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.
Although the exact cause of Bell's palsy—a type of facial paralysis—is unknown, it may be related to reactivation of HSV-1. 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. Antivirals may improve the condition slightly when used together with corticosteroids in those with severe disease.
Neonatal herpes simplex is a HSV infection in an infant. It is a rare but serious condition, usually caused by vertical transmission of HSV-1 or -2) from mother to newborn. During immunodeficiency, herpes simplex can cause unusual lesions in the skin. One of the most striking is the appearance of clean linear erosions in skin creases, with the appearance of a knife cut. Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicles.:369 Eczema herpeticum is an infection with herpesvirus in patients with chronic atopic dermatitis may result in spread of herpes simples throughout the eczematous areas.:373
As with almost all sexually transmitted infections, women are more susceptible to acquiring genital HSV-2 than men. On an annual basis, without the use of antivirals or condoms, the transmission risk of HSV-2 from infected male to female is about 8–11%. This is believed to be due to the increased exposure of mucosal tissue to potential infection sites. Transmission risk from infected female to male is around 4–5% annually. Suppressive antiviral therapy reduces these risks by 50%. Antivirals also help prevent the development of symptomatic HSV in infection scenarios, meaning the infected partner will be seropositive but symptom-free by about 50%. Condom use also reduces the transmission risk significantly. Condom use is much more effective at preventing male-to-female transmission than vice versa. Previous HSV-1 infection may reduce the risk for acquisition of HSV-2 infection among women by a factor of three, although the one study that states this has a small sample size of 14 transmissions out of 214 couples.
During these periods, it is especially important to abstain from kissing and any form of physical contact with the blistering area, saliva, or sexual discharge. If you are infected, be sure to wash your hands after touching an infected area on either the oral or genital regions. Herpes medications can also help reduce your risk of transmitting the virus to another individual.
Herpes is contracted through direct contact with an active lesion or body fluid of an infected person. Herpes transmission occurs between discordant partners; a person with a history of infection (HSV seropositive) can pass the virus to an HSV seronegative person. Herpes simplex virus 2 is typically contracted through direct skin-to-skin contact with an infected individual, but can also be contracted by exposure to infected saliva, semen, vaginal fluid, or the fluid from herpetic blisters. To infect a new individual, HSV travels through tiny breaks in the skin or mucous membranes in the mouth or genital areas. Even microscopic abrasions on mucous membranes are sufficient to allow viral entry.
Some people experience very mild genital herpes symptoms or no symptoms at all. Frequently, people infected with the virus don't even know they have it. However, when it causes symptoms, it can be described as extremely painful. This is especially true for the first outbreak, which is often the worst. Outbreaks are described as aches or pains in or around the genital area or burning, pain, or difficulty urinating. Some people experience discharge from the vagina or penis.
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.
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).
However, asymptomatic carriers of the HSV-2 virus are still contagious. In many infections, the first symptom people will have of their own infections is the horizontal transmission to a sexual partner or the vertical transmission of neonatal herpes to a newborn at term. Since most asymptomatic individuals are unaware of their infection, they are considered at high risk for spreading HSV.
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
There’s herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2). “HSV-1 and HSV-2 are different but closely related viruses,” says Dr. Christine Johnston, MPH, who is the Associate Medical Director of the Virology Research Clinic at the University of Washington. Johnston explains that both are transmitted through close mucosal or skin contact with infected secretions. HSV-1 primarily causes oral outbreaks, also known as cold sores, and HSV-2 usually causes genital outbreaks. But HSV-1 can also cause genital outbreaks through oral-to-genital contact, according to the CDC. According to Johnston, genital HSV-1 is less likely to recur than HSV-2, and there’s less asymptomatic shedding (transmitting the virus without realizing it) with HSV-1 than with HSV-2.
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
HSV-1 has been proposed as a possible cause of Alzheimer's disease. In the presence of a certain gene variation (APOE-epsilon4 allele carriers), HSV-1 appears to be particularly damaging to the nervous system and increases one's risk of developing Alzheimer's disease. The virus interacts with the components and receptors of lipoproteins, which may lead to its development.
HSV asymptomatic shedding occurs at some time in most individuals infected with herpes. It can occur more than a week before or after a symptomatic recurrence in 50% of cases. Virus enters into susceptible cells by entry receptors such as nectin-1, HVEM and 3-O sulfated heparan sulfate. Infected people who show no visible symptoms may still shed and transmit viruses through their skin; asymptomatic shedding may represent the most common form of HSV-2 transmission. Asymptomatic shedding is more frequent within the first 12 months of acquiring HSV. Concurrent infection with HIV increases the frequency and duration of asymptomatic shedding. Some individuals may have much lower patterns of shedding, but evidence supporting this is not fully verified; no significant differences are seen in the frequency of asymptomatic shedding when comparing persons with one to 12 annual recurrences to those with no recurrences.