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{{Redirect|herpes|all types of herpes viruses|Herpesviridae}}
{{Redirect|herpes|all types of herpes viruses|Herpesviridae}}


'''Herpes simplex''' is a [[viral disease]] caused by [[Herpes simplex virus]]es; both herpes simplex virus 1 (HSV–1) and herpes simplex virus 2 (HSV–2) cause herpes simplex. Infection with the herpes virus is categorized into one of several distinct disorders based on the site of infection. ''Oral herpes'', the visible symptoms of which are colloquially called ''cold sores'', infects the face and mouth. Oral herpes is the most common form of infection. Infection of the [[genital]]s, commonly known as ''herpes'', is the second most common form of herpes. Other disorders such as [[herpetic whitlow]], [[herpes gladiatorum]], ocular herpes (keratitis), cerebral herpes infection [[encephalitis]], [[Mollaret's meningitis]], neonatal herpes, and possibly [[Bell's palsy]] are all caused by herpes simplex viruses. Most individual disorders may be caused by HSV–1 or HSV–2, though some disorders have significantly different rates of infection by type. Herpes simplex is not typically life-threatening for [[Immunocompetence|immunocompetent]] people.


== Towelie ==
Herpes viruses cycle between periods of active disease—presenting as blisters containing infectious [[virus]] particles—that last 2–21 days, followed by a [[remission (medicine)|remission]] period, during which the sores disappear. Genital herpes, however, is often [[asymptomatic]], though [[viral shedding]] may still occur. After initial infection, the viruses move to [[Sensory neuron|sensory nerves]], where they reside as life-long, [[Virus latency|latent]] viruses. Causes of recurrence are uncertain, though some potential triggers have been identified. Over time episodes of active disease reduce in frequency.


Herpes simplex is most easily transmitted by direct contact with a lesion or the body fluid of an infected individual. Transmission may also occur through skin-to-skin contact during periods of asymptomatic shedding. Barrier protection methods are the most reliable, but not failsafe, method of preventing transmission of herpes. Oral herpes is easily diagnosed if the patient presents with visible sores or ulcers. Early stages of orofacial herpes and genital herpes are harder to diagnose; laboratory testing is usually required. Prevalence of HSV infections varies throughout the world. Poor hygiene, overcrowding, lower [[socioeconomic]] status, and birth in an undeveloped country have been identified as risk factors associated with increased HSV-1 childhood infection. Additional studies have identified other risk factors for both types of HSV.


<gallery>
There is currently no cure for herpes; no [[vaccine]] is currently available to prevent or eliminate herpes. However, treatments are available to reduce viral reproduction and shedding, prevent the virus from entering the skin, and alleviate the severity of symptomatic episodes.
Image:1131519160towelie.jpg|Caption1
</gallery>


<font size=7> TOWELIE SAYS DONT FORGET TO BRING A TOWEL!!!</font>
== Disorders ==


HSV infection causes several distinct medical [[Disorder (medicine)|disorders]]. Common infection of the skin or mucosa may affect the face and mouth (orofacial herpes), genitalia (genital herpes), or hands (herpes whitlow). More serious disorders occur when the virus infects and damages the eye (herpes keratitis), or invades the central nervous system, damaging the brain (herpes encephalitis). Patients with immature or suppressed immune systems, such as newborn infants, transplant recipients, or AIDS patients are prone to severe complications from HSV infections.


<gallery>
In all cases HSV is never removed from the body by the [[immune system]]. Following a primary infection, the virus enters the nerves at the site of primary infection, migrates to the [[cell body]] of the neuron, and becomes latent in the [[ganglion]].<ref name="pmid18156035"/> 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, [[seroconversion]] after an oral infection will prevent additional HSV-1 infections such as whitlow, genital herpes, and keratitis. Prior HSV-1 seroconversion seems to ameliorate the symptoms of a later HSV-2 infection, however HSV-2 can still be contracted. Most indications are that an HSV-2 infection contracted prior to HSV-1 seroconversion will immunize that person against HSV-1 infection. <ref name=Brown1997 Aug 21>{{cite journal
| author = Brown Za, Selke S., Zeh J, Kopelman J, Maslow A, Asley RL, Watts DH, Berry S, Herd M, Corey L
| year = 1997 Aug 21
| title = The acquisition of herpes simplex virus during pregnancy
| journal = N Engl J Med
| volume = 337(8)
| pages = 509-15
| Pubmed = 9262493
| url = http://content.nejm.org/cgi/content/full/337/8/509
}}</ref> This not neccessarily good, as prior HSV-1 infection has the tendency to ameliorate the effects of symptomatic HSV-2 reoccurences.


<gallery>
===Orofacial infection===
Image:lmao SUPER FUNNY.jpg|towelie
{{Infobox_Disease |
Image:lmao SUPER FUNNY.jpg|says
Name = Herpesviral vesicular dermatitis |
Image:lmao SUPER FUNNY.jpg|dont
Image = Herpes labialis - opryszczka wargowa.jpg |
Image:lmao SUPER FUNNY.jpg|forget
Caption = Herpes lesion on upper lip and face |
Image:lmao SUPER FUNNY.jpg|a
DiseasesDB = |
Image:lmao SUPER FUNNY.jpg|towel
ICD10 = {{ICD10|B|00|1|b|00}} |
Image:lmao SUPER FUNNY.jpg|ass
ICD9 = |
Image:lmao SUPER FUNNY.jpg|ass
ICDO = |
OMIM = |
MedlinePlus = |
eMedicineSubj = |
eMedicineTopic = |
MeshID = |
}}


</gallery>
Orofacial herpes affects the face and mouth. Infection occurs when the virus comes into contact with oral mucosa or abraded skin. Infection by the type 1 strain of herpes simplex virus (HSV-1) is the most common cause of orofacial herpes, though cases of oral infection by the type 2 strain are increasing.<ref>{{cite journal |author=Bruce AJ, Rogers RS |title=Oral manifestations of sexually transmitted diseases |journal=Clin. Dermatol. |volume=22 |issue=6 |pages=520–7 |year=2004 |pmid=15596324 |doi=10.1016/j.clindermatol.2004.07.005}}</ref>

Herpes infections are largely asymptomatic; when symptoms appear they will typically resolve within two weeks.<ref name="pmid15596324">{{cite journal
|author=Bruce AJ, Rogers RS
|title=Oral manifestations of sexually transmitted diseases
|journal=Clin. Dermatol.
|volume=22
|issue=6
|pages=520–7
|year=2004
|pmid=15596324
|doi=10.1016/j.clindermatol.2004.07.005}}</ref> The main symptom of oral infection is acute herpetic [[gingivostomatitis]] (inflammation of the mucosa of the cheek and gums), which occurs within 5–10 days of infection. Other symptoms may also develop, including painful [[ulcer]]s—sometimes confused with [[canker sores]]—fever, and sore throat.<ref name="pmid15596324"/> Primary HSV infection in adolescents frequently manifests as severe [[pharyngitis]] with [[lesion]]s developing on the cheek and gums. Some individuals develop difficulty in swallowing ([[dysphagia]]) and swollen [[lymph node]]s ([[lymphadenopathy]]).<ref name="pmid15596324"/> Primary HSV infections in adults often results in pharyngitis similar to that observed in glandular fever ([[infectious mononucleosis]]), but gingivostomatitis is less likely.

Recurrent oral infection is more common with HSV-1 infections than with HSV-2. [[Prodromal]] symptoms often precede a recurrence. Symptoms typically begin with tingling (itching) and reddening of the skin around the infected site. Eventually, fluid-filled [[blister]]s form on the lip (labial) tissue and the area between the lip and skin (vermilion border). The recurrent infection is thus often called ''herpes simplex labialis''. Rare reinfections occur inside the mouth (''intraoral HSV stomatitis'') affecting the gums, [[alveolar ridge]], [[hard palate]], and the back of the tongue, possibly accompanied by ''herpes labialis''.<ref name="pmid15596324"/><ref>{{Who| title =Herpes Online: Exploring the "H" Community | pages =1-4 | format = PDF| language =English | publisher =American Social Health Association | date= 1996 | url =http://www.ashastd.org/pdfs/HELPER_SPRING_05.pdf | accessdate = 2007-03-29 }}</ref>

===Genital infection===
{{Infobox_Disease |
Name = Anogenital herpesviral infection |
Image = SOA-Herpes-genitalis-female.jpg|
Caption = Genital herpes in a female|
DiseasesDB = |
ICD10 = {{ICD10|A|60||a|50}} |
ICD9 = |
ICDO = |
OMIM = |
MedlinePlus = |
eMedicineSubj = |
eMedicineTopic = |
MeshID = D006558 |
}}
[[Image:SOA-Herpes-genitalis-male.jpg|thumb|right|190px|Genital herpes in a male]]

Genital herpes is caused by HSV-2 more often than it is caused by HSV-1, although infections of the genitals by HSV-1 are increasing. The typical symptom a primary HSV-1 or HSV-2 genital infection is clusters of inflamed [[papule]]s and [[vesicle]]s on the outer surface of the genitals resembling cold sores.<ref name="titleSTD Facts - Genital Herpes">{{cite web
|url=http://www.cdc.gov/std/Herpes/STDFact-Herpes.htm
|title=STD Facts - Genital Herpes
|accessdate=2008-02-22 }}</ref> These usually appear 4–7 days after sexual exposure to HSV for the first time.<ref name="pmid18156035">{{cite journal
|author=Gupta R, Warren T, Wald A
|title=Genital herpes
|journal=Lancet
|volume=370
|issue=9605
|pages=2127–37
|year=2007
|pmid=18156035
|doi=10.1016/S0140-6736(07)61908-4}}</ref> Genital HSV-1 infection recurs at rate of about one sixth of that of genital HSV-2. In males, the lesions occur on the shaft of the [[penis]] or other parts of the genital region, on the inner thigh, buttocks, or [[anus]]. In females, lesions appear on or near the [[Mons pubis|pubis]], [[Labium (genitalia)|labia]], [[clitoris]], [[vulva]], buttocks or anus.<ref name="titleSTD Facts - Genital Herpes"/> Other common symptoms include pain, itching, and burning. Less frequent, yet still common, symptoms include discharge from the penis or [[vagina]], [[fever]], [[headache]], muscle pain ([[myalgia]]), swollen and enlarged lymph nodes and [[malaise]].<ref name="pmid18156035"/> Women often experience additional symptoms that include painful urination ([[dysuria]]) and [[cervicitis]]. Herpetic [[proctitis]] (inflammation of the anus and rectum) is common for individuals participating in anal intercourse.<ref name="pmid18156035"/> After 2–3 weeks, existing lesions progress into ulcers and then crust and heal, although lesions on mucosal surfaces may never form crusts.<ref name="pmid18156035"/>

===Herpes whitlow===

Herpes whitlow ([[herpetic whitlow]]) is a painful infection that typically affects the fingers or thumbs. Occasionally infection occurs on the toes or on the nail cuticle. Herpes whitlow can be caused by infection by HSV-1 or HSV-2.<ref name="pmid14677662">{{cite journal |author=Clark DC |title=Common acute hand infections |journal=Am Fam Physician |volume=68 |issue=11 |pages=2167–76 |year=2003 |pmid=14677662 |doi=}}</ref> HSV-1 whitlow is often contracted by health care workers that come in contact with the virus; it is most commonly contracted by dental workers and medical workers exposed to oral secretions.<ref name="pmid15119801">{{cite journal |author=Lewis MA |title=Herpes simplex virus: an occupational hazard in dentistry |journal=Int Dent J |volume=54 |issue=2 |pages=103–11 |year=2004 |pmid=15119801 |doi=}}</ref><ref name="pmid12236568">{{cite journal |author=Avitzur Y, Amir J |title=Herpetic whitlow infection in a general pediatrician--an occupational hazard |journal=Infection |volume=30 |issue=4 |pages=234–6 |year=2002 |pmid=12236568 |doi=}}</ref> It is also often observed in thumb-sucking children with primary HSV-1 oral infection ([[autoinoculation]]) prior to seroconversion,<ref name="pmid14677662"/> and in adults aged 20 to 30 following contact with HSV-2-infected genitals.<ref name="pmid17674583">{{cite journal |author=Wu IB, Schwartz RA |title=Herpetic whitlow |journal=Cutis |volume=79 |issue=3 |pages=193–6 |year=2007 |pmid=17674583 |doi=}}</ref>

Symptoms of herpetic whitlow include swelling, reddening and tenderness of the skin of infected finger. This may be accompanied by fever and swollen lymph nodes. Small, clear vesicles initially form individually, then merge and become cloudy. Associated pain often seems large relative to the physical symptoms. The herpes whitlow lesion usually heals in two to three weeks.<ref name="pmid5125276">{{cite journal |author= Anonymous|title=Herpetic whitlow: a medical risk |journal=Br Med J |volume=4 |issue=5785 |pages=444 |year=1971 |pmid=5125276 |doi=}}</ref>

===Herpes gladiatorum===

Individuals that participate in [[contact sport]]s such as [[wrestling]], [[Rugby football|rugby]], and [[soccer]] sometimes acquire a condition caused by HSV-1 known as herpes gladiatorum, ''[[scrumpox]]'', ''wrestler’s herpes'', or ''mat herpes''. Abraded skin provides an area of entry for HSV-1. Symptoms present within 2 weeks of direct skin-to-skin contact with an infected person. They include skin ulceration on the face, ears, and neck, fever, headache, sore throat and swollen glands. It occasionally affects the eyes. Physical symptoms sometimes recur in the skin.<ref name="pmid17939933"/> Previous adolescent HSV-1 seroconversion would preclude most herpes gladiatorum, but being that stress and trauma are recognized triggers, such a person would be likely to infect others.

