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"Herpes" redirects here. For other uses, see .

For the virus that causes herpes simplex, see . For all types of herpes viruses, see .

Herpes simplex is a caused by the . Infections are categorized based on the part of the body infected. involves the face or mouth. It may result in small in groups often called cold sores or fever blisters or may just cause a sore throat., often simply known as herpes, may have minimal symptoms or form blisters that break open and result in small . These typically heal over two to four weeks. Tingling or shooting pains may occur before the blisters appear.Herpes cycles between periods of active disease followed by periods without symptoms. The first episode is often more severe and may be associated with fever, muscle pains, swollen and headaches. Over time, episodes of active disease decrease in frequency and severity. Other disorders caused by herpes simplex include: when it involves the fingers,,, and when it affects a newborn, among others.

There are two types of herpes simplex virus, type 1 (HSV-1) and type 2 (HSV-2). HSV-1 more commonly causes infections around the mouth while HSV-2 more commonly causes genital infections. They are transmitted by direct contact with body fluids or lesions of an infected individual. Transmission may still occur when symptoms are not present. Genital herpes is classified as a . It may be spread to an infant during childbirth. After infection, the viruses are transported along to the nerve cell bodies, where they . Causes of recurrence may include: , stress, and sunlight exposure. Oral and genital herpes is usually diagnosed based on the presenting symptoms. The diagnosis may be confirmed by or detecting herpes DNA in fluid from blisters. Testing the blood for against the virus can confirm a previous infection but will be negative in new infections.

The most effective method of avoiding genital infections is by avoiding vaginal, oral, and anal sex. use decreases the risk. Daily taken by someone who has the infection can also reduce spread. There is no available and once infected, there is no cure. (acetaminophen) and topical lidocaine may be used to help with the symptoms. Treatments with antiviral medication such as or can lessen the severity of symptomatic episodes.

Worldwide rates of either HSV-1 or HSV-2 are between 60% and 95% in adults. HSV-1 is usually acquired during childhood. Rates of both increase as people age. 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. 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. Most people with HSV-2 do not realize that they are infected. The name is from : ἕρπης herpēs which means "to creep", referring to spreading blisters. The name does not refer to latency.



Herpes simplex is divided into two types; HSV-1 causes primarily mouth, throat, face, eye, and infections, whereas HSV-2 causes primarily anogenital infections. However, each may cause infections in all areas.

Signs and symptoms

Herpes infection

HSV infection causes several distinct medical . Common infection of the skin or mucosa may affect the face and mouth (orofacial herpes), genitalia (genital herpes), or hands (). More serious disorders occur when the virus infects and damages the eye (), or invades the central nervous system, damaging the brain (herpes encephalitis). People with immature or suppressed immune systems, such as newborns, transplant recipients, or people with AIDS, are prone to severe complications from HSV infections. HSV infection has also been associated with cognitive deficits of , and , although this is often dependent on the of the infected person.

In all cases, HSV is never removed from the body by the . Following a primary infection, the virus enters the nerves at the site of primary infection, migrates to the of the neuron, and becomes latent in the . As a result of primary infection, the body produces antibodies to the particular type of HSV involved, preventing a subsequent infection of that type at a different site. In HSV-1-infected individuals, after an oral infection prevents additional HSV-1 infections such as whitlow, genital herpes, and herpes of the eye. Prior HSV-1 seroconversion seems to reduce the symptoms of a later HSV-2 infection, although HSV-2 can still be contracted.

Many people infected with HSV-2 display no physical symptoms—individuals with no symptoms are described as asymptomatic or as having herpes.

Condition Description Illustration Herpetic gingivostomatitis is often the initial presentation during the first herpes infection. It is of greater severity than herpes labialis, which is often the subsequent presentations. Herpesgingiva.JPG Infection occurs when the virus comes into contact with oral mucosa or abraded skin. Cold sore.jpg When symptomatic, the typical manifestation of a primary HSV-1 or HSV-2 genital infection is clusters of inflamed and on the outer surface of the genitals resembling cold sores. SOA-Herpes-genitalis-female.jpg and Herpes whitlow is a painful infection that typically affects the fingers or thumbs. On occasion, infection occurs on the toes or on the nail cuticle. Individuals who participate in such as , , and (soccer), sometimes acquire a condition caused by HSV-1 known as , scrumpox, wrestler's herpes, or mat herpes, which presents as skin ulceration on the face, ears, and neck. Symptoms include fever, headache, sore throat, and swollen glands. It occasionally affects the eyes or eyelids. Herpetic whitlow in young child.jpg and A herpetic infection of the brain thought to be caused by the transmission of virus from a peripheral site on the face following HSV-1 reactivation, along the , to the brain. HSV is the most common cause of viral encephalitis. When infecting the brain, the virus shows a preference for the . HSV-2 is the most common cause of Mollaret's meningitis, a type of recurrent viral meningitis. Hsv encephalitis.jpg Symptoms may include painful swallowing () and difficulty swallowing (). It is often associated with impaired immune function (e.g. , in solid ). Herpes esophagitis.JPG


is a HSV infection in an infant. It is a rare but serious condition, usually caused by 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. is a recurrent or initial herpes simplex infection affecting primarily the hair follicles.:369 is an infection with herpesvirus in patients with chronic may result in spread of herpes simples throughout the eczematous areas.:373

, a primary infection, typically presents as swelling of the and eyelids (), accompanied by small white itchy lesions on the surface of the .

Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the .:369

Bell's palsy

Although the exact cause of —a type of facial —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 in those with severe disease.

Alzheimer's disease

HSV-1 has been proposed as a possible cause of . In the presence of a certain gene variation (-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 , which may lead to its development.


Herpes shedding HSV-2 genital 15–25% of days HSV-1 oral 6–33% of days HSV-1 genital 5% of days HSV-2 oral 1% of days

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.

HSV asymptomatic 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.

Antibodies that develop following an initial infection with a type of HSV prevents reinfection with the same virus type—a person with a history of orofacial infection caused by HSV-1 cannot contract herpes whitlow or a genital infection caused by HSV-1.[] In a couple, a seronegative female runs a greater than 30% per year risk of contracting an HSV infection from a seropositive male partner. If an oral HSV-1 infection is contracted first, seroconversion will have occurred after 6 weeks to provide protective antibodies against a future genital HSV-1 infection. Herpes simplex is a double-stranded .


Primary orofacial herpes is readily identified by clinical examination of persons with no previous history of lesions and contact with an individual with known HSV-1 infection. The appearance and distribution of sores in these individuals typically presents as multiple, round, superficial oral ulcers, accompanied by acute . Adults with atypical presentation are more difficult to diagnose. Prodromal symptoms that occur before the appearance of herpetic lesions help differentiate HSV symptoms from the similar symptoms of other disorders, such as . When lesions do not appear inside the mouth, primary orofacial herpes is sometimes mistaken for , a bacterial . Common mouth ulcers () also resemble intraoral herpes, but do not present a stage.

Genital herpes can be more difficult to diagnose than oral herpes, since most HSV-2-infected persons have no classical symptoms. Further confusing diagnosis, several other conditions resemble genital herpes, including , , , and . testing is often used to confirm a diagnosis of genital herpes. Laboratory tests include culture of the virus, (DFA) studies to detect virus, , and to test for presence of viral DNA. Although these procedures produce highly sensitive and specific diagnoses, their high costs and time constraints discourage their regular use in clinical practice.

Until the 1980s tests for antibodies to HSV were rarely useful to diagnosis and not routinely used in clinical practice. The older IgM serologic assay could not differentiate between antibodies generated in response to HSV-1 or HSV-2 infection. However, a glycoprotein G-specific (IgG) HSV test introduced in the 1980s is more than 98% specific at discriminating HSV-1 from HSV-2.

It should not be confused with conditions caused by other viruses in the family such as , which is caused by . The includes due to similar lesions on the skin.


Barrier protection, such as a , can reduce the risk of herpes transmission.

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.

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.

In October 2011, the anti-HIV drug , when used topically in a microbicidal vaginal gel, was reported to reduce herpes virus sexual transmission by 51%.

Barrier methods

Condoms offer moderate protection against HSV-2 in both men and women, with consistent condom users having a 30%-lower risk of HSV-2 acquisition compared with those who never use condoms. A can provide greater protection than the male condom, as it covers the labia. The virus cannot pass through a synthetic condom, but a male condom's effectiveness is limited because herpes ulcers may appear on areas not covered by it. Neither type of condom prevents contact with the scrotum, anus, buttocks, or upper thighs, areas that may come in contact with ulcers or genital secretions during sexual activity. Protection against herpes simplex depends on the site of the ulcer; therefore, if ulcers appear on areas not covered by condoms, abstaining from sexual activity until the ulcers are fully healed is one way to limit risk of transmission. The risk is not eliminated, however, as viral shedding capable of transmitting infection may still occur while the infected partner is asymptomatic. The use of condoms or also limits the transmission of herpes from the genitals of one partner to the mouth of the other (or vice versa) during . When one partner has a herpes simplex infection and the other does not, the use of antiviral medication, such as , in conjunction with a condom, further decreases the chances of transmission to the uninfected partner. Topical that contain chemicals that directly inactivate the virus and block viral entry are being investigated.


Antivirals may reduce asymptomatic shedding; asymptomatic genital HSV-2 viral shedding is believed to occur on 20% of days per year in patients not undergoing antiviral treatment, versus 10% of days while on antiviral therapy.


