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, keratitis, in immunocompromised (transplant) patients, or disseminated herpes zoster. The original compounds used were 5-iodo-2'-deoxyuridine, AKA idoxuridine, IUdR, or(IDU) and 1-β-D-arabinofuranosylcytosine or ara-C, later marketed under the name cytosar or cytarabine. The usage expanded to include topical treatment of herpes simplex, zoster, and varicella. Some trials combined different antivirals with differing results. 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, trifluorothymidine (TFT), Ribivarin, interferon, Virazole, and 5-methoxymethyl-2'-deoxyuridine (MMUdR). The introduction of 9-(2-hydroxyethoxymethyl)guanine, AKA aciclovir, in the late 1970s raised antiviral treatment another notch and led to vidarabine vs. aciclovir trials in the late 1980s. 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. 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. However, aciclovir seems to inhibit antibody response, and newborns on aciclovir antiviral treatment experienced a slower rise in antibody titer than those on vidarabine.
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.
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.
The most effective method of avoiding genital infections is by avoiding vaginal, oral, and anal sex. Condom use decreases the risk. Daily antiviral medication taken by someone who has the infection can also reduce spread. There is no available vaccine and once infected, there is no cure. Paracetamol (acetaminophen) and topical lidocaine may be used to help with the symptoms. Treatments with antiviral medication such as aciclovir or valaciclovir can lessen the severity of symptomatic episodes.
Primary Infection: This is the first stage wherein the contagion reproduces upon entering from the mucous membrane or skin. Typical symptom is the appearance of oral lesions which may not be present initially resulting in an asymptotic infection. In this case due to lack of symptoms one will be unaware of the presence of an infection. The sores usually takes 21 days to form and become visible, then the blisters will persist up to 10 days before beginning to heal.
Not every person with a herpes infection actually experiences breakouts of cold sores throughout his or her lifetime or even after initially becoming infected. How often someone has a herpes cold sore outbreak, how severe the outbreaks are, how contagious someone is after infection and how long the sores take to heal all depend on someone’s individual immune response.
Herpes simplex type 1, which is transmitted through oral secretions or sores on the skin, can be spread through kissing or sharing objects such as toothbrushes or eating utensils. In general, a person can only get herpes type 2 infection during sexual contact with someone who has a genital HSV-2 infection. It is important to know that both HSV-1 and HSV-2 can be spread even if sores are not present.
"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."