===Ocular herpes===
{{Infobox_Disease |
Name = Herpesviral ocular disease |
Image =Herpes2.JPG|
Caption =Herpes infection of the cornea |
DiseasesDB = |
ICD10 = {{ICD10|B|00|5|b|00}} |
ICD9 = |
ICDO = |
OMIM = |
MedlinePlus = |
eMedicineSubj = |
eMedicineTopic = |
MeshID = D016849 |
}}
Ocular herpes is a special case of facial herpes infection, known as herpes keratitis. Occular herpes is generally caused by HSV-1. It begins with infection of epithelial cells on the surface of the eye and retrograde infection of nerves serving the [[cornea]].<ref name="pmid11393165">{{cite journal |author=Carr DJ, Härle P, Gebhardt BM |title=The immune response to ocular herpes simplex virus type 1 infection |journal=Exp. Biol. Med. (Maywood) |volume=226 |issue=5 |pages=353–66 |year=2001 |pmid=11393165 |doi=}}</ref> Primary infection typically presents as swelling of the [[conjunctiva]] and eye-lids ([[blepharoconjunctivitis]]), accompanied by small white itchy lesions on the surface of the [[cornea]]. The effect of the lesions varies, from minor damage to the [[epithelium]] ([[Punctate epithelial erosions|superficial punctate keratitis]]), to formation of [[Corneal ulcer|dendritic ulcers]].<ref name="pmid10858770">{{cite journal |author=Suresh PS, Tullo AB |title=Herpes simplex keratitis |journal=Indian J Ophthalmol |volume=47 |issue=3 |pages=155–65 |year=1999 |pmid=10858770 |doi=}}</ref> Infection is unilateral, affecting one eye at a time. Additional symptoms include dull pain deep inside the eye, mild to acute dryness, and [[sinusitis]]. Most primary infections resolve spontaneously in a few weeks. Healing can be aided by the use of oral and topical [[antiviral]]s.

Subsequent recurrences may be more severe, with infected epithelial cells showing larger dendritic ulceration, and lesions forming white plaques.<ref name="pmid10858770"/> The epithelial layer is sloughed off as the dendritic ulcer grows, and mild inflammation ([[iritis]]) may occur in the underlying [[stroma of iris]]. Sensation loss occurs in lesional areas, producing generalised corneal anaesthesia with repeated recurrences.<ref name="pmid10858770"/> Recurrence can be accompanied by chronic dry eye, low grade intermittent conjunctivitis, or chronic unexplained sinusitis. Following persistent infection the concentration of viral DNA reaches a critical limit. Antibody responses against the viral [[antigen]] expression in the stroma can trigger a massive [[autoimmune]] response in the eye. The response may result in the destruction of the [[Substantia propria|corneal stroma]],<ref name="pmid10858770"/> resulting in loss of vision due to opacification of the cornea. This is known as immune-mediated stromal keratitis.
}}

Herpes simplex [[encephalitis]] (HSE) is one of the most severe viral infections of the human [[central nervous system]]. It is estimated to affect at least 1 in 500,000 individuals per year.<ref name="pmid16675036">{{cite journal |author=Whitley RJ |title=Herpes simplex encephalitis: adolescents and adults |journal=Antiviral Res. |volume=71 |issue=2-3 |pages=141–8 |year=2006 |pmid=16675036 |doi=10.1016/j.antiviral.2006.04.002}}</ref> About 1 in 3 cases of HSE result from primary HSV-1 infection, predominantly occurring in individuals under the age of 18; 2 in 3 cases occur in seropositive persons, few of whom have history of recurrent orofacial herpes. Approximately 50% of individuals that develop HSE are over 50 years of age.<ref name="pmid11853816">{{cite journal |author=Whitley RJ, Gnann JW |title=Viral encephalitis: familiar infections and emerging pathogens |journal=Lancet |volume=359 |issue=9305 |pages=507–13 |year=2002 |pmid=11853816 |doi=}}</ref>

HSE is thought to be caused by the [[Retrograde infection|retrograde transmission]] of virus from a peripheral site on the face following HSV-1 reactivation, along a nerve [[axon]], to the brain.<ref name="pmid16675036"/> The virus lies dormant in the [[ganglion]] of the trigeminal [[cranial nerve]], but the reason for reactivation, and its pathway to gain access to the brain, remains unclear. The olfactory nerve may also be involved in HSE.<ref>{{cite journal | author = Dinn J | title = Transolfactory spread of virus in herpes simplex encephalitis. | journal = Br Med J | volume = 281 | issue = 6252 | pages = 1392 | year = 1980 | pmid = 7437807}}</ref> For unknown reasons the virus seems to target the [[temporal lobe]]s of the brain.

Most individuals with HSE show a decrease in their level of consciousness and an altered mental state presenting as [[Mental confusion|confusion]], and changes in personality. Increased numbers of white blood cells can be found in patient's [[cerebrospinal fluid]], without the presence of [[pathogen]]ic [[bacteria]] and [[fungi]]. Patients typically have a fever.<ref name="pmid16675036"/> and may have seizures. The electrical activity of the brain changes as the disease progresses, first showing abnormalities in one [[temporal lobe]] of the brain, which spread to the other temporal lobe 7–10 days later.<ref name="pmid16675036"/>

Without treatment, HSE results in rapid death in approximately 70% of cases.<ref name="pmid16675036"/> HSE is fatal in around 20% of cases treated, and causes serious long-term neurological damage in over half of survivors. Only a small population of survivors (2.5%) regain completely normal brain function.<ref name="pmid11853816"/>

===Neonatal herpes simplex===
{{DiseaseDisorder infobox |
Name = Congenital herpesviral (herpes simplex) infection |
Image = SOA-Herpes-neonatorum.jpg|
Caption = HSV disease in a newborn child|
ICD10 = {{ICD10|P|35|2|p|35}} |
ICD9 = {{ICD9|771.2}} |
}}

[[Infant|Neonatal]] HSV infection is a rare but serious condition, usually caused by [[vertical transmission]] of HSV from mother to newborn. Only an estimated 10% of cases are acquired [[postnatal]]ly. Neonatal HSV rates in the U.S. are estimated to be between 1 in 3,000 and 1 in 20,000 live births. Approximately 22% of pregnant women in the U.S. have had previous exposure to HSV-2, and an additional 2% acquire the virus during pregnancy, mirroring the infection rate in the general population.<ref name="pmid16199646">{{cite journal
|author=Brown ZA, Gardella C, Wald A, Morrow RA, Corey L
|title=Genital herpes complicating pregnancy
|journal=Obstet Gynecol
|volume=106
|issue=4
|pages=845–56
|year=2005
|pmid=16199646
|doi=10.1097/01.AOG.0000180779.35572.3a
|doi_brokendate=2008-06-25}}</ref> The risk of transmission to the newborn is 30-57% in cases where the mother acquired a primary infection in the [[Pregnancy#physiology|third trimester]] of pregnancy. Risk of transmission by a mother with existing antibodies for both HSV-1 and HSV-2 has a much lower (1-3%) transmission rate. This in part is due to the transfer of significant titer of protective maternal antibodies to the fetus from about the seventh month of pregnancy.<ref name="pmid12517231">{{cite journal
|author=Brown ZA, Wald A, Morrow RA, Selke S, Zeh J, Corey L
|title=Effect of serologic status and cesarean delivery on transmission rates of herpes simplex virus from mother to infant
|journal=JAMA
|volume=289
|issue=2
|pages=203–9
|year=2003
|pmid=12517231}}</ref> However, shedding of HSV-1 from both primary genital infection and reactivations is associated with higher transmission from mother to infant.<ref name="pmid12517231"/>
Complications of neonatal herpes rates are low birth weight and premature birth. Approximately one quarter of NHSV infected babies will have [[sepsis]] before the onset of herpes symptoms, further complicating diagnosis.

HSV-1 neonatal herpes is extremely rare in [[developing country|developing countries]] because development of HSV-1 specific antibodies usually occurs in childhood or adolescence, precluding a genital HSV-1 infection. HSV-2 infections are much more common in these countries. In industrialized nations, the adolescent HSV-1 seroprevalance has been dropping steadily for the last 5 decades. The resulting increase in the number of young women becoming sexually active while HSV-1 seronegative has contributed to increased HSV-1 genital herpes rates, and as a result, increased HSV-1 neonatal herpes in developed nations. A recent three year study in Canada (2000-2003) revealed a neonatal HSV incidence of 5.9 per 100,000 live births. HSV-1 was the cause of 62.5% of cases of neonatal herpes of known type, and 98.3% of transmission was asymptomatic.<ref name=Kropp>{{cite journal
| author=Kropp RY., Wong T, et al
| title=Neonatal Herpes Simplex Virus Infections in Canada: Results of a 3-Year National Prospective Study
| journal=Pediatrics
| year=2006
| pages=1955–1962
| volume=117
| issue=61
| pmid=16740836
|url=http://pediatrics.aappublications.org/cgi/content/abstract/117/6/1955 }}</ref> Asymptomatic genital HSV-1 has been shown to be more infectious to the neonate, and is more likely to produce neonatal herpes, than HSV-2,<ref name=ZA_Brown>{{cite journal
| author=Brown ZA, Wald A, Morrow RA, Selke S, Zeh J, Corey L
| title=Effect of Serologic Status and Cesarean Delivery on Transmission Rates of Herpes Simplex Virus From Mother to Infant
| journal=JAMA
| year=2003
| pages=203–209
| volume=289
| issue=2
| pmid=12517231
|url=http://jama.ama-assn.org/cgi/reprint/289/2/203}}</ref><ref name=EL_Brown>{{cite journal
| author=Brown ZA, Gardella C, Malm G, Prober CG, Forsgren M, Krantz EM, Arvin AM, Yasukawa LL, Mohan K, Brown Z, Corey L, Wald A
| title=Effect of maternal herpes simplex virus (HSV) serostatus and HSV type on risk of neonatal herpes
| journal=Acta Obstet et Gynecol Scand
| year=2007
| pages=523–529
| volume=86
| issue=5
| pmid=17564578
|url=http://www.informaworld.com/smpp/content~content=a777727985~db=all}}</ref>. However, with prompt application of antiviral therapy, the prognosis of neonatal HSV-1 infection is better than that for HSV-2.

Neonatal herpes manifests itself in three forms: skin, eyes, and mouth herpes (SEM) sometimes referred to as "localized", disseminated herpes (DIS), and central nervous system herpes(CNS).<ref name="pmid15685144">{{cite journal
|author=Kimberlin DW, Whitley RJ
|title=Neonatal herpes: what have we learned
|journal=Semin Pediatr Infect Dis
|volume=16
|issue=1
|pages=7–16
|year=2005
|pmid=15685144
|doi=10.1053/j.spid.2004.09.006}}</ref> SEM herpes is characterized by external lesions but no internal organ involvement. Lesions are likely to appear on trauma sites such as the attachment site of fetal scalp electrodes, forceps or vacuum extractors that are used during delivery, in the margin of the eyes, the [[nasopharynx]], and in areas associated with trauma or surgery (including circumcision).<ref name="pmid12517231"/> DIS herpes affects internal organs, particularly the liver. CNS herpes is an infection of the nervous system and the brain that can lead to encephalitis. Infants with CNS herpes present with [[seizure]]s, [[tremor]]s, [[lethargy]], and irritability, they feed poorly, have unstable temperatures, and their [[fontanelle]] (soft spot of the skull) may bulge.<ref name="pmid12517231"/> CNS herpes is associated with highest [[morbidity]], and DIS herpes has a higher [[mortality]] rate. These categories are not mutually exclusive and there is often overlap of two or more types. SEM herpes has the best prognosis of the three, however, if left untreated it may progress to disseminated or CNS herpes with its attendant increases in mortality and morbidity. Death from neonatal HSV disease in the U.S. is currently decreasing; The current death rate is about 25%, down from as high as 85% in untreated cases just a few decades ago. Other complications from neonatal herpes include prematurity with approximately 50% of cases having a gestation of 38 weeks or less, and a concurrent sepsis in approximately one quarter of cases that further clouds speedy diagnosis.