The risk of transmission from mother to baby is highest if the mother becomes infected around the time of delivery (30% to 60%), since insufficient time will have occurred for the generation and transfer of protective maternal antibodies before the birth of the child. In contrast, the risk falls to 3% if the infection is recurrent, and is 1–3% if the woman is seropositive for both HSV-1 and HSV-2, and is less than 1% if no lesions are visible. Women seropositive for only one type of HSV are only half as likely to transmit HSV as infected seronegative mothers. To prevent neonatal infections, seronegative women are recommended to avoid unprotected oral-genital contact with an HSV-1-seropositive partner and conventional sex with a partner having a genital infection during the last trimester of pregnancy. Mothers infected with HSV are advised to avoid procedures that would cause trauma to the infant during birth (e.g. fetal scalp electrodes, forceps, and vacuum extractors) and, should lesions be present, to elect to reduce exposure of the child to infected secretions in the birth canal. The use of antiviral treatments, such as aciclovir, given from the 36th week of pregnancy, limits HSV recurrence and shedding during childbirth, thereby reducing the need for caesarean section.

Aciclovir is the recommended antiviral for herpes suppressive therapy during the last months of pregnancy. The use of valaciclovir and famciclovir, while potentially improving compliance, have less-well-determined safety in pregnancy.


No method eradicates herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks. such as and (acetaminophen) can reduce pain and fever. Topical anesthetic treatments such as , , , or can also relieve itching and pain.


The antiviral medication aciclovir

Several are effective for treating herpes, including (acyclovir), , , and . Aciclovir was the first discovered and is now available in . Valaciclovir is also available as a generic and is slightly more effective than aciclovir for reducing lesion healing time.

Evidence supports the use of aciclovir and valaciclovir in the treatment of herpes labialis as well as herpes infections in people with . The evidence to support the use of aciclovir in primary herpetic gingivostomatitis is weaker.


A number of antivirals are effective for herpes labialis, including aciclovir, penciclovir, and .

Alternative medicine

Evidence is insufficient to support use of many of these compounds, including , , , , bee products, and . While a number of small studies show possible benefit from monolaurin, L-lysine, , lemon balm, topical zinc, or licorice root cream in treatment, these preliminary studies have not been confirmed by higher-quality .


Following active infection, herpes viruses establish a infection in sensory and autonomic of the nervous system. The double-stranded DNA of the virus is incorporated into the cell physiology by infection of the of a nerve's . HSV latency is static; no virus is produced; and is controlled by a number of viral genes, including .

Many HSV-infected people experience recurrence within the first year of infection. precedes development of lesions. Prodromal symptoms include tingling (), itching, and pain where lumbosacral nerves innervate the skin. Prodrome may occur as long as several days or as short as a few hours before lesions develop. Beginning antiviral treatment when prodrome is experienced can reduce the appearance and duration of lesions in some individuals. During recurrence, fewer lesions are likely to develop and are less painful and heal faster (within 5–10 days without antiviral treatment) than those occurring during the primary infection. Subsequent outbreaks tend to be periodic or episodic, occurring on average four or five times a year when not using antiviral therapy.

The causes of reactivation are uncertain, but several potential triggers have been documented. A 2009 study showed the protein plays a key role in reactivation of the dormant virus. Changes in the immune system during may play a role in HSV-1 reactivation. Concurrent infections, such as viral or other febrile diseases, can cause outbreaks. Reactivation due to other infections is the likely source of the historic terms 'cold sore' and 'fever blister'.

Other identified triggers include local injury to the face, lips, eyes, or mouth; trauma; surgery; ; and exposure to wind, , or sunlight.

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 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. 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.


Main article:

Worldwide rates of either HSV-1 and/or HSV-2 are between 60 and 95% in adults. HSV-1 is more common than HSV-2, with rates of both increasing as people age. HSV-1 rates are between 70% and 80% in populations of low socioeconomic status and 40% to 60% in populations of improved socioeconomic status. An estimated 536 million people or 16% of the population worldwide were infected with HSV-2 as of 2003 with greater rates among women and in those in the developing world. Rates of infection are determined by the presence of against either .

In the , 58% of the population is infected with HSV-1 and 16% are infected with HSV-2. Among those HSV-2-seropositive, only 19% were aware they were infected. During 2005–2008, the prevalence of HSV-2 was 39% in blacks and 21% in women.

The annual incidence in Canada of genital herpes due to HSV-1 and HSV-2 infection is not known (for a review of HSV-1/HSV-2 prevalence and incidence studies worldwide, see Smith and Robinson 2002). As many as one in seven Canadians aged 14 to 59 may be infected with herpes simplex type 2 virus and more than 90 per cent of them may be unaware of their status, a new study suggests. In the United States, it is estimated that about 1,640,000 HSV-2 seroconversions occur yearly (730,000 men and 910,000 women, or 8.4 per 1,000 persons).

In British Columbia in 1999, the seroprevalence of HSV-2 antibody in leftover serum submitted for antenatal testing revealed a prevalence of 17%, ranging from 7% in women 15–19 years old to 28% in those 40–44 years.

In Norway, a study published in 2000 found that up to 70–90% of genital initial infections were due to HSV-1.

In Nova Scotia, 58% of 1,790 HSV isolates from genital lesion cultures in women were HSV-1; in men, 37% of 468 isolates were HSV-1.


