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.
At least 80 to 90 percent of people in the U.S. have already been exposed to the HSV-1 virus.sup style="font-size: 10px;">21 Meanwhile, around 3.7 billion HSV-1 infections were recorded in 2012 all over the world, according to the World Health Organization. Africa was home to the highest number of cases, with 87 percent of occurrences coming from this continent.22
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).
Recurrent outbreaks of genital herpes may happen, with some patients having four to six outbreaks in the span of a year. Compared to the first infection, subsequent recurrences are less painful and occur in shorter periods than the first infection. There are some patients, however, who don’t have another outbreak for many years or even once more during their lifetime.11
Pain, itching and the appearance of sores called lesions are common symptoms of genital herpes. Lesions may appear inside or outside the vagina, and on or around the penis. In both women and men, these sores may appear in and around the anus.6 Lesions typically appear from two days to two weeks after you first get infected with the virus, and will take seven to 14 days or more to heal.7
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]
Mouth herpes{also known as oral herpes) primarily affects children of more than 6 months of age or who are aged 1-2 years  and it affects adults also.  When this virus is inside your mouth it is sometimes confused with a canker sore. It results in painful red fluid-filled blisters or lesions on the tongue, lips, inside of the cheeks, and gums often accompanied with an itchy or burning sensation. Muscle pain and fever can also be suffered at a later stage.  If treatment is ignored, a herpes infection inside your mouth can be dangerous.

HSV-2 is commonly referred to as genital herpes because it usually causes cold sores to erupt around the genitalia. In fact, genital herpes is the No. 1 cause of genital ulcers worldwide, according to the Centers for Disease Control and Prevention (CDC), and affects up to 1 in 3 adults (although most who are infected don’t even know it). (5) Both types of herpes viruses are highly contagious, and both can cause cold sores in either area of the body (or sometimes both). 


You should stop having sexual contact as soon as you feel warning signs of an outbreak. Warning signs may include a burning, itching, or tingling feeling on the genitals or around the mouth. Do not have vaginal, anal, or oral sex — even with a condom — until seven days after the warning signs stop or the sore heals. The virus can spread from sores not covered by the condom. It can also spread in sweat or vaginal fluids to places the condom doesn't cover.
A scary finding is that more cases of genital herpes than ever before are now being caused by HSV-1 (the type most people assume only causes mouth sores), and about 85 percent of people with genital herpes don’t even know it. (7) Studies show that about 50 percent of the new genital herpes infections in young adults are due to HSV-1 and about 40 percent in older adults. The fact that most people don’t ever find out they’re infected is one of the reasons that transmission rates are steadily climbing.
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