Reductions in morbidity and mortality are due to the use of antiviral treatments such as [[vidarabine]] and [[acyclovir]].<ref name="pmid15685144"/><ref name="pmid11269641">{{cite journal
|author=Kesson AM
|title=Management of neonatal herpes simplex virus infection
|journal=Paediatr Drugs
|volume=3
|issue=2
|pages=81–90
|year=2001
|pmid=11269641 }}</ref><ref>{{cite web
|url=http://www.merck.com/mmpe/sec19/ch279/ch279h.html
|title=The Merck Manual, Neonatal Herpes Simplex Virus (HSV) Infection</ref><ref name=neonatal>{{cite journal
|author=Brocklehurst P, Kinghorn GA et al.
|title=randomised placebo controlled trial of suppressive acyclovir in late pregnancy in women with recurrent genital herpes infection
|journal= Br J Obstet Gynaecol
|year= 1998
|volume=105
|issue=3
|pages=275–80 }}</ref> However, morbidity and mortality still remain high due to diagnosis of DIS and CNS herpes coming too late for effective antiviral administration; early diagnosis is difficult in the 20-40% of infected neonates that have no visible lesions.<ref name="pmid9523400">{{cite journal
|author=Jacobs RF
|title=Neonatal herpes simplex virus infections
|journal=Semin. Perinatol.
|volume=22
|issue=1
|pages=64–71
|year=1998
|pmid=9523400 }}</ref> Herpes simplex virus infection in the newborn "carries high mortality and morbidity rates from central nervous system involvement", according to [[Harrison's Principles of Internal Medicine]], which recommends that pregnant women with active genital herpes lesions at the time of labor be delivered by [[cesarean section]]. Women whose herpes is not active can be managed with acyclovir.<ref>Ch. 6, "Medical Disorders during Pregnancy," in Harrison's Principles of Internal Medicine, 16th ed., 2005</ref> The current practice is to deliver women with primary or first episode non primary infection via ceasarian section, and those with recurrrent infection vaginally, even in the presence of lesions because of the low risk (1-3%) of vertical transmission associated with recurrent herpes.

=== Viral meningitis ===

HSV-2 is the most common cause of Mollaret's meningitis, a type of recurrent viral [[meningitis]].<ref name="pmid15319091">{{cite journal |author=Tyler KL |title=Herpes simplex virus infections of the central nervous system: encephalitis and meningitis, including Mollaret's |journal=Herpes |volume=11 Suppl 2 |issue= |pages=57A–64A |year=2004 |pmid=15319091 |doi=}}</ref><ref name=viral_meningitis>{{cite web | title=Recurring viral meningitis & herpes II | publisher=Med Help International | url=http://www.medhelp.org/forums/neuro/archive/9599.html | accessdate=2006-11-21}}</ref> This condition was first described in 1944 by French [[neurologist]] [[Pierre Mollaret]]. Recurrences usually last a few days or a few weeks, and resolve without treatment. They may recur weekly or monthly for approximately 5 years following primary infection.<ref name="pmid16754896">{{cite journal |author=Sendi P, Graber P |title=Mollaret's meningitis |journal=CMAJ |volume=174 |issue=12 |pages=1710 |year=2006 |pmid=16754896 |doi=10.1503/cmaj.051688}}</ref>

===Bell's palsy===

In a mouse model a type of facial [[paralysis]] called [[Bell's palsy]] has been linked to the presence and reactivation of latent HSV-1 inside the sensory nerves of the face ([[geniculate ganglion|geniculate ganglia]]).<ref name="pmid1336296">{{cite journal
|author=Takasu T, Furuta Y, Sato KC, Fukuda S, Inuyama Y, Nagashima K
|title=Detection of latent herpes simplex virus DNA and RNA in human geniculate ganglia by the polymerase chain reaction
|journal=Acta Otolaryngol.
|volume=112
|issue=6
|pages=1004–11
|year=1992
|pmid=1336296 }}</ref><ref name="pmid7598372">{{cite journal
|author=Sugita T, Murakami S, Yanagihara N, Fujiwara Y, Hirata Y, Kurata T
|title=Facial nerve paralysis induced by herpes simplex virus in mice: an animal model of acute and transient facial paralysis
|journal=Ann. Otol. Rhinol. Laryngol.
|volume=104
|issue=7
|pages=574–81
|year=1995
|pmid=7598372 }}</ref> This is supported by findings that show the presence of HSV-1 DNA in saliva at a higher frequency in patients with Bell's palsy relative to those without the condition.<ref name="pmid16917546">{{cite journal
|author=Lazarini PR, Vianna MF, Alcantara MP, Scalia RA, Caiaffa Filho HH
|title=Herpes simplex virus in the saliva of peripheral Bell's palsy patients
|language=Portuguese
|journal=Rev Bras Otorrinolaringol (Engl Ed)
|volume=72
|issue=1
|pages=7–11
|year=2006
|pmid=16917546 }}</ref>

However, since HSV can also be detected in these ganglia in large numbers of individuals that have never experienced facial paralysis, and high titers of antibodies for HSV are not found in HSV-infected individuals with Bell's palsy relative to those without, this theory has been contested.<ref name="pmid15699730">{{cite journal
|author=Linder T, Bossart W, Bodmer D
|title=Bell's palsy and Herpes simplex virus: fact or mystery?
|journal=Otol. Neurotol.
|volume=26
|issue=1
|pages=109–13
|year=2005
|pmid=15699730 }}</ref> In other studies HSV-1 DNA was not detected in the [[cerebrospinal fluid]] of Bell's palsy sufferers, raising questions whether HSV-1 is the causative agent in this type of facial paralysis.<ref name="pmid17573575">{{cite journal
|author=Kanerva M, Mannonen L, Piiparinen H, Peltomaa M, Vaheri A, Pitkäranta A
|title=Search for Herpesviruses in cerebrospinal fluid of facial palsy patients by PCR
|journal=Acta Otolaryngol.
|volume=127
|issue=7
|pages=775–9
|year=2007
|pmid=17573575
|doi=10.1080/00016480601011444}}</ref><ref name="pmid16676828">{{cite journal
|author=Stjernquist-Desatnik A, Skoog E, Aurelius E
|title=Detection of herpes simplex and varicella-zoster viruses in patients with Bell's palsy by the polymerase chain reaction technique
|journal=Ann. Otol. Rhinol. Laryngol.
|volume=115
|issue=4
|pages=306–11
|year=2006
|pmid=16676828 }}</ref> The potential effect of HSV-1 in the etiology of Bell's palsy has prompted the use of antiviral medication to treat the condition. The benefits of acyclovir and valacyclovir have been studied.<ref name="pmid17956069">{{cite journal
|author=Tiemstra JD, Khatkhate N
|title=Bell's palsy: diagnosis and management
|journal=Am Fam Physician
|volume=76
|issue=7
|pages=997–1002
|year=2007
|pmid=17956069 }}</ref>

===Alzheimer's disease===

Scientists discovered a link between HSV-1 and [[Alzheimer’s disease]] in 1979.<ref>{{cite journal|author=Middleton PJ, Peteric M, Kozak M, Rewcastle NB, McLachlan DR. |title=Herpes simplex viral genome and senile and presenile dementias of Alzheimer and Pick. |journal=Lancet |year=1980 |volume= 315|issue= |pages=1038 |doi=10.1016/S0140-6736(80)91490-7}}</ref> 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 the development of Alzheimer's disease.<ref name=Dobson1999>{{cite journal
| author = Dobson, C.B.
| coauthors = Itzhaki, R.F.
| year = 1999
| title = Herpes simplex virus type 1 and Alzheimer's disease.
| journal = Neurobiol Aging
| volume = 20
| issue = 4
| pages = 457–65
| url = http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=10604441&cmd=showdetailview&indexed=google
| accessdate = 2008-03-15
| doi = 10.1016/S0197-4580(99)00055-X
}}</ref> This research identifies HSVs as the pathogen most clearly linked to the establishment of Alzheimer’s.<ref name=Pyles2001>{{cite journal
| author = Pyles, R.B.
| year = 2001
| title = The association of herpes simplex virus and Alzheimer's disease: a potential synthesis of genetic and environmental factors
| journal = Herpes
| volume = 8
| issue = 3
| pages = 64–68
| url = http://www.ihmf.com/journal/download/83pyles(64)vol864.pdf
| accessdate = 2008-03-15
}}</ref>

Without the presence of the gene allele, HSV type 1 does not appear to cause any neurological damage and thus increase the risk of Alzheimer’s.<ref name=Itzhaki1997>{{cite journal
| author = Itzhaki, R.F.
| coauthors = Lin, W.R.; Shang, D.; Wilcock, G.K.; Faragher, B.; Jamieson, G.A.
| year = 1997
| title = Herpes simplex virus type 1 in brain and risk of Alzheimer's disease.
| journal = Lancet
| volume = 349
| issue = 9047
| pages = 241–4
| url = http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=97167222&cmd=showdetailview&indexed=google
| accessdate = 2008-03-15
| doi = 10.1016/S0140-6736(96)10149-5
}}</ref>

==Recurrence==

Following active infection herpes viruses establish a latent infection in sensory and autonomic [[ganglia]] of the nervous system. The double-stranded DNA of the virus is incorporated into the cell physiology by infection of the [[cell nucleus|nucleus]] of a nerve's [[Soma (biology)|cell body]]. HSV latency is static—no virus is produced—and is controlled by a number of viral genes, including [[HHV LAT|Latency Associated Transcript]] (LAT).<ref name="pmid12409612">{{cite journal |author=Stumpf MP, Laidlaw Z, Jansen VA |title=Herpes viruses hedge their bets |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=99 |issue=23 |pages=15234–7 |year=2002 |pmid=12409612 |doi=10.1073/pnas.232546899}}</ref>

Many HSV infected people experience recurrence within the first year of infection.<ref name="pmid18156035"/> [[Prodrome]] precedes development of lesions. Prodromal symptoms include tingling ([[paresthesia]]), 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, lesions are less painful, and lesions heal faster (within 5–10 days without antiviral treatment), than those occurring during the primary infection.<ref name="pmid18156035"/> Subsequent outbreaks tend to be periodic or episodic, occurring on average four to five times a year when not using [[antiviral therapy.]]

The causes of reactivation are uncertain, but several potential triggers have been documented. Physical or psychological stress can trigger an outbreak of herpes.<ref name="pmid11359358">{{cite journal |author=Sainz B, Loutsch JM, Marquart ME, Hill JM |title=Stress-associated immunomodulation and herpes simplex virus infections |journal=Med. Hypotheses |volume=56 |issue=3 |pages=348–56 |year=2001 |pmid=11359358 |doi=10.1054/mehy.2000.1219}}</ref> Changes in the immune system during [[menstruation]] may play a role in HSV-1 reactivation.<ref name="pmid11022124">{{cite journal |author=Myśliwska J, Trzonkowski P, Bryl E, Lukaszuk K, Myśliwski A |title=Lower interleukin-2 and higher serum tumor necrosis factor-a levels are associated with perimenstrual, recurrent, facial Herpes simplex infection in young women |journal=Eur. Cytokine Netw. |volume=11 |issue=3 |pages=397–406 |year=2000 |pmid=11022124 |doi=}}</ref><ref name="pmid4526372">{{cite journal |author=Segal AL, Katcher AH, Brightman VJ, Miller MF |title=Recurrent herpes labialis, recurrent aphthous ulcers, and the menstrual cycle |journal=J. Dent. Res. |volume=53 |issue=4 |pages=797–803 |year=1974 |pmid=4526372 |doi=}}</ref> Concurrent infections, such as viral [[upper respiratory tract infection]] or other febrile diseases, can cause outbreaks. Reactivation due to infection 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, [[radiotherapy]], and exposure to wind, [[ultraviolet light]], or sunlight.<ref name="pmid18083428">{{cite journal |author=Chambers A, Perry M |title=Salivary mediated autoinoculation of herpes simplex virus on the face in the absence of "cold sores," after trauma |journal=J. Oral Maxillofac. Surg. |volume=66 |issue=1 |pages=136–8 |year=2008 |pmid=18083428 |doi=10.1016/j.joms.2006.07.019}}</ref><ref name="pmid2821086">{{cite journal |author=Perna JJ, Mannix ML, Rooney JF, Notkins AL, Straus SE |title=Reactivation of latent herpes simplex virus infection by ultraviolet light: a human model |journal=J. Am. Acad. Dermatol. |volume=17 |issue=3 |pages=473–8 |year=1987 |pmid=2821086 |doi=}}</ref><ref name="pmid1323616">{{cite journal |author=Rooney JF, Straus SE, Mannix ML, ''et al'' |title=UV light-induced reactivation of herpes simplex virus type 2 and prevention by acyclovir |journal=J. Infect. Dis. |volume=166 |issue=3 |pages=500–6 |year=1992 |pmid=1323616 |doi=}}</ref><ref name="pmid9377190">{{cite journal |author=Oakley C, Epstein JB, Sherlock CH |title=Reactivation of oral herpes simplex virus: implications for clinical management of herpes simplex virus recurrence during radiotherapy |journal=Oral Surg Oral Med Oral Pathol Oral Radiol Endod |volume=84 |issue=3 |pages=272–8 |year=1997 |pmid=9377190 |doi=}}</ref><ref name="pmid15603217">{{cite journal |author=Ichihashi M, Nagai H, Matsunaga K |title=Sunlight is an important causative factor of recurrent herpes simplex |journal=Cutis |volume=74 |issue=5 Suppl |pages=14–8 |year=2004 |pmid=15603217 |doi=}}</ref>

The frequency and severity of recurrent outbreaks may vary greatly between patients. An immunity to the virus is built over time; immunocompromised individuals may experience episodes that are longer, more frequent and more severe. Antiviral medication has been proven to shorten the frequency and duration of outbreaks.<ref name="pmid18192785">{{cite journal |author=Martinez V, Caumes E, Chosidow O |title=Treatment to prevent recurrent genital herpes |journal=Curr Opin Infect Dis |volume=21 |issue=1 |pages=42–48 |year=2008 |pmid=18192785 |doi=10.1097/QCO.0b013e3282f3d9d3 |doi_brokendate=2008-06-25}}</ref> Outbreaks may occur at the original site of the infection or in close 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, back of the thighs.