Herpes has been known for at least 2,000 years. Emperor is said to have banned kissing in Rome for a time due to so many people having cold sores. In the 16th-century , blisters "o'er ladies' lips" are mentioned. In the 18th century, it was so common among prostitutes that it was called "a vocational disease of women". The term 'herpes simplex' appeared in 's A System of Rational and Practical Chirurgery in 1713, where the terms 'herpes miliaris' and 'herpes exedens' also appeared. Herpes was not found to be a virus until the 1940s.

Herpes antiviral therapy began in the early 1960s with the experimental use of medications that interfered with viral replication called (DNA) inhibitors. The original use was against normally fatal or debilitating illnesses such as adult encephalitis, keratitis, in immunocompromised (transplant) patients, or . 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 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.

Society and culture

Genital herpes simplex was not always . It was merely considered a cold sore until the 1970s. As late as 1975, a study of "Psychological morbidity in a clinic for sexually transmitted disease" does not mention herpes simplex because at that time, no significant problem (i.e. mental anxiety or illness) was associated with the virus.

Pedro Cuatrecasas states, "during the R&D of , marketing [department of ] insisted that there were 'no markets' for this compound. Most had hardly heard of genital herpes..." Thus, the medical condition—separating the 'normal cold sore' from the 'stigmatized genital infection' was to become the key to marketing the drug, a process now known as 'disease mongering'.

Since the creation of the herpes hype, some people experience negative feelings related to the condition following diagnosis, in particular if they have acquired the genital form of the disease. Feelings can include , fear of rejection, feelings of , fear of being found out, and self-destructive feelings. These feelings usually lessen over time. Much of the hysteria and stigma surrounding herpes stems from a media campaign beginning in the late 1970s and peaking in the early 1980s. Multiple articles were worded in fear-mongering and anxiety-provoking terminology, such as the now-ubiquitous "attacks", "outbreaks", "victims", and "sufferers". At one point, the term "herpetic" even entered the popular lexicon. The articles were published by , U.S. News, and Time magazine, among others. A made-for-TV movie was named Intimate Agony. The peak was when Time magazine had 'Herpes: The New Scarlet Letter' on the cover in August 1982, forever stigmatizing the word in the public mind. have been formed in the United States and the UK, providing information about herpes and running message forums and dating websites for sufferers. People with the herpes virus are often hesitant to divulge to other people, including friends and family, that they are infected. This is especially true of new or potential sexual partners whom they consider casual.

In a 2007 study, 1,900 people (25% of which had herpes) ranked genital herpes second for social stigma, out of all sexually transmitted diseases ( took the top spot for STD stigma).[111]

Support groups

United States

An important source of support is the National Herpes Resource Center which arose from the work of the American Social Health Association (ASHA). The ASHA was created in 1914 to in response to the increase in sexually transmittes diseases that had spread during . During the 1970s, there was an increase in sexually transmitted diseases. One of the diseases that increased dramatically was genital herpes. In response, ASHA created the National Herpes Resource Center in 1979. The HRC was designed to meet the growing need for education and awareness about the virus. One of the projects of The Herpes Resource Center (HRC) was to create a network of local support (HELP) groups. The goal of these HELP groups was to provide a safe, confidential environment where participants can get accurate information and share experiences, fears, and feelings with others who are concerned about herpes.


In the UK, the Herpes Association (now the ) was started in 1982, becoming a registered charity with a Dept of Health grant in 1985. The charity started as a string of local group meetings before acquiring an office and a national spread.


Main article:

Research has gone into vaccines for both prevention and treatment of herpes infections. Unsuccessful clinical trials have been conducted for some glycoprotein subunit vaccines. As of 2017, the future pipeline includes several promising replication-incompetent vaccine proposals while two replication-competent (live-attenuated) HSV vaccine are undergoing human testing.

A study of the herpes simplex type 1 virus confirmed the human migration pattern theory known as the .


