Worldwide rates of either HSV-1 or HSV-2 are between 60% and 95% in adults.[4] HSV-1 is usually acquired during childhood.[1] Rates of both increase as people age.[4] Rates of HSV-1 are between 70% and 80% in populations of low socioeconomic status and 40% to 60% in populations of improved socioeconomic status.[4] An estimated 536 million people worldwide (16% of the population) were infected with HSV-2 as of 2003 with greater rates among women and those in the developing world.[10] Most people with HSV-2 do not realize that they are infected.[1] The name is from Greek: ἕρπης herpēs which means "to creep", referring to spreading blisters.[11] The name does not refer to latency.[12]
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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]
Herpes virus type 1 (HSV-1) is the cause of cold sores or fever blisters around the mouth. Usually, the sores or blisters can show up on the outside of the mouth or on the lips. But sometimes, they can be inside the mouth, on the face, nose, cheeks or fingers. HSV-1 can also lead to infection of the genitals, called genital herpes. This occurs when you have a cold sore and perform oral sex on another person. HSV-1 infections are highly contagious. Apart from oral-genital contact, they can be spread through skin-to-skin contact. If you come into contact with a person or a thing that carries HSV-1, you will be likely to get it, too. Often, people get HSV-1 from kissing someone with a cold sore or when they share eating utensils, razors, or towels.
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.
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

Herpesviral encephalitis and herpesviral meningitis Herpes simplex encephalitis (HSE) is a rare life-threatening condition that is thought to be caused by the transmission of HSV-1 either from the nasal cavity to the brain's temporal lobe or from a peripheral site on the face, along the trigeminal nerve axon, to the brainstem.[16][17][18][19] Despite its low incidence, HSE is the most common sporadic fatal encephalitis worldwide. HSV-2 is the most common cause of Mollaret's meningitis, a type of recurrent viral meningitis.
“You don’t want an infant delivered through infected birth canal or vulva because the infant can be infected,” Cullins explains. A neonatal herpes infection is a real risk because it can cause problems with brain development and eye and skin infections, or even be fatal. And since there is more risk for transmission from mother to baby during an initial outbreak than during a recurrent outbreak, the CDC stresses that it’s incredibly important for pregnant women to avoid contracting a new herpes infection.
The frequency and severity of recurrent outbreaks vary greatly between people. Some individuals' outbreaks can be quite debilitating, with large, painful lesions persisting for several weeks, while others experience only minor itching or burning for a few days. Some evidence indicates genetics play a role in the frequency of cold sore outbreaks. An area of human chromosome 21 that includes six genes has been linked to frequent oral herpes outbreaks. An immunity to the virus is built over time. Most infected individuals experience fewer outbreaks and outbreak symptoms often become less severe. After several years, some people become perpetually asymptomatic and no longer experience outbreaks, though they may still be contagious to others. Immunocompromised individuals may experience longer, more frequent, and more severe episodes. Antiviral medication has been proven to shorten the frequency and duration of outbreaks.[79] Outbreaks may occur at the original site of the infection or in proximity to nerve endings that reach out from the infected ganglia. In the case of a genital infection, sores can appear at the original site of infection or near the base of the spine, the buttocks, or the back of the thighs. HSV-2-infected individuals are at higher risk for acquiring HIV when practicing unprotected sex with HIV-positive persons, in particular during an outbreak with active lesions.[80]
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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