==Transmission and prevention==

Herpes is contracted through direct contact with an active lesion or body fluid of an infected person.<ref name="titleAHMF: Preventing Sexual Transmission of Genital Herpes">{{cite web |url=http://www.ahmf.com.au/health_professionals/guidelines/preventing_gh_transmission.htm |title=AHMF: Preventing Sexual Transmission of Genital Herpes |accessdate=2008-02-24 |format= |work=}}</ref> Herpes transmission occurs between discordant partners; a person with a history of infection (HSV seropositive) can pass the virus to an HSV seronegative person.<ref name="pmid18156035"/> There are no documented cases of infection via an inanimate object (e.g. a towel, toilet seat, drinking vessels).{{Facts|date=July 2008}} 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 [[viral shedding|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.<ref name="pmid16238897"/> Infected people that show no visible symptoms may still shed and transmit virus through their skin; asymptomatic shedding may represent the most common form of HSV-2 transmission.<ref name="pmid16238897">{{cite journal |author=Leone P |title=Reducing the risk of transmitting genital herpes: advances in understanding and therapy |journal=Curr Med Res Opin |volume=21 |issue=10 |pages=1577–82 |year=2005 |pmid=16238897 |doi=10.1185/030079905X61901}}</ref> Asymptomatic shedding is more frequent within the first 12 months of acquiring HSV. Concurrent infection with [[Human Immunodeficiency Virus|HIV]] increases the frequency and duration of asymptomatic shedding.<ref>{{cite journal | author = Kim H, Meier A, Huang M, Kuntz S, Selke S, Celum C, Corey L, Wald A | title = Oral herpes simplex virus type 2 reactivation in HIV-positive and -negative men. | journal = J Infect Dis | volume = 194 | issue = 4 | pages = 420–7 | year = 2006 | pmid = 16845624 | doi = 10.1086/505879}}</ref> There are indications that 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 1 to 12 annual recurrences to those that have no recurrences.<ref name="pmid16238897"/>

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 [[monogamy|monogamous]] couple, a seronegative female runs a greater than 30% per year risk of contracting an HSV-1 infection from a seropositive male partner.<ref name=Mertz1993>{{cite journal
| author = Mertz, G.J.
| year = 1993
| title = Epidemiology of genital herpes infections.
| journal = Infect Dis Clin North Am
| volume = 7
| issue = 4
| pages = 825-39
| url = /scholar?hl=en&lr=&ie=UTF-8&sa=G&as_publication=Infect+Dis+Clin+North+Am&oi=qs&q=epidemiology+of+genital+herpes+infections+author:g-mertz
| accessdate = 2008-07-24
}}</ref> 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.

[[Image:Kondom.jpg|thumb|left|200px|Barrier protection, such as a [[condom]], can reduce the risk of herpes transmission in some cases.]]
For genital herpes, [[condom]]s are highly effective in limiting transmission of herpes simplex infection.<ref name=Wald>{{cite journal | author=Wald A, Langenberg AG, Link K, Izu AE, Ashley R, Warren T, Tyring S, Douglas JM Jr, Corey L. | title=Effect of condoms on reducing the transmission of herpes simplex virus type 2 from men to women | journal=JAMA | year=2001 | pages=3100–3106 | volume=285 | issue=24 | pmid=11427138 | doi=10.1001/jama.285.24.3100}}</ref><ref name=Casper>{{cite journal | author=Casper C, Wald A. | title=Condom use and the prevention of genital herpes acquisition, | journal=Herpes | year=2002 | pages=10–14 | volume=9 | issue=1 | pmid=11916494}}</ref> The virus cannot pass through latex, but a condom's effectiveness is somewhat limited on a [[public health]] scale by their limited use in the community,<ref name=Visser>{{cite journal | author=de Visser RO, Smith AM, Rissel CE, Richters J, Grulich AE. | title=Sex in Australia: safer sex and condom use among a representative sample of adults | journal=Aust. N. Z. J. Public Health. | year=2003 | pages=223–229 | volume=27 | issue=2 | pmid=14696715 | doi=10.1111/j.1467-842X.2003.tb00812.x}}</ref> and on an individual scale because the condom may not completely cover blisters on the penis of an infected male, or the base of the penis or testicles not covered by the condom may come into contact with free virus in vaginal fluid of an infected female. In such cases, abstinence from sexual activity or washing of the genitals after sex is recommended. The use of condoms or [[dental dams]] also limits the transmission of herpes from the genitals of one partner to the mouth of the other (or vice versa) during [[oral sex]]. When one partner has a herpes simplex infection and the other does not, the use of antiviral medication, such as [[valaciclovir]], in conjunction with a condom, further decreases the chances of transmission to the uninfected partner.<ref name="pmid18156035"/> Topical [[microbicide]]s which contain chemicals that directly inactivate the virus and block viral entry are currently being investigated.<ref name="pmid18156035"/> [[Vaccines]] for HSV are currently undergoing trials. Once developed, they may be used to help with prevention or minimize initial infections as well as treatment for existing infections.<ref>{{cite news | last =Seppa | first =Nathan | title =One-Two Punch: Vaccine fights herpes with antibodies, T cells | pages =5 | language =English | publisher =Science News | date= 2005-01-05 | url =http://www.sciencenews.org/articles/20050101/fob6.asp | accessdate = 2007-03-29}}</ref>

As with almost all sexually transmitted infections, women are more susceptible to acquiring genital HSV-2 than men.<ref> {{cite news | author=Carla K. Johnson | title=Percentage of people with herpes drops | url=http://www.newsobserver.com/150/story/477928.html | publisher=Associated Press | date= August 23, 2006}}</ref> On an annual basis, without the use of antivirals or condoms, the transmission risk of HSV-2 from infected male to female is approximately 8-10%.{{Fact|date=May 2008}} 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 approximately 4-5% annually.{{Fact|date=May 2008}} Suppressive antiviral therapy reduces these risks by 50%. <ref name=Corey2004>{{cite journal
| author = Corey L, Wald A, Patel R, et al
| year = 2004
| title = Once-daily valacyclovir to reduce the risk of transmission of genital herpes
| journal = N Engl J Med
| volume = 350(1)
| pages = 11-20
| PMID = 1402423
| url = http://content.nejm.org/cgi/reprint/350/1/11.pdf
}}</ref> 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 by 50%.{{Fact|date=May 2008}} Condom use is much more effective at preventing male to female transmission than vice-versa.<ref name=Wald/> The effects of combining antiviral and condom use is roughly additive, thus resulting in approximately a 75% combined reduction in annual transmission risk.{{Fact|date=May 2008}} These figures reflect experiences with subjects having frequently-recurring genital herpes (>6 recurrences per year). Subjects with low recurrence rates and those with no clinical manifestations were excluded from these studies.{{Fact|date=May 2008}}

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 [[caesarean section]] to reduce exposure of the child to infected secretions in the birth canal.<ref name="pmid18156035"/> 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.<ref name="pmid18156035"/>

HSV-2 infected individuals are at higher risk for acquiring [[HIV]] when practicing unprotected sex with HIV positive persons, particularly during an outbreak with active lesions.<ref name="pmid18186706">{{cite journal |author=Koelle DM, Corey L |title=Herpes Simplex: Insights on Pathogenesis and Possible Vaccines |journal=Annu Rev Med |volume=59 |issue= |pages=381–395 |year=2008 |pmid=18186706 |doi=10.1146/annurev.med.59.061606.095540}}</ref>

==Diagnosis==

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 [[gingivitis]].<ref name="pmid17939933">{{cite journal |author=Fatahzadeh M, Schwartz RA |title=Human herpes simplex virus infections: epidemiology, pathogenesis, symptomatology, diagnosis, and management |journal=J. Am. Acad. Dermatol. |volume=57 |issue=5 |pages=737–63; quiz 764–6 |year=2007 |pmid=17939933 |doi=10.1016/j.jaad.2007.06.027}}</ref> Adults with non-typical 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 [[allergy|allergic]] [[stomatitis]]. When lesions do not appear inside the mouth primary orofacial herpes is sometimes mistaken for [[impetigo]], a bacterial [[infection]]. Common mouth ulcers ([[aphthous ulcer]]) also resemble intraoral herpes, but do not present a vesicular stage.<ref name="pmid17939933"/>

Genital herpes can be more difficult to diagnose than oral herpes since most HSV-2-infected persons have no classical symptoms.<ref name="pmid17939933"/> Further confusing diagnosis, several other conditions resemble genital herpes, including [[lichen planus]], [[atopic dermatitis]], and [[urethritis]].<ref name="pmid17939933"/> [[Laboratory]] testing is often used to confirm a diagnosis of genital herpes. Laboratory tests include: culture of the virus, [[direct fluorescent antibody]] (DFA) studies to detect virus, [[skin biopsy]], and [[polymerase chain reaction]] (PCR) 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.<ref name="pmid17939933"/>

[[Serology|Serological]] tests for antibodies to HSV are rarely useful to diagnosis and not routinely used in clinical practice<ref name="pmid17939933"/>, but are important in epidemiological studies. Serologic assays cannot differentiate between antibodies generated in response to a genital versus an oral HSV infection, and as such cannot confirm the site of infection. Absence of antibody to HSV-2 does not exclude gential infection because of the increasing incidence of genital infections caused by HSV-1.

==Epidemiology==

Although many people infected with HSV develop labial or genital lesions, many more are either undiagnosed or display no physical symptoms—individuals with no symptoms are described as asymptomatic or as having [[Subclinical infection|subclinical]] herpes.<ref name="pmid11095834">{{cite journal |author=Handsfield HH |title=Public Health Strategies to Prevent Genital Herpes: Where Do We Stand? |journal=Curr Infect Dis Rep |volume=2 |issue=1 |pages=25–30 |year=2000 |pmid=11095834 |doi=}}</ref> Since asymptomatic individuals are often unaware of their infection, they are considered at high risk for spreading HSV. Many studies have been performed around the world to estimate the numbers of individuals infected with HSV-1 and HSV-2 by determining if they have developed antibodies against either viral species.<ref name="pmid12353183">{{cite journal |author=Smith JS, Robinson NJ |title=Age-specific prevalence of infection with herpes simplex virus types 2 and 1: a global review |journal=J. Infect. Dis. |volume=186 Suppl 1 |issue= |pages=S3–28 |year=2002 |pmid=12353183 |doi=}}</ref> This information provides population prevalence of HSV viral infections in individuals with or without active disease.