  1. ^ . cdc.gov. December 8, 2014. from the original on 31 December 2014. Retrieved 31 December 2014.
  2. ^ Balasubramaniam, R; Kuperstein, AS; Stoopler, ET (April 2014). "Update on oral herpes virus infections". Dental clinics of North America. 58 (2): 265–80. :.  .
  3. ^ Elad S, Zadik Y, Hewson I, et al. (August 2010). . Support Care Cancer. 18 (8): 993–1006. :.  .
  4. ^ Chayavichitsilp P, Buckwalter JV, Krakowski AC, Friedlander SF (April 2009). "Herpes simplex". Pediatr Rev. 30 (4): 119–29, quiz 130. :.  .
  5. Mosby (2013). (9 ed.). Elsevier Health Sciences. pp. 836–37.  . from the original on 2017-09-06.
  6. Wu, IB; Schwartz, RA (March 2007). "Herpetic whitlow". Cutis. 79 (3): 193–06.  .
  7. Rowe, AM; St Leger, AJ; Jeon, S; Dhaliwal, DK; Knickelbein, JE; Hendricks, RL (January 2013). . Progress in retinal and eye research. 32: 88–101. :.  .  .
  8. Steiner, I; Benninger, F (December 2013). "Update on herpes virus infections of the nervous system". Current Neurology and Neuroscience Reports. 13 (12): 414. :.  .
  9. Stephenson-Famy, A; Gardella, C (December 2014). "Herpes Simplex Virus Infection During Pregnancy". Obstetrics and gynecology clinics of North America. 41 (4): 601–14. :.  .
  10. ^ Looker, KJ; Garnett, GP; Schmid, GP (October 2008). . Bulletin of the World Health Organization. 86 (10): 805–12, A. :.  .  .
  11. Beswick, TSL (1962). "The Origin and the Use of the Word Herpes". Med Hist (6): 214–232.
  12. Reese, Vail. . Online Journal of Community and Person-Centered Dermatology. Dr. David Elpern. Retrieved 22 September 2018.
  13. Dickerson FB, Boronow JJ, Stallings C, et al. (March 2004). "Infection with herpes simplex virus type 1 is associated with cognitive deficits in bipolar disorder". Biol. Psychiatry. 55 (6): 588–93. :.  .
  14. ^ Gupta R, Warren T, Wald A (December 2007). . Lancet. 370 (9605): 2127–37. :.  .
  15. Handsfield HH (2000). "Public Health Strategies to Prevent Genital Herpes: Where Do We Stand?". Curr Infect Dis Rep. 2 (1): 25–30. :.  .
  16. at
  17. Jocelyn A. Lieb; Stacey Brisman; Sara Herman; Jennifer MacGregor; Marc E. Grossman (2008). "Linear erosive Herpes Simplex Virus infection in immunocompromised patients: the "Knife-Cut Sign"". Clin Infect Dis. 47 (11): 1440–41. :.  .
  18. ^ James, William D.; Berger, Timothy G. (2006). Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier.  .
  19. Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby.  .
  20. Tankéré F, Bernat I (September 2009). "[Bell's palsy: from viral aetiology to diagnostic reality]". Rev Med Interne (in French). 30 (9): 769–75. :.  .
  21. Linder T, Bossart W, Bodmer D (January 2005). "Bell's palsy and Herpes simplex virus: fact or mystery?". Otol. Neurotol. 26 (1): 109–13. :.  .
  22. Gagyor, Ildiko; Madhok, Vishnu B.; Daly, Fergus; Somasundara, Dhruvashree; Sullivan, Michael; Gammie, Fiona; Sullivan, Frank (2015-11-09). "Antiviral treatment for Bell's palsy (idiopathic facial paralysis)". The Cochrane Database of Systematic Reviews (11): CD001869. :.  .  .
  23. Itzhaki RF, Wozniak MA (May 2008). "Herpes simplex virus type 1 in Alzheimer's disease: the enemy within". J. Alzheimers Dis. 13 (4): 393–405.  .
  24. Holmes C, Cotterell D (December 2009). "Role of infection in the pathogenesis of Alzheimer's disease: implications for treatment". CNS Drugs. 23 (12): 993–1002. :.  .
  25. Dobson CB, Itzhaki RF (1999). . Neurobiol. Aging. 20 (4): 457–65. :.  .
  26. Pyles RB (2001). "The association of herpes simplex virus and Alzheimer's disease: a potential synthesis of genetic and environmental factors". Herpes. 8 (3): 64–68.  .
  27. Warren, Terri (2009). . New Harbinger Publications. p. 28.  . from the original on 2016-05-27.
  28. . Archived from on January 21, 2008. Retrieved 2008-02-24.
  29. Anita L. Nelson; Jo Ann Woodward (2007-12-14). . Springer Science & Business Media. pp. 50–.  .
  30. ^ Leone P (2005). "Reducing the risk of transmitting genital herpes: advances in understanding and therapy". Curr Med Res Opin. 21 (10): 1577–82. :.  .
  31. Akhtar, Jihan; Shukla, Deepak (December 2009). . FEBS Journal. 276 (24): 7228–36. :.  .  .
  32. Shukla, Deepak; Liu, Jian; Blaiklock, Peter; Shworak, Nicholas W.; Bai, Xiaomei; Esko, Jeffrey D.; Cohen, Gary H.; Eisenberg, Roselyn; et al. (1999). . Cell. 99 (1): 13–22. :.  .
