If abstinence is not possible, using a sexual barrier (such as a condom or dental dam) can reduce the likelihood of transmission, although there is still a risk that these methods will not be sufficient to prevent the spread of the virus. It’s also a good idea to keep a visual reminder of your infection at hand to avoid any accidental food or beverage sharing.
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]
We usually do this for short durations of time. Not something that can be taken as lifelong therapy. I know it might not make sense to some of you. You’re probably asking why it is that we can’t just take the suppressive antiviral medications for the rest of our lives and with that, have no flares of herpes? Well basically, we know that having a high viral load is not the definitive factor in determining a herpetic flare. It is how the body is coping with the virus. So ultimately, you can be taking medications for months on end with your body in good shape to contain the virus so that there are no breakouts but that does not mean that the virus is eliminated from your body.
The flares are caused when your immune system falters. This can be due to a number of reasons. Anything from daily stressors, lack of sleep, poor nutrition, weight gain, concurrent illnesses etc may cause your immune system to be distracted from the Herpes Simplex Virus (HSV) infection. The moment that happens, the virus will flare resulting in rashes, cold sores, ulcers or blisters on your body.
Genital herpes is passed on by skin-to-skin contact during vaginal, oral or anal sex, or by sharing sex toys. You can get genital herpes even if there are no visible sores or blisters, and once you have the virus, there is no cure. 'Herpes is more likely to be passed on just before, during or straight after an outbreak, as herpes blisters and sores are highly infectious,' says O’Sullivan.
Transmission of HSV-1 occurs by direct exposure to saliva or droplets formed in the breath of infected individuals. In addition, skin contact with the lesions on an infected individual can spread the disease to another individual. Although close personal contact is usually required for transmission of the virus, it is possible to transmit HSV-1 when people share toothbrushes, drinking glasses, or eating utensils.
Particularly when someone is on suppressive antiviral medication and practicing safer sex, risk of transmission can be greatly reduced. Cullins suggests female condoms (condoms that go inside the vagina and cover most of the vulva, though it's important to note that not all people with vaginas are female) to provide the most protection against transmission, though condoms that go over the penis will protect what they cover.
"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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