{| class = "prettytable" style = "width:300px; float:right; font-size:80%; margin-left:15px; text-align:center"
| align="center" colspan="5"|'''Seroprevalence estimates for HSV-1 and HSV-2'''<ref name="pmid12353183"/>
|-align="left" style="color: black; background: #ccccff" |
|width="200px" rowspan="3" | '''Location'''
|width="50px" align="center" colspan="1" rowspan="3"|'''Year(s)'''
|width="150px" align="center" colspan="3"|'''Prevalence (%)'''
|-align="center" style="color: black; background: #ccccff"
|width="50px" align="center" colspan="1"|'''HSV-1'''|| width="100px" align="center" colspan="2"|'''HSV-2'''
|-
|width="50px" align="center" colspan="1"|'''Total'''||width="50px" align="center" colspan="1"|'''Female'''|| width="50px" align="center" colspan="1"|'''Male'''
|-
|width="300px" align="center" colspan="5"|'''[[Africa]]'''
|-
|align="left"|[[Benin]]||1997-8||-||30||12
|-
|align="left"|[[Cameroon]]||1997-8||-||46-51||24-27
|-
|align="left"|[[Central African Republic]]||1998-9||99||82||-
|-
|align="left"|[[Eritrea]]||1995||84-97||23||24-27
|-
|align="left"|[[The Gambia]]||1998-9||-||29-32||5
|-
|align="left"|[[Kenya]]||1997-8||-||68||35
|-
|align="left"|[[Mali]]<ref name="pmid18080353">{{cite journal |author=Patnaik P, Herrero R, Morrow RA, ''et al'' |title=Type-specific seroprevalence of herpes simplex virus type 2 and associated risk factors in middle-aged women from 6 countries: the IARC multicentric study |journal=Sex Transm Dis |volume=34 |issue=12 |pages=1019–24 |year=2007 |pmid=18080353 |doi=}}</ref>||1991-7||93||43||-
|-
|align="left"|[[Morocco]]<ref name="pmid18080353"/>||1991-7||99||26||-
|-
|align="left"|[[South Africa]]||1999||-||53||17
|-
|align="left"|[[Tanzania]]||1992||-||42||19
|-
|align="left"|[[Uganda]]||1989-93||91||71||36
|-
|align="left"|[[Zambia]]||1997-8||-||55||36
|-
|align="left"|[[Zimbabwe]]||1993-8||-||67||36-53
|-
|width="300px" align="center" colspan="5"|'''[[Asia]]'''
|-
|align="left"|[[Bangladesh]]||1996-8||46<sup>#</sup>||8-14||-
|-
|align="left"|[[China]]||1987-95||-||18-29||17
|-
|align="left"|[[Israel]]||1998-9||70||5||4
|-
|align="left"|[[Japan]]||1985-93||50-60||1-17||2
|-
|align="left"|[[Jordan]]||<2000||-||41||53
|-
|align="left"|[[South Korea]]<ref name="pmid18162706">{{cite journal |author=Shin HS, Park JJ, Chu C, ''et al'' |title=Herpes simplex virus type 2 seroprevalence in Korea: rapid increase of HSV-2 seroprevalence in the 30s in the southern part |journal=J. Korean Med. Sci. |volume=22 |issue=6 |pages=957–62 |year=2007 |pmid=18162706 |doi=}}</ref>||2004||-||28||22
|-
|align="left"|[[Philippines]]||1991-3||-||9||-
|-
|align="left"|[[Syria]]||1995-8||80-100||0||0-1
|-
|align="left"|[[Thailand]]<ref name="pmid18080353"/><ref name="pmid12353183"/>||1991-7||51||35||15
|-
|align="left"|[[Turkey]]||1991-2||97||42||-
|-
|width="300px" align="center" colspan="5"|'''[[Australasia]]'''
|-
|align="left"|[[Australia]]||<1992-8||79-80||11-15||-
|-
|align="left"|[[New Zealand]]||1993-8||-||4-15||3-7
|-
|width="300px" align="center" colspan="5"|'''[[Central America|Central]]/[[South America]]'''
|-
|align="left"|[[Brazil]]||1990-7||-||23-42||-
|-
|align="left"|[[Colombia]]<ref name="pmid18080353"/>||1985-97||89||57||-
|-
|align="left"|[[Costa Rica]]||1984-5||-||39||-
|-
|align="left"|[[Haiti]]||<1992||-||54||-
|-
|align="left"|[[Mexico]]||1992-7||-||30||-
|-
|align="left"|[[Peru]]<ref name="pmid18080353"/>||1991-7||92||36||-
|-
|width="300px" align="center" colspan="5"|'''[[Europe]]'''
|-
|align="left"|[[Bulgaria]]<ref name="pmid15170000">{{cite journal |author=Pebody RG, Andrews N, Brown D, ''et al'' |title=The seroepidemiology of herpes simplex virus type 1 and 2 in Europe |journal=Sex Transm Infect |volume=80 |issue=3 |pages=185–91 |year=2004 |pmid=15170000 |doi=}}</ref>||1999||84||15->40||15-30
|-
|align="left"|[[Denmark]]||1986||76||31||-
|-
|align="left"|[[Finland]]||1966-89||-||26-31||-
|-
|align="left"|[[Germany]]||1996-7||87||15||11
|-
|align="left"|[[Greenland]]||1986||98||68||-
|-
|align="left"|[[Italy]]||1981-8||81-93||1-5||0-5
|-
|align="left"|[[Norway]]||1992-4||79||27||-
|-
|align="left"|[[Spain]]||1992-3||79||4||4
|-
|align="left"|[[Sweden]]||1989-93||41<sup>#</sup>||21-33||-
|-
|align="left"|[[Switzerland]]||1997||65-87||22||11
|-
|align="left"|[[UK]]||1984-95||69-78||5||3
|-
|width="300px" align="center" colspan="5"|'''[[North America]]'''
|-
|align="left"|[[Canada]]||1999||57||13||-
|-
|align="left"|[[USA]]||1988-94||68||26||18
|-
|align="left" colspan="5"|''<sup>#</sup> in children''
|}

===Europe===

Large differences in HSV-1 seroprevalence are seen in different [[Europe|European countries]]. HSV-1 seroprevalence is high in [[Bulgaria]] (83.9%) and The [[Czech Republic]] (80.6%), and lower in [[Belgium]] (67.4%), The [[Netherlands]] (56.7%), and [[Finland]] (52.4%).<ref name="pmid15170000"/> The typical age at which HSV-1 infection is acquired ranges from 5 to 9 years in [[Eastern Europe]]an countries like Bulgaria and the Czech Republic, to over 25 years of age in [[Northern Europe]]an countries such as Finland, The Netherlands, [[Germany]], and [[England]] and [[Wales]]. Young adults in Northern European countries are less likely to be infected with HSV-1. European women are more likely to be HSV-1 seropositive than men.<ref name="pmid15170000"/>

HSV-2 seropositivity is widely distributed in Europeans older than 12, although there are large differences in the percentage of the population exposed to HSV-2. Bulgaria has a high (23.9%) HSV-2 seroprevalence relative to other European countries: Germany (13.9%), Finland (13.4%),
Belgium (11.1%), The Netherlands (8.8%), the Czech Republic (6.0%), and England and Wales (4.2%).<ref name="pmid15170000"/> Women are more likely to be seropositive than men, and likely acquire the virus at an earlier age. In each country of Europe, HSV-2 seropositivity becomes more common from adolescence onwards and increases in the population with age, with a decline in the older age groups in some countries.<ref name="pmid15170000"/>

===North America===
====United States====
African Americans and immigrants from [[developing country|developing countries]] typically have an HSV-1 seroprevalance in their adolescent population that is two or three times higher than that of [[White American|Caucasian Americans]], possibly reflecting differences in their [[Socioeconomics|socioeconomic]] backgrounds.<ref name="pmid17939933"/> Many white Americans become sexually active while seronegative for HSV-1. The absence of antibodies from a prior oral HSV-1 infection leaves these individuals susceptible to primary HSV-1 genital infections. This brings with it a risk of vertical transmission to the neonate if the mother contracts a primary infection during the third trimester of pregnancy. A seronegative mother has up to a 57% chance of conveying an HSV infection to her baby during childbirth whereas a woman seropositive for both HSV-1 and HSV-2 has around a 1-3% chance of transmitting infection to her infant.<ref name=Whitley_RJ>{{cite journal
| author= Whitley RJ, Kimberlin DW, Roizman B
| title=Herpes simplex viruses
| journal=Clin Infect Dis
| year=1998
| pages=541–53
| volume=26
| issue=3
| pmid=9524821
|doi= |url=http://www.journals.uchicago.edu/doi/pdf/10.1086/514600
}}</ref>

Women that are seropositive for only one type of HSV are only half as likely to transmit HSV as the seronegative mother. In the U.S. the number of genital infections caused by HSV-1 is now thought to be about 50% of first episodes of genital infection.<ref name=Mertz_GJ>{{cite journal
| author= Mertz GJ, Rosenthal SL, Stanberry LR
| title=Is Herpes Simplex Virus Type 1 (HSV-1) Now More Common than HSV-2 in First Episodes of Genital Herpes?
| journal=Sex Transm Dis
| year=2003
| pages=797–800
| volume=30
| issue=10
| pmid=14520182
| url=http://www.stdjournal.com/pt/re/std/pdfhandler.00007435-200310000-00013.pdf
}}</ref><ref name=Roberts_CM>{{cite journal
| author= Roberts CM, Pfister JR, Spear SJ
| title=Increasing proportion of herpes simplex virus type 1 as a cause of genital herpes infection in college students
| journal=Sex Transm Dis
| year=2003
| pages=797–800
| volume=30
| issue=10
| pmid=14520181
| url=http://www.stdjournal.com/pt/re/std/pdfhandler.00007435-200310000-00012.pdf
}}</ref>

In healthy adults, HSV-2 infection occurs more frequently in the [[USA]] than in Europe, and infection rates appear to be increasing. In individuals over 12 years old, HSV-2 seroprevalence has increased from 16.4% in 1976 to 21.8% in 1994 and is still rising.<ref name="pmid15115626">{{cite journal
|author=Malkin JE
|title=Epidemiology of genital herpes simplex virus infection in developed countries
|journal=Herpes
|volume=11 Suppl 1
|issue=
|pages=2A–23A
|year=2004
|pmid=15115626 }}</ref>
The current incidence of genital herpes caused by HSV-2 in the U.S. is roughly one in four or five adults, with approximately 50 million people infected with genital herpes and an estimated 0.5 million new genital herpes infections occurring each year.<ref name="pmid17939933"/> [[African American]]s appear more susceptible to HSV-2, although the presence of active genital symptoms is more likely in [[White American|Caucasian Americans]]. The largest increase in HSV-2 acquisition during the past few years is in white adolescents. People with many lifetime sexual partners and those who are sexually active from a young age are also at higher-risk for the transmission of HSV-2 in the U.S.<ref name = "ummc">{{cite web
| url =http://www.umm.edu/patiented/articles/who_gets_herpes_simplex_virus_000052_4.htm
| title = Herpes simplex
| accessdate = 2007-09-03
| format = HTML
| work =
| publisher = [[University of Maryland]] Medical Center
| pages =
| language = English
| archiveurl =
| archivedate =
}}
</ref><ref name = "asha">{{cite web
| url = http://www.ashastd.org/herpes/herpes_learn.cfm
| title = LEARN ABOUT HERPES > Fast Facts
| accessdate = 2007-09-03
| format = HTML
| work =
| publisher = [[ASHA]] Herpes Resource Center
| pages =
| language = English
| archiveurl =
| archivedate =
}}
</ref><ref name = "cdc">{{cite web
| url = http://www.cdc.gov/std/Herpes/STDFact-Herpes.htm
| title = STD Facts - Genital Herpes
| accessdate = 2007-09-03
| format = HTML
| work =
| publisher = [[Centers for Disease Control and Prevention]]
| pages =
| language = English
| archiveurl =
| archivedate =
}}
</ref><ref name = "stanford">{{cite web
| url = http://www.stanford.edu/group/SHPRC/ch4_her.html
| title = Herpes
| accessdate = 2007-09-03
| format = HTML
| work =
| publisher = [[Stanford University]] Sexual Health Peer Resource Center
| pages =
| language = English
| archiveurl =
| archivedate =
}}
</ref>
Women are at higher risk than men for acquiring HSV-2 infection, and the chance of being infected increases with age.<ref name="pmid17939933"/>

====Canada====
According to a study in [[Ontario]], up to 55% of [[Canadian]]s age of 15 to 16, and 89% of individuals in their early forties have antibodies to HSV-1.<ref name=Howard2003>{{cite journal
| author = Howard M, Sellors J.W., Jang D, Robinson NJ, Fearon M, Kaczorowski J, Chernesky M
| year = 2003
| title = Regional Distribution of Antibodies to Herpes Simplex Virus Type 1 (HSV-1) and HSV-2 in Men and Women in Ontario, Canada
| journal = J Clin Microbiol
| volume = 41(1)
| pages = 84-89
| pubmed = PMCID: PMC149555
| url = http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=149555&blobtype=pdf
}}</ref> Teenagers are less likely to be seropositive for HSV-2—antibodies against this virus are only found in 0–3.8% of 15-16 year olds. However, 21% of individuals in their early forties have antibodies against HSV-2, reflecting the sexually transmitted nature of this virus. When standardising for age, HSV-2 seroprevalence in Ontario for individuals between the ages of 15 to 44 was 9.1%. This is much lower than estimated levels of HSV-2 seroprevalence in people of a similar age range in the United States.<ref name="pmid12517830">{{cite journal
|author=Howard M, Sellors JW, Jang D, ''et al''
|title=Regional distribution of antibodies to herpes simplex virus type 1 (HSV-1) and HSV-2 in men and women in Ontario, Canada
|journal=J. Clin. Microbiol.
|volume=41
|issue=1
|pages=84–9
|year=2003
|pmid=12517830 }}</ref>
HSV-2 seroprevalence in pregnant women between the ages of 15-44 in [[British Columbia]] is similar, with 57% having antibodies for HSV-1 and 13% having antibodies for HSV-2.<ref name="pmid12353183"/>

===Africa===
====Sub-Saharan Africa====
HSV-2 is more common in [[Sub-Saharan Africa]] than in Europe or the North America. Up to 82% of women and 53% of men in Sub-Saharan Africa are seropositive for HSV-2. <!-- Referenced in table. -->These are the highest levels of HSV-2 infection in the world, although exact levels vary from country to country in this continent.<ref name="pmid15115627">{{cite journal
|author=Weiss H
|title=Epidemiology of herpes simplex virus type 2 infection in the developing world
|journal=Herpes
|volume=11 Suppl 1
|issue=
|pages=24A–35A
|year=2004
|pmid=15115627 }}</ref>
In most African countries, HSV-2 prevalence increases with age. However, age-associated decreases in HSV-2 seroprevalence has been observed for women in [[Uganda]] and [[Zambia]], and in men in [[Ethiopia]], [[Benin]], and Uganda.<ref name="pmid12353183"/>