  33. Kim H, Meier A, Huang M, Kuntz S, Selke S, Celum C, Corey L, Wald A (2006). "Oral herpes simplex virus type 2 reactivation in HIV-positive and -negative men". J Infect Dis. 194 (4): 420–27. :.  .
  34. ^ Mertz, G.J. (1993). "Epidemiology of genital herpes infections". Infect Dis Clin North Am. 7 (4): 825–39.  .
  35. Reuven NB, Staire AE, Myers RS, Weller SK (2003). . J. Virol. 77 (13): 7425–33. :.  .  .
  36. ^ Fatahzadeh M, Schwartz RA (2007). "Human herpes simplex virus infections: epidemiology, pathogenesis, symptomatology, diagnosis, and management". J. Am. Acad. Dermatol. 57 (5): 737–63, quiz 764–6. :.  .
  37. Ashley RL, et al. (1988). . J. Clin. Microbiol. 26 (4): 662–67.  .  . from the original on 2011-07-01.
  38. Carla K. Johnson (August 23, 2006). . Associated Press. Archived from on 2012-03-18. Retrieved 2011-04-12.
  39. ^ Kulhanjian JA, Soroush V, Au DS, et al. (April 2, 1992). . N. Engl. J. Med. 326 (14): 916–20. :.  . from the original on February 5, 2009.
  40. Corey L, Wald A, Patel R, et al. (January 2004). (PDF). N Engl J Med. 350 (1): 11–20. :.  . (PDF) from the original on 2008-12-04.
  41. ^ Wald A, Langenberg AG, Link K, Izu AE, Ashley R, Warren T, Tyring S, Douglas JM Jr, Corey L (2001). . JAMA. 285 (24): 3100–06. :.  . from the original on 2008-12-05.
  42. Wald A, Langenberg AG, Krantz E, et al. (November 2005). . Annals of Internal Medicine. 143 (10): 707–13. :.  . from the original on 2008-07-08.
  43. Mertz, GJ; Benedetti J; Ashley R; Selke SA; Corey L. (1 February 1992). "Risk factors for the sexual transmission of genital herpes". Annals of Internal Medicine. 116 (3): 197–202. :.  .
  44. . Center for Disease Control and Prevention. from the original on 2014-01-30. Retrieved 2014-01-30.
  45. McNeil DG. 2017-04-09 at the .. NY Times. Research article: Andrei G; Lisco A; Vanpouille C; et al. (October 2011). . Cell Host. 10 (4): 379–89. :.  .  .
  46. Martin ET, Krantz E, Gottlieb SL, Magaret AS, Langenberg A, Stanberry L, Kamb M, Wald A (July 2009). . Archives of Internal Medicine. 169 (13): 1233–40. :.  .  .
  47. . UBM Medica. Retrieved 20 July 2011.
  48. . Center for Disease Control and Prevention. from the original on 2011-10-02. Retrieved 2011-10-01.
  49. . Center for Disease Control and Prevention. from the original on 2011-10-01. Retrieved 2011-10-01.
  50. Koelle, D.M.; Wald, A. (April 2000). . J. Antimicrob. Chemother. 45 (Suppl T3): 1–8. :.  .
  51. Brown ZA, Selke S, Zeh J, et al. (1997). "The acquisition of herpes simplex virus during pregnancy". N Engl J Med. 337 (8): 509–15. :.  .
  52. Brown ZA, Wald A, Morrow RA, Selke S, Zeh J, Corey L (2003). "Effect of serologic status and cesarean delivery on transmission rates of herpes simplex virus from mother to infant". JAMA. 289 (2): 203–09. :.  .
  53. ^ Brown ZA, Benedetti J, Ashley R, et al. (May 1991). "Neonatal herpes simplex virus infection in relation to asymptomatic maternal infection at the time of labor". N. Engl. J. Med. 324 (18): 1247–52. :.  .
  54. Whitley RJ, Kimberlin DW, Roizman B (1998). "Herpes simplex viruses". Clin Infect Dis. 26 (3): 541–53. :.  .
  55. O'Mahony C, Timms MS, Ramsden RT (December 1988). . BMJ. 297 (6661): 1468. :.  .  .
  56. Kaminester LH, Pariser RJ, Pariser DM, et al. (December 1999). "A double-blind, placebo-controlled study of topical tetracaine in the treatment of herpes labialis". J. Am. Acad. Dermatol. 41 (6): 996–1001. :.  .
  57. Leung DT, Sacks SL (October 2003). "Current treatment options to prevent perinatal transmission of herpes simplex virus". Expert Opin Pharmacother. 4 (10): 1809–19. :.  .
  58. Robert L. LaFemina (2009). . Washington, DC: ASM Press. p. 1.  . from the original on 2016-05-02.
  59. Agrawal, Caroline A. Hastings, Joseph Torkildson, Anurag Kishor (2012-04-30). (2nd ed.). Chichester, West Sussex: Wiley-Blackwell. p. 360.  . from the original on 2016-04-30.
  60. Chen, Fangman; Xu, Hao; Liu, Jinli; Cui, Yuan; Luo, Xiaobo; Zhou, Yu; Chen, Qianming; Jiang, Lu (2017). "Efficacy and safety of nucleoside antiviral drugs for treatment of recurrent herpes labialis: a systematic review and meta-analysis". Journal of Oral Pathology & Medicine. 46 (8): 561. :.  .
