and cause new sores and symptoms. The following factors may contribute to or trigger recurrence: stress, illness, ultraviolet light (UV rays including sunshine), fever, fatigue, hormonal changes (for example, menstruation), immune depression, and trauma to a site or a nerve region where previous HSV infection occurred.
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]
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.
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.
Human herpes virus 6 (HHV6) is a recently observed agent found in the blood cells of a few patients with a variety of diseases. It causes roseola (a viral disease causing high fever and a skin rash in small children) and a variety of other illnesses associated with fever in that age group. This infection accounts for many of the cases of convulsions associated with fever in infancy (febrile seizures).
Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.

Herpes type 2 (HSV-2) can cause genital herpes. This is one of the most common sexually transmitted infections (STIs) in the US. It causes sores or painful blisters on the penis, vagina, scrotum, anus and buttocks. Along with blisters, people with HSV-2 may experience tingling, itching or pain. Like HSV-1, HSV-2 infections are highly contagious. They can be spread easily through skin-to-skin contact. Sexual intercourse is the main route of transmission.
"Oral herpes is an infection found in the mouth, or on and around the lips, caused by the Herpes Simplex Virus (HSV)," Michael explains. "There are two types or strains of this virus called HSV1 and HSV2. Usually, the HSV1 strain infects the mouth and lips, and the HSV2 strain infects the genitals. It is however possible for HSV2 to infect your mouth and lips."
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