====Northern Africa====
Genital herpes appears less common in [[North Africa|Northern Africa]] compared to Sub-Saharan Africa. For example, only 26% of middle-aged women have antibodies for HSV-2 in [[Morocco]].<ref name="pmid18080353"/> Women are more likely to be infected with HSV-2 once they are over the age of 40.<ref name="pmid18080353"/> Children in [[Egypt]] are often infected with HSV from a young age—HSV-1 or HSV-2 antibodies are present in an estimated 54% of children under the age of 5, and 77% in children over 10 years of age.<ref name="pmid16883441">{{cite journal
|author=Loutfy SA, Alam El-Din HM, Ibrahim MF, Hafez MM
|title=Seroprevalence of herpes simplex virus types 1 and 2, Epstein-Barr virus, and cytomegalovirus in children with acute lymphoblastic leukemia in Egypt
|journal=Saudi Med J
|volume=27
|issue=8
|pages=1139–45
|year=2006
|pmid=16883441 }}</ref>
[[Algeria]]n children are also likely to acquire HSV-1 infection at a young age (under 6) and 81.25% of the population has antibodies to HSV-1 by the age of 15.<ref name="pmid2562258">{{cite journal
|author=Meguenni S, Djenaoui T, Bendib A, ''et al''
|title=Herpes simplex virus infections in Algiers
|language=French
|journal=Arch Inst Pasteur Alger
|volume=57
|pages=61–72
|year=1989
|pmid=2562258}}</ref>

===Central and South America===

Relative to rates in Europe and North America, HSV-2 seroprevalency is high in Central and South America. Infection levels are estimated at 20% to 60%.<ref name="pmid12353183"/><ref name="pmid15115627"/>
During the mid 1980s, HSV-2 prevalence was 33% in 25–29 year old women and 45% in those aged 40 and over in [[Costa Rica]]. In the early 1990s HSV-2 prevalence was approximately 45% among women over 60 in [[Mexico]].<ref name="pmid12353183"/> The highest HSV-2 prevalence in Central or South America—60%—has been found in [[Colombia]]n middle-aged women, although similar HSV-2 prevalence has been observed in younger women in [[Haiti]] (54%).<ref name="pmid12353183"/> HSV-2 infects about 30% of women over 30 years old in [[Colombia]], Costa Rica, Mexico, and [[Panama]]. HSV-2 antibodies were found in more than 41% of women of childbearing age in [[Brazil]].<ref name="pmid12353183"/> However, no increase in seroprevalence was associated with age in women over 40 years old in Brazil—HSV-2 prevalence was estimated at 50% among women aged 40–49, 33% among women 50–59, and 42% among women over 60. Women in Brazil are more likely to acquire an HSV-2 infection if their male partners had history of anal sex and had many sexual partners in his lifetime.<ref name="pmid18080353"/> In [[Peru]], HSV-2 prevalence is also high among women in their 30s but is lower in men.<ref name="pmid12353183"/>

===Asia===
====Eastern and South East Asia====
HSV-1 seroprevalence in some Asian countries is low, relative to other countries worldwide, with only 51% women in [[Thailand]], and between 50-60% in [[Japan]] possessing antibodies.<ref name="pmid18080353"/><ref name="pmid12353183"/> HSV-2 seroprevalence in developing [[Asia]]n countries is comparable (10-30%) to that observed in North America and Northern Europe.<ref name="pmid15115627"/> However, estimates of HSV-2 infectivity in Thailand are higher than observed in other [[Eastern Asia]]n countries; total HSV-2 seroprevalence is approximately 37% in this country.<ref name="pmid18080353"/> HSV-2 seroprevalence is low in women in the [[Philippines]] (9%), although commencing activity while young is associated with an increase risk of acquiring HSV-2 infection; woman starting sexual activity by the time they reach 17 are seven times more likely to be HSV-2 seropositive that those starting sexual activity when over 21.<ref name="pmid11318248">{{cite journal
|author=Smith JS, Herrero R, Muñoz N, ''et al''
|title=Prevalence and risk factors for herpes simplex virus type 2 infection among middle-age women in Brazil and the Philippines
|journal=Sex Transm Dis
|volume=28
|issue=4
|pages=187–94
|year=2001
|pmid=11318248}}</ref>
In South Korea, incidence of HSV-2 infection in those under the age of 20 is low, only 2.7% in men and 3.0% in women.<ref name="pmid18162706"/> Seroprevalence levels increase in older South Koreans however, such that the population over 20 that has antibodies against HSV-2 is 21.7% of men and 28% of women.<ref name="pmid18162706"/>
====Southern Asia====
In India 33.3% of individuals are seropositive for HSV-1 and 16.6% are seropositive for HSV-2. Those with both HSV-1 and HSV-2 antibodies are estimated at 13.3% of the population. Indian men are more likely to be infected with HSV-2 than women, and increasing seroprevalence of this virus is associated with an increasing age.<ref name="pmid17278662">{{cite journal |author=Kaur R, Gupta N, Baveja UK |title=Seroprevalence of HSV1 and HSV2 infections in family planning clinic attenders |journal=J Commun Dis |volume=37 |issue=4 |pages=307–9 |year=2005 |pmid=17278662 |doi=}}</ref>
====Middle East====
Turky-
High levels of HSV-1 (97%) and HSV-2 (42%) were found amongst pregnant women in the city of [[Erzurum]] in [[Eastern Anatolia Region, Turkey]].<ref name="pmid12353183"/> In [[Istanbul]] however, lower HSV-2 seroprevalence was observed; HSV-2 antibodies were found in 4.8% of sexually active adults, while HSV-1 antibodies were found in 85.3%.<ref name="pmid17062037">{{cite journal
|author=Dolar N, Serdaroglu S, Yilmaz G, Ergin S
|title=Seroprevalence of herpes simplex virus type 1 and type 2 in Turkey
|journal=J Eur Acad Dermatol Venereol
|volume=20
|issue=10
|pages=1232–6
|year=2006
|pmid=17062037
|doi=10.1111/j.1468-3083.2006.01766.x}}</ref>
Only 5% of pregnant women were infected with HSV-2, and 98% were infected with HSV-1. Prevalence of these viruses was higher in sex workers of Istanbul, reaching levels of 99% and 60% for HSV-1 and HSV-2 prevalence respectively.<ref name="pmid17062037"/>

Jordan-
The prevalence of HSV-2 in [[Jordan]] is 52.8% for men and 41.5% for women.<ref name="pmid10939038">{{cite journal
|author=Abuharfeil N, Meqdam MM
|title=Seroepidemiologic study of herpes simplex virus type 2 and cytomegalovirus among young adults in northern Jordan
|journal=New Microbiol.
|volume=23
|issue=3
|pages=235–9
|year=2000
|pmid=10939038 }}</ref>

Israel-
HSV-1 seroprevalence is 59.8% in the population of [[Israel]] and increases with age in both genders and but the adolescent seroprevalence has been declining as in most industrialized nations. <ref name=Davidovici2006-Nov>{{cite journal
| author = Davidovici Bb, Grotto I., Balicer RD, Robinson NJ, Cohen D
| year = 2006-Nov
| title = Decline in the prevalence of antibodies to herpes simplex virus types 1 and 2 among Israeli young adults between 1984 and 2002
| journal = Sex Transm Dis
| volume = 33(11)
| pages = 641-5.
| pubmed = PMID: 16614586 [PubMed - indexed for MEDLINE]
| url = http://www.stdjournal.com/pt/re/std/pdfhandler.00007435-200611000-00001.pdf
}}</ref>An estimated 9.2% of Israeli adults are infected with HSV-2. Infection of either HSV-1 or HSV-2 is higher in females; HSV-2 seroprevalence reaches 20.5% in females in their 40s. These values are similar to levels in HSV infection in Europe.<ref name="pmid16213591">{{cite journal
|author=Davidovici BB, Green M, Marouni MJ, Bassal R, Pimenta JM, Cohen D
|title=Seroprevalence of herpes simplex virus 1 and 2 and correlates of infection in Israel
|journal=J. Infect.
|volume=52
|issue=5
|pages=367–73
|year=2006
|pmid=16213591
|doi=10.1016/j.jinf.2005.08.005}}</ref>
Antibodies for HSV-1 or HSV-2 are also more likely to be found individuals born outside of Israel, and individuals residing in [[Jerusalem]] and Southern Israel; people of [[Jewish]] origin living in Israel are less likely to possess antibodies against herpes.<ref name="pmid16213591"/>
Among pregnant women in Israel a small scale cross sectional study found the prevalence of HSV-2 infection was 13.3% and that of HSV-1 was 94.9%. The HSV-2 infection rate was 3-fold higher among immigrants from the former Soviet Union (27.5%) than among
Israeli-born Jewish and Arab women (9%). <ref name=Dan2003>{{cite journal
| author = Dan M, Sadan O., Glezerman M, Raveh D, Samra Z
| year = 2003
| title = Prevalence and risk factors for herpes simplex virus type 2 infection among pregnant women in Israel
| journal = Sex Transm Dis
| volume = 30(11)
| pages = 835-8
| pmid = 14603091
| url = http://www.stdjournal.com/pt/re/std/pdfhandler.00007435-200311000-00007.pdf
}}</ref> Approximately 78% of HSV-2 infections in Israel are asymptomatic.<ref name=Feldman2003>{{cite journal
| author = Feldman Pa, Steinberg J., Madeb R, Bar G, Nativ O, Tal J, Srugo I
| year = 2003
| title = Herpes simplex virus type 2 seropositivity in a sexually transmitted disease clinic in Israel
| journal = Isr Med Assoc J
| volume = 5(9)
| pages = 626-8
| Pubmed = PMID: 14509150 [PubMed - indexed for MEDLINE]
|url = http://www.ima.org.il/imaj/ar03sep-5.pdf
}}</ref>HSV-1 causes 66.3% of genital herpes in the [[Tel Aviv]] area.<ref name="pmid14520180">{{cite journal
|author=Samra Z, Scherf E, Dan M
|title=Herpes simplex virus type 1 is the prevailing cause of genital herpes in the Tel Aviv area, Israel
|journal=Sex Transm Dis
|volume=30
|issue=10
|pages=794–6
|year=2003
|pmid=14520180
|doi=10.1097/01.OLQ.0000079517.04451.79}}</ref>

Syria-
Genital herpes infection from HSV-2 is predicted to be low in [[Syria]] although HSV-1 levels are high. HSV-1 infections is common (95%) among healthy Syrians over the age of 30, while HSV-2 prevalence is low in healthy individuals (0.15%), and persons infected with other sexually transmitted diseases (9.5%). High risk groups for acquiring HSV-2 in Syria, include prostitutes and bar girls; they have 34% and 20% seroprevalence respectively.<ref name="pmid11533818">{{cite journal |author=Ibrahim AI, Kouwatli KM, Obeid MT |title=Frequency of herpes simplex virus in Syria based on type-specific serological assay |journal=Saudi Med J |volume=21 |issue=4 |pages=355–60 |year=2000 |pmid=11533818 |doi=}}</ref>

===Oceania===

In [[Australia]] the seroprevalence of HSV-1 is 76%, with differences associated with age, gender and Indigenous status.<ref name="pmid16581748">{{cite journal |author=Cunningham AL, Taylor R, Taylor J, Marks C, Shaw J, Mindel A |title=Prevalence of infection with herpes simplex virus types 1 and 2 in Australia: a nationwide population based survey |journal=Sex Transm Infect |volume=82 |issue=2 |pages=164–8 |year=2006 |pmid=16581748 |doi=10.1136/sti.2005.016899}}</ref>
An estimated 12% of Australian adults are seropositive for HSV-2, with higher prevalence in women (16%) than in men (8%).<ref name="pmid16581748"/> Larger cities have higher HSV-2 seroprevalence (13%) than rural populations (9%). Higher prevalence is found in [[Indigenous Australians]] (18%) than non-Indigenous Australians (12%) but is lower than HSV-2 prevalence observed in the United States.<ref name="pmid16581748"/> As in the U.S., HSV-1 is increasingly identified as the cause of genital herpes in Australians; HSV-1 was identified in the [[Perineum|anogenital area]] of only 3% of the population in 1980, but had risen to 41% in 2001.<ref name="pmid16731681">{{cite journal |author=Haddow LJ, Dave B, Mindel A, ''et al'' |title=Increase in rates of herpes simplex virus type 1 as a cause of anogenital herpes in western Sydney, Australia, between 1979 and 2003 |journal=Sex Transm Infect |volume=82 |issue=3 |pages=255–9 |year=2006 |pmid=16731681 |doi=10.1136/sti.2005.018176}}</ref> This was most common in females and persons under 25.<ref name="pmid16731681"/>

The number of genital herpes infections appears to be rising in [[New Zealand]] with three times more cases in 1993 compared to 1977.<ref name="pmid8001945">{{cite journal |author=Lyttle PH |title=Surveillance report: disease trends at New Zealand sexually transmitted disease clinics 1977-1993 |journal=Genitourin Med |volume=70 |issue=5 |pages=329–35 |year=1994 |pmid=8001945 |doi=}}</ref> In this country, HSV-2 affects 60% more women than men of similar age.<ref name="pmid12353183"/>