  61. ^ Chon T, Nguyen L, Elliott TC (July 2007). "Clinical inquiries. What are the best treatments for herpes labialis?". J Fam Pract. 56 (7): 576–78.  .
  62. Glenny AM, Fernandez Mauleffinch LM, Pavitt S, Walsh T (January 2009). "Interventions for the prevention and treatment of herpes simplex virus in patients being treated for cancer". The Cochrane Database of Systematic Reviews (1): CD006706. :.  .
  63. Nasser M, Fedorowicz Z, Khoshnevisan MH, Shahiri Tabarestani M (October 2008). "Acyclovir for treating primary herpetic gingivostomatitis". The Cochrane Database of Systematic Reviews (4): CD006700. :.  .
  64. Treister NS, Woo SB (April 2010). "Topical n-docosanol for management of recurrent herpes labialis". Expert Opin Pharmacother. 11 (5): 853–60. :.  .
  65. Perfect MM, Bourne N, Ebel C, Rosenthal SL (October 2005). "Use of complementary and alternative medicine for the treatment of genital herpes". Herpes. 12 (2): 38–41.  .
  66. Beauman, JG (Oct 15, 2005). "Genital herpes: a review". American Family Physician. 72 (8): 1527–34.  .
  67. Stumpf MP, Laidlaw Z, Jansen VA (2002). . Proc. Natl. Acad. Sci. U.S.A. 99 (23): 15234–37. :. :.  .  . from the original on 2011-09-18.
  68. Thompson, Richard L.; Preston, Chris M.; Sawtell, Nancy M. (2009-03-01). . PLOS Pathogens. 5 (3): e1000352. :.  .  .  .
  69. Myśliwska J, Trzonkowski P, Bryl E, Lukaszuk K, Myśliwski A (2000). "Lower interleukin-2 and higher serum tumor necrosis factor-a levels are associated with perimenstrual, recurrent, facial herpes simplex infection in young women". Eur. Cytokine Netw. 11 (3): 397–406.  .
  70. Segal AL, Katcher AH, Brightman VJ, Miller MF (1974). "Recurrent herpes labialis, recurrent aphthous ulcers, and the menstrual cycle". J. Dent. Res. 53 (4): 797–803. :.  .
  71. Chambers A, Perry M (2008). "Salivary mediated autoinoculation of herpes simplex virus on the face in the absence of "cold sores," after trauma". J. Oral Maxillofac. Surg. 66 (1): 136–38. :.  .
  72. Perna JJ, Mannix ML, Rooney JF, Notkins AL, Straus SE (1987). "Reactivation of latent herpes simplex virus infection by ultraviolet light: a human model". J. Am. Acad. Dermatol. 17 (3): 473–78. :.  .
  73. Rooney JF, Straus SE, Mannix ML, et al. (1992). "UV light-induced reactivation of herpes simplex virus type 2 and prevention by acyclovir". J. Infect. Dis. 166 (3): 500–06. :.  .
  74. Oakley C, Epstein JB, Sherlock CH (1997). "Reactivation of oral herpes simplex virus: implications for clinical management of herpes simplex virus recurrence during radiotherapy". Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 84 (3): 272–78. :.  .
  75. Ichihashi M, Nagai H, Matsunaga K (2004). "Sunlight is an important causative factor of recurrent herpes simplex". Cutis. 74 (5 Suppl): 14–18.  .
  76. Martinez V, Caumes E, Chosidow O (2008). "Treatment to prevent recurrent genital herpes". Current Opinion in Infectious Diseases. 21 (1): 42–48. :.  .
  77. Koelle DM, Corey L (2008). "Herpes Simplex: Insights on Pathogenesis and Possible Vaccines". Annu Rev Med. 59: 381–95. :.  .
  78. Smith JS, Robinson NJ (2002). . J. Infect. Dis. 186 (Suppl 1): S3–28. :.  .
  79. Xu, Fujie; Fujie Xu; Maya R. Sternberg; Benny J. Kottiri; Geraldine M. McQuillan; Francis K. Lee; Andre J. Nahmias; Stuart M. Berman; Lauri E. Markowitz (2006-10-23). . JAMA. AMA. 296 (8): 964–73. :.  . from the original on 2010-04-24.
  80. Xu, F; MR Sternberg; SL Gottlieb; SM Berman; LE Markowitz; et al. (23 April 2010). . Morbidity and Mortality Weekly Report (MMWR). 59 (15): 456–59. from the original on 25 June 2011. Retrieved 12 April 2011.
  81. (PDF). Center for Disease Control and Prevention. 2010-03-09. (PDF) from the original on 2016-03-06. Retrieved 2012-02-19.
  82. Rotermann, Michelle; Langlois, Kellie A.; Severini, Alberto; Totten, Stephanie (2013-04-01). "Prevalence of Chlamydia trachomatis and herpes simplex virus type 2: Results from the 2009 to 2011 Canadian Health Measures Survey". Health Reports. 24 (4): 10–15.  .  .
  83. . National Post. Retrieved 2017-02-20.
  84. Smith JS, Robinson NJ (2002). "Age-specific prevalence of infection with herpes simplex virus types 2 and 1: a global review". J Infect Dis. 186 (suppl 1): S3–28. :.
  85. Armstrong GL, Schillinger J, Markowitz L, Nahmias AJ, Johnson RE, McQuillan GM, St Louis ME (May 2001). "Incidence of herpes simplex virus type 2 infection in the United States". American Journal of Epidemiology. 153 (9): 912–20. :.  .
  86. Nilsen A, Myrmel H (2000). "Changing trends in genital herpes simplex virus infection in Bergen, Norway". Acta Obstet Gynecol Scand. 79 (8): 693–96. :.  .
  87. Forward KR, Lee SHS (2003). "Predominance of herpes simplex virus type 1 from patients with genital herpes in Nova Scotia". Can J Infect Dis. 14 (2): 94–96. :.
  88. ^ John Leo (1982-08-02). . . from the original on 2010-02-02.
  89. ^ Chow AW, Roland A, Fiala M, et al. (March 1973). . Antimicrob. Agents Chemother. 3 (3): 412–17. :.  .  .
  90. Kaufman HE, Howard GM (August 1962). "Therapy of experimental herpes simplex keratitis". Investigative Ophthalmology. 1: 561–4.  .
  91. Ch'ien LT, Whitley RJ, Alford CA, Galasso GJ (June 1976). "Adenine arabinoside for therapy of herpes zoster in immunosuppressed patients: preliminary results of a collaborative study". J. Infect. Dis. 133 (Suppl): A184–91. :.  .
  92. McKelvey EM, Kwaan HC (November 1969). . Blood. 34 (5): 706–11.  .
  93. Fiala M, Chow A, Guze LB (April 1972). . Antimicrob. Agents Chemother. 1 (4): 354–57. :.  .  .
  94. Allen LB, Hintz OJ, Wolf SM, et al. (June 1976). "Effect of 9-beta-D-arabinofuranosylhypoxanthine 5'-monophosphate on genital lesions and encephalitis induced by Herpesvirus hominis type 2 in female mice". J. Infect. Dis. 133 (Suppl): A178–83. :.  .
  95. Juel-Jensen BE (March 1970). "Varicella and cytosine arabinoside". Lancet. 1 (7646): 572. :.  .
  96. Nahmias AJ, Kibrick S (May 1964). . J. Bacteriol. 87 (5): 1060–66.  .  .
  97. Allen LB, Sidwell RW (September 1972). . Antimicrob. Agents Chemother. 2 (3): 229–33. :.  .  .
  98. Allen LB, Wolf SM, Hintz CJ, Huffman JH, Sidwell RW (March 1977). "Effect of ribavirin on Type 2 Herpesvirus hominis (HVH/2) in vitro and in vivo". Annals of the New York Academy of Sciences. 284: 247–53. :. :.  .
  99. Allen LB, Cochran KW (November 1972). . Infection and Immunity. 6 (5): 819–23.  .  .
  100. Sidwell RW, Huffman JH, Khare GP, Allen LB, Witkowski JT, Robins RK (August 1972). . Science. 177 (4050): 705–06. :. :.  .
  101. Babiuk LA, Meldrum B, Gupta VS, Rouse BT (December 1975). . Antimicrob. Agents Chemother. 8 (6): 643–50. :.  .  .
  102. O'Meara A, Deasy PF, Hillary IB, Bridgen WD (December 1979). "Acyclovir for treatment of mucocutaneous herpes infection in a child with leukaemia". Lancet. 2 (8153): 1196. :.  .
  103. Whitley R, Arvin A, Prober C, et al. (February 1991). . N. Engl. J. Med. 324 (7): 444–49. :.  . from the original on 2008-12-08.
  104. ^ Kimberlin DW, Lin CY, Jacobs RF, et al. (August 2001). . Pediatrics. 108 (2): 230–38. :.  .
  105. Mayou, R (1975). . The British journal of venereal diseases. 51 (1): 57–60. :.  .  .
  106. Moynihan R, Heath I, Henry D (April 2002). . BMJ. 324 (7342): 886–91. :.  .  .
  107. Cuatrecasas P (November 2006). . J. Clin. Invest. 116 (11): 2837–42. :.  .  . from the original on 2011-05-11.
  108. Vezina C, Steben M (2001). (PDF). The Canadian Journal of CME (June): 125–34. (PDF) from the original on 2008-12-16.
  109. Green, J; Ferrier, S; Kocsis, A; Shadrick, J; Ukoumunne, OC; Murphy, S; Hetherton, J (February 2003). . Sexually transmitted infections. 79 (1): 42–44. :.  .  .
  110. Miranda Hitti (24 August 2007). . WebMD. Archived from on 16 November 2013.
  111. . www.herpesdatesites.com. from the original on 2017-04-06. Retrieved 2017-02-20.
  112. . genitalherpesdatingsites.org. from the original on 2017-05-22. Retrieved 2017-02-20.
  113. . from the original on 4 May 2016. Retrieved 15 May 2016.
  114. . from the original on 21 October 2014. Retrieved 19 October 2014. ASHA was founded in 1914 in New York City, formed out of early 20th century social reform movements focused on fighting sexually transmitted infections (known then as venereal disease, or VD) and prostitution.
  115. . Archived from on 2008-08-20.
  116. . Archived from on 2011-10-03.
  117. . Herpes Viruses Association. from the original on 2015-07-26. Retrieved 2017-02-20.
  118. Foley, James A. (21 Oct 2013). . NatureWorldNews.com. from the original on 22 October 2013. Retrieved 22 October 2013.

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