==Treatment==

There is currently no treatment that can eradicate herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks. Antiviral drugs also reduce asymptomatic shedding; it is believed asymptomatic shedding occurs on 10.8% of days in patients not undergoing antiviral treatment, versus 2.9% of days while on antiviral therapy.<ref name="pmid16238897"/> Non-prescription [[analgesic]]s can reduce pain and fever during initial outbreaks. Topical anesthetic treatments such as [[prilocaine]], [[lidocaine]] or [[tetracaine]] can also relieve itching and pain.<ref name="pmid3147021">{{cite journal
|author=
|title=Local anesthetic creams
|journal=BMJ
|volume=297
|issue=6661
|pages=1468
|year=1988
|pmid=3147021
|doi=}}</ref><ref name="pmid10570387">{{cite journal
|author=Kaminester LH, Pariser RJ, Pariser DM, ''et al''
|title=A double-blind, placebo-controlled study of topical tetracaine in the treatment of herpes labialis
|journal=J. Am. Acad. Dermatol.
|volume=41
|issue=6
|pages=996–1001
|year=1999
|pmid=10570387 }}</ref>

===Antiviral medication===

[[Antiviral drug|Antiviral medications]] used against herpes viruses work by interfering with [[viral replication]], effectively slowing the replication rate of the virus and providing a greater opportunity for the immune response to intervene. All drugs in this class depend on the activity of the viral [[enzyme]] [[thymidine kinase]] to convert the drug sequentially from its [[prodrug]] form to monophosphate (with one [[phosphate]] group), diphosphate (with two phosphate groups), and finally to the triphosphate (with three phosphate groups) form which interferes with viral [[DNA replication]].<ref name="pmid16284630">{{cite journal
|author=De Clercq E, Field HJ
|title=Antiviral prodrugs - the development of successful prodrug strategies for antiviral chemotherapy
|journal=Br. J. Pharmacol.
|volume=147
|issue=1
|pages=1–11
|year=2006
|pmid=16284630
|doi=10.1038/sj.bjp.0706446}}</ref>
[[Image:Acyclovir pills.jpg|thumb|left|200px|The antiviral medication acyclovir]]

There are several prescription [[antiviral]] medications for controlling herpes simplex outbreaks, including [[aciclovir]] (Zovirax), [[valaciclovir]] (Valtrex), [[famciclovir]] (Famvir), and [[penciclovir]]. Aciclovir was the original, and prototypical, member of this drug class; it is now available in generic brands at a greatly reduced cost. Valaciclovir and famciclovir—prodrugs of aciclovir and penciclovir, respectively—have improved solubility in water and better [[bioavailability]] when taken orally.<ref name="pmid16284630"/> Aciclovir is the recommended antiviral for suppressive therapy for use during the last months of pregnancy to prevent transmission of herpes simplex to the [[neonate]].<ref name="Leung">{{cite journal
| author=Leung DT, Sacks SL.
| title=Current treatment options to prevent perinatal transmission of herpes simplex virus
| journal=Expert Opin. Pharmacother.
| year=2003
| pages=1809–1819
| volume=4
| issue=10
| pmid=14521490
| doi=10.1517/14656566.4.10.1809}}</ref>
The use of valaciclovir and famciclovir, while potentially improving treatment compliance and efficacy, are still undergoing safety evaluation in this context.

Several studies with mice provide evidence that treatment with famciclovir soon after initial infection can help lower the incidence of future outbreaks, by reducing the amount of latent virus in the neural ganglia.<ref>The effects of antiviral therapy on the distribution of herpes simplex virus type 1 to ganglionic neurons and its consequences during, immediately following and several months after treatment"[http://vir.sgmjournals.org/cgi/content/full/81/10/2385]"</ref><ref>Famciclovir and Valaciclovir Differ in the Prevention of Herpes Simplex Virus Type 1 Latency in Mice: a Quantitative Study"[http://aac.asm.org/cgi/content/full/42/7/1555]"</ref><ref>Persistence of Infectious Herpes Simplex Virus Type 2 in the Nervous System in Mice after Antiviral Chemotherapy"[http://aac.asm.org/cgi/content/full/44/1/97]"</ref> A review of human subjects treated with famciclovir during their first herpes episode supports these findings, with only 4.2 percent of famciclovir-treated patients experiencing a recurrence within one to six months after the first outbreak, compared to 19 percent of acyclovir-treated patients.<ref>Observation May Indicate A Possible Clinical Effect On Latency"[http://www.pslgroup.com/dg/D29E.htm]"</ref> Despite these promising results, early famciclovir treatment for herpes has yet to find mainstream adoption. However, the potential effect on latency drops to zero a few months post-infection.<ref name=Thackray>{{cite journal
| author=Thackray AM, Field HJ.
| title=Differential effects of famciclovir and valaciclovir on the pathogenesis of herpes simplex virus in a murine infection model including reactivation from latency
| journal=J. Infect. Dis.
| year=1996
| pages=291–299
| volume=173
| issue=2
| pmid=8568288}}</ref>

Antiviral medications are also available as topical creams for treating recurrent outbreaks on the lips, although their effectiveness is disputed.<ref name="pmid8664786">{{cite journal
|author=Worrall G
|title=Evidence for efficacy of topical acyclovir in recurrent herpes labialis is weak
|journal=BMJ
|volume=313
|issue=7048
|pages=46
|year=1996
|pmid=8664786 </ref>
Penciclovir cream has a 7-17 hour longer cellular [[biological half-life|half-life]] than aciclovir cream, increasing its effectiveness relative to aciclovir when topically applied.<ref name="pmid9134943">{{cite journal
|author=Spruance SL, Rea TL, Thoming C, Tucker R, Saltzman R, Boon R
|title=Penciclovir cream for the treatment of herpes simplex labialis. A randomized, multicenter, double-blind, placebo-controlled trial. Topical Penciclovir Collaborative Study Group
|journal=JAMA
|volume=277
|issue=17
|pages=1374–9
|year=1997
|pmid=9134943 </ref>

===Topical treatments===

[[Docosanol]] is available as a cream for direct application to the affected area of skin. It prevents HSV from fusing to cell membranes, thus barring the entry of the virus into the skin. Docosanol was approved for use after clinical trials by the [[FDA]] in July 2000.<ref>{{cite web
| title = Drug Name: ABREVA (docosanol) - approval
| publisher = centerwatch.com
| date = July 2000
| url = http://www.centerwatch.com/patient/drugs/dru627.html
| accessdate = 2007-10-17 }}</ref>
Docosanol is marketed by Avanir Pharmaceuticals under the name Abreva. It was the first [[over-the-counter drug|over-the-counter]] [[antiviral drug]] approved for sale in the United States and Canada. Avanir Pharmaceuticals and GlaxoSmithKiline Consumer Healthcare were the subject of a U.S. nationwide class-action suit in [[March, 2007]] due to the misleading claim that it cut recovery times in half.<ref>{{cite web
| title = California Court Upholds Settlement Of Class Action Over Cold Sore Medicationl
| publisher = BNA Inc.
| date = July 2000
| url = http://subscript.bna.com/SAMPLES/plp.nsf/85256269004a991e8525611300214487/29d5bb623a50fd25852572ad0074f772?OpenDocument
| accessdate = 2007-10-17 }}</ref>

[[Tromantadine]] is available as a gel that inhibits the entry and spread of the virus by altering the surface composition of skin cells and inhibiting release of viral genetic material. Zilactin is a topical [[analgesic]] barrier treatment, which forms a "shield" at the area of application to prevent a sore from increasing in size, and decrease viral spreading during the healing process.

There is some limited research that has shown that [[tea tree oil]] may have topical anti-viral activity, especially with the [[Herpes]] virus<ref>{{cite journal | author=Bishop, C.D. | title=Anti-viral Activity of the Essential Oil of Melaleuca alternifolia | journal=Journal of Essential Oil Research | pages=641–644| year=1995 }}</ref>

===Other drugs===

[[Cimetidine]], a common component of [[heartburn]] medication, has been shown to lessen the severity of [[herpes zoster]] outbreaks in several different instances.<ref name=kapinska>
{{cite journal
| author=Kapinska-Mrowiecka M, Toruwski G
| title=Efficacy of cimetidine in treatment of herpes zoster in the first 5 days from the moment of disease manifestation.
| journal= Pol Tyg Lek.
| year=1996
| pages=338–339
| volume=51
| issue=23-26
| pmid=9273526}}</ref><ref name=hayne>{{cite journal
| author=Hayne ST, Mercer JB
| title=Herpes zoster:treatment with cemetidine.
| journal=Can Med Assoc J
| year= 1983
| pages=1284–1285
| volume=129
| issue=12
| pmid=6652595}}</ref><ref name=komlos> {{cite journal
| author=Komlos L, Notmann J, Arieli J, et.al.
| title=In vitro cell-mediated immune reactions in herpes zoster patients treated with cimetidine.
| journal=Asian Pac J Allelrgy Immunol
| year= 1994
| pages=51–58
| volume=12
| issue=1
| pmid=7872992 }}</ref> This is an [[off-label use]] of the drug. It and [[probenecid]] have been shown to reduce the [[Clearance (medicine)|renal clearance]] of aciclovir.<ref name=debony>{{cite journal
| author=De Bony F, Tod M, Bidault R, On NT, Posner J, Rolan P.
| title=Multiple interactions of cimetidine and probenecid with valaciclovir and its metabolite acyclovir
| journal=Antimicrob. Agents Chemother.
| year=2002
| pages=458–463
| volume=46
| issue=2
| pmid=11796358
| doi=10.1128/AAC.46.2.458-463.2002}}</ref> These compounds also reduce the rate, but not the extent, at which valaciclovir is converted into aciclovir.

Limited evidence suggests that low dose [[aspirin]] (125 mg daily) might be beneficial in patients with recurrent HSV infections. Aspirin (acetylsalicylic acid) is an [[non-steroidal anti-inflammatory drug]] which reduces the level of [[prostaglandin]]s—naturally occurring lipid compounds—that are essential in creating [[inflammation]].<ref name=Karadi>{{cite journal
| author=Karadi I, Karpati S, Romics L.
| title=Aspirin in the management of recurrent herpes simplex virus infection
| journal=Ann. Intern. Med.
| year=1998
| pages=696–697
| volume=128
| issue=8
| pmid=9537952}}</ref> A recent study in animals showed inhibition of thermal (heat) [[Stress (medicine)|stress]] induced [[viral shedding]] of HSV-1 in the eye by aspirin, and a possible benefit in reducing the frequency of recurrences.<ref name=Gebhardt>{{cite journal
| author=Gebhardt BM, Varnell ED, Kaufman HE.
| title=Acetylsalicylic acid reduces viral shedding induced by thermal stress
| journal=Curr. Eye Res.
| year=2004
| pages=119–125
| volume=29
| issue=2-3
| pmid=15512958
| doi=10.1080/02713680490504588 }}</ref>
Another treatment is the use of petroleum jelly. Healing of cold sores is sped by barring water or saliva from reaching the sore.

===Vaccines===

The [[National Institutes of Health]] (NIH) in the [[United States]] is currently conducting [[Clinical trial|phase III trials]] of [[Herpevac]], a vaccine against HSV-2.<ref name="titleHerpevac Trial for Women">{{cite web
|url=http://www.niaid.nih.gov/dmid/stds/herpevac/
|title=Herpevac Trial for Women |accessdate=2008-02-25}}</ref>
The vaccine has only been shown to be effective for women who have never been exposed to HSV-1. Overall, the vaccine is approximately 48% effective in preventing HSV-2 seropositivity and about 78% effective in preventing symptomatic HSV-2.<ref name="titleHerpevac Trial for Women">{{cite web |url=http://www.niaid.nih.gov/dmid/stds/herpevac/studyover_faqs.htm
|title=Herpevac Trial for Women
|accessdate=2008-03-04 }}</ref> Assuming FDA approval, a commercial version of the vaccine is estimated to become available in 2008.{{Fact|date=July 2008}} During initial trials, the vaccine did not exhibit any evidence of preventing HSV-2 in males.<ref name="titleHerpevac Trial for Women"/> Additionally, the vaccine only reduced the acquisition of HSV-2 and symptoms due to newly acquired HSV-2 among women who did not have HSV-2 infection at the time they got the vaccine.<ref name="titleHerpevac Trial for Women"/> Because about 20% of persons in the United States have HSV-2 infection, this further reduces the population for whom this vaccine might be appropriate.<ref name="titleHerpevac Trial for Women"/>

Researchers at the [[University of Florida]] have made a hammerhead [[ribozyme]] that targets and cleaves the mRNA of essential genes in HSV-1. The hammerhead which targets the mRNA of the UL20 gene greatly reduced the level of HSV-1 ocular infection in rabbits and reduced the viral yield in vivo.<ref>{{cite web
|url=http://www.nature.com/mt/journal/v13/n1s/abs/mt2006942a.html
|title=Molecular Therapy - Abstract of article: 801. RNA Gene Therapy Targeting Herpes Simplex Virus }}</ref>

===Natural compounds===
{| class = "prettytable" style = "width:150px; float:right; font-size:80%; margin-left:15px"
|[[Image:RedoxonVitaminC.jpg|150px]]
|-
|[[Image:Koeh-094.jpg|150px]]
|-
|[[Image:Garlic.jpg|150px]]
|-
|Many people seek benefits in natural products and dietary supplements for treatment of herpes
|}

Certain dietary adjustments, [[dietary supplement]]s, and [[Complementary and alternative medicine|alternative remedies]] are believed to be beneficial in the treatment of herpes, either alone, or in conjunction with prescribed antiviral therapy. There is currently insufficient scientific and clinical evidence to support the effective use of many of these compounds to treat herpes in humans.<ref name="pmid16209859">{{cite journal
|author=Perfect MM, Bourne N, Ebel C, Rosenthal SL
|title=Use of complementary and alternative medicine for the treatment of genital herpes
|journal=Herpes
|volume=12
|issue=2
|pages=38–41
|year=2005
|pmid=16209859 }}</ref>

[[Lysine]] supplementation has been used for the [[prophylaxis]] and treatment of herpes simplex Doses smaller than 1 gram per day appear to be ineffective.<ref name=McCune>{{cite journal
| author=McCune MA, Perry HO, Muller SA, O'Fallon WM.
| title=Treatment of recurrent herpes simplex infections with L-lysine monohydrochloride
| journal=Cutis.
| year=2005
| pages=366–373
| volume=34
| issue=4
| pmid=6435961}}</ref><ref name=Griffith>{{cite journal
| author=Griffith RS, Walsh DE, Myrmel KH, Thompson RW, Behforooz A.
| title=Success of L-lysine therapy in frequently recurrent herpes simplex infection. Treatment and prophylaxis
| journal=Dermatologica.
| year=1987
| pages=183–190
| volume=175
| issue=4
| pmid=3115841}}</ref><ref name=Griffith2>{{cite journal
| author=Griffith RS, Norins AL, Kagan C.
| title=A multicentered study of lysine therapy in Herpes simplex infection
| journal=Dermatologica.
| year=1978
| pages=257–267
| volume=156
| issue=5
| pmid=640102}}</ref>
[[Aloe vera]], available as a cream or gel, makes an affected area heal faster and may prevent recurrences.<ref>{{cite journal
| author=Vogler BK and Ernst E.
| title=Aloe vera: a systematic review of its clinical effectiveness.
| journal=British Journal of General Practice
| volume=49
| pages=823–828
| url=http://www.jr2.ox.ac.uk/bandolier/booth/alternat/AT125.html}}</ref>
[[Lemon balm]] (Melissa officinalis) has antiviral activity against HSV-2 in cell culture and may reduce HSV symptoms in herpes infected people.<ref name=Allahverdiyev>{{cite journal
| author=Allahverdiyev A, Duran N, Ozguven M, Koltas S.
| title=Antiviral activity of the volatile oils of Melissa officinalis L. against Herpes simplex virus type-2.
| journal=Phytomedicine.
| year=2004
| pages=657–661
| volume=11
| issue=7-8
| pmid=15636181
| doi=10.1016/j.phymed.2003.07.014 }}</ref><ref name="pmid10589440">{{cite journal
|author=Koytchev R, Alken RG, Dundarov S
|title=Balm mint extract (Lo-701) for topical treatment of recurring herpes labialis
|journal=Phytomedicine
|volume=6
|issue=4
|pages=225–30
|year=1999
|pmid=10589440
|doi=}}</ref><ref name="pmid10589440" />
[[Carrageenan]]s—linear sulphated [[polysaccharide]]s extracted from red [[seaweed]]s—have been shown to have antiviral effects in HSV-infected cells and in mice.<ref name=Zacharopoulos>{{cite journal
| author=Zacharopoulos VR, Phillips DM.
| title=Vaginal formulations of carrageenan protect mice from herpes simplex virus infection
| journal=Clin. Diagn. Lab. Immunol.
| year=1997
| pages=465–468
| volume=4
| issue=4
| pmid=9220165}}</ref> However, there is no evidence that this compound is effective as a treatment in humans.<ref name=Carlucci>{{cite journal
| author=Carlucci MJ, Scolaro LA, Damonte EB.
| title=Inhibitory action of natural carrageenans on Herpes simplex virus infection of mouse astrocytes
| journal=Chemotherapy
| year=1999
| pages=429–436
| volume=45
| issue=6
| pmid=10567773
| doi=10.1159/000007236 }}</ref>
There is conflicting evidence on a possible benefit from extracts from the plant [[echinacea]] in treating oral<ref name="pmid12357386">{{cite journal
|author=Binns SE, Hudson J, Merali S, Arnason JT
|title=Antiviral activity of characterized extracts from echinacea spp. (Heliantheae: Asteraceae) against herpes simplex virus (HSV-I)
|journal=Planta Med.
|volume=68
|issue=9
|pages=780–3
|year=2002
|pmid=12357386
|doi=10.1055/s-2002-34397}}</ref>, but not genital, herpes.<ref name="pmid11231867">{{cite journal
|author=Vonau B, Chard S, Mandalia S, Wilkinson D, Barton SE
|title=Does the extract of the plant Echinacea purpurea influence the clinical course of recurrent genital herpes?
|journal=Int J STD AIDS
|volume=12
|issue=3
|pages=154–8
|year=2001
|pmid=11231867 }}</ref>
[[Resveratrol]], a compound naturally produced by plants and a component of red wine, prevents HSV replication in cultured cells and reduces cutaneous HSV lesion formation in mice. It is not considered potent enough to be an effective treatment on its own.<ref name=Docherty99>
{{cite journal
| author=Docherty JJ, Fu MM, Stiffler BS, Limperos RJ, Pokabla CM, DeLucia AL.
| title=Resveratrol inhibition of herpes simplex virus replication
| journal=Antiviral Res.
| year=1999
| pages=145–155
| volume=43
| issue=3
| pmid=10551373
| doi=10.1016/S0166-3542(99)00042-X }}</ref><ref name=Docherty04>{{cite journal
| author=Docherty JJ, Smith JS, Fu MM, Stoner T, Booth T.
| title=Effect of topically applied resveratrol on cutaneous herpes simplex virus infections in hairless mice
| journal=Antiviral Res.
| year=2004
| pages=19–26
| volume=61
| issue=1
| pmid=14670590
| doi=10.1016/j.antiviral.2003.07.001}}</ref>

Extracts from [[garlic]] have shown antiviral activity against HSV in cell culture experiments, although the extremely high concentrations of the extracts required to produce an antiviral effect was also toxic to the cells.<ref name="pmid1470664">{{cite journal
|author=Weber ND, Andersen DO, North JA, Murray BK, Lawson LD, Hughes BG
|title=In vitro virucidal effects of Allium sativum (garlic) extract and compounds
|journal=Planta Med.
|volume=58
|issue=5
|pages=417–23
|year=1992
|pmid=1470664 }}</ref>
The plant [[Prunella vulgaris]], commonly known as ''selfheal'', also prevents expression of both type 1 and type 2 herpes in cultured cells.<ref name=saritamackita> {{cite journal
| author=Chiu LC, Zhub W, Oo VE
| title=A polysaccharide fraction from medicinal herb Prunella vulgaris downregulates the expression of herpes simplex virus antigen in Vero cells
| journal=Journal of Ethnopharmacology
| year=2004
| pages=63–68
| volume=93
| issue=1
| doi=10.1016/j.jep.2004.03.024 }}</ref>

[[Lactoferrin]], a component of [[whey]] protein, has been shown to have a synergistic effect with aciclovir against HSV in vitro.<ref name=Andersen>
{{cite journal
| author=Andersen JH, Jenssen H, Gutteberg TJ.
| title=Lactoferrin and lactoferricin inhibit Herpes simplex 1 and 2 infection and exhibit synergy when combined with acyclovir
| journal=Antiviral Res.
| year=2003
| pages=209–215
| volume=58
| issue=3
| pmid=12767468
| doi=10.1016/S0166-3542(02)00214-0 }}</ref>

Some dietary supplements have been suggested to positively treat herpes. These include [[vitamin C]], [[vitamin A]], [[vitamin E]], and [[zinc]].<ref name="pmid16813459">{{cite journal
|author=Gaby AR
|title=Natural remedies for Herpes simplex
|journal=Altern Med Rev
|volume=11
|issue=2
|pages=93–101
|year=2006
|pmid=16813459 }}</ref><ref name="pmid16405618">{{cite journal
|author=Yazici AC, Baz K, Ikizoglu G
|title=Recurrent herpes labialis during isotretinoin therapy: is there a role for photosensitivity?
|journal=J Eur Acad Dermatol Venereol
|volume=20
|issue=1
|pages=93–5
|year=2006
|pmid=16405618
|doi=10.1111/j.1468-3083.2005.01358.x}}</ref>
[[Butylated hydroxytoluene]] (BHT), commonly available as a [[food preservative]], has been shown in cell culture and animal studies to inactivate herpes virus.<ref>{{cite journal
|author= Snipes W, Person S, Keith A, Cupp J.
|title=Butylated hydroxytoluene inactivates lipid-containing viruses" Science. 1975;188(4183):64-6</ref><ref>Richards JT, Katz ME, Kern ER. "Topical butylated hydroxytoluene treatment of genital herpes simplex virus infections of guinea pigs
|journal=Antiviral Res
|year=1985
|volume=5
issue=5;
pages=281-90 }}</ref> However, BHT has not been clinically tested and approved to treat herpes infections in humans.

==Psychological and social effects==

Some people experience negative feelings related to the condition following diagnosis, particularly if they have acquired the genital form of the disease. Feelings can include depression, fear of rejection, feelings of isolation, fear of being found out, self-destructive feelings, and fear of masturbation.<ref name=Vezina>{{cite journal
| author=Vezina C, Steben M.
| title=Genital Herpes: Psychosexual Impacts and Counselling
| journal=The Canadian Journal of CME
| year=2001
| pages=125–134
| issue=June}}</ref> These feelings usually lessen over time. [[Herpes support groups]] have been formed in the United States and the UK, providing information about herpes and running message forums and dating websites for sufferers.<ref>{{cite web
|url=http://www.herpesaz.com/html/groups.html
|title=A to Z Herpes Support Groups }}</ref><ref>{{cite web
|url=http://www.herpes-coldsores.com/support/herpes.htm
|title=Herpes Support Groups }}</ref><ref>{{cite web
|url=http://www.herpes.org.uk
|title=Herpes Viruses Association}}</ref><ref>{{cite web
|url=http://www.herpes-coldsores.com/messageforum
|title=Herpes & Cold Sore Support Forum }}</ref><ref>{{cite web
|url=http://www.h-date.com
|title=Herpes Dating H-Date.com - genital herpes dating/HPV picture }}</ref><ref>{{cite web
|url=http://www.mpwh.net/
|title=Herpes Dating, HPV Dating, and Support on Antopia's MPwH.net }}</ref>

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 that they consider casual.<ref name=Green>{{cite journal
| author=Green J, Ferrier S, Kocsis A, Shadrick J, Ukoumunne OC, Murphy S, Hetherton J.
| title=Determinants of disclosure of genital herpes to partners.
| journal=Sex. Transm. Infect.
| year=2003
| pages=42–44
| volume=79
| issue=1
| pmid=12576613
| doi=10.1136/sti.79.1.42}}</ref> A perceived reaction is sometimes taken into account before making a decision about whether to inform new partners and at what point in the relationship. Many people choose not to disclose their herpes status when they first begin dating someone, but wait until it later becomes clear that they are moving towards a sexual relationship. Other people disclose their herpes status upfront. Still others choose only to date other people who already have herpes.

==References==
{{reflist|2}}

== External links ==
<!-- BEFORE inserting new links here you should first post it to the talk page, otherwise your edit is likely to be reverted-->

'''General'''
*[http://www.cdc.gov/std/Herpes/STDFact-Herpes.htm Genital Herpes Fact Sheet] at [[The Centers for Disease Control and Prevention]]
*[http://www.fda.gov/fdac/features/2002/202_herp.html Paper - Genital Herpes: A Hidden Epidemic] at [[FDA]]

'''Images'''
*[http://www.lib.uiowa.edu/hardin/md/herpespictures.html Links to genital herpes pictures] (Hardin MD/[[University of Iowa]]
*[http://www.dermnet.com/moduleSearch.cfm?searchterm=herpes Herpes photo library at Dermnet]
*[http://www.visualdxhealth.com/adult/orofacialHerpesSimplexVirusHSV.htm Pictures of Orofacial Herpes (Coldsores)] (VisualDxHealth)
*[http://herpespictures.blogspot.com/ Genital Herpes Pictures]

'''Other'''
<!-- BEFORE inserting new links here you should first post it to the talk page, otherwise your edit is likely to be reverted. -->
*[http://www.ashastd.org/pdfs/blood_test.pdf Herpes Blood Tests Quick Reference Guide]
*[http://www.westoverheights.com/genital_herpes/handbook.html Updated Herpes Handbook from Westover Heights Clinic]
*[http://www.medscape.com/viewarticle/489964 "The Importance and Practicalities of Patient Counseling in the Prevention and Management of Genital Herpes"] (2004) at [[Medscape]]
*[http://www.ihmf.org/default.asp International Herpes Management Forum]
*[http://www.herpes.com/Nutrition.shtml Provides Ratios of Lysine to Arginine in Common Foods]
*[http://www.sexhealthguru.com/index.php?id=136,311,0,0,1,0 How Valtrex Works]

{{STD/STI}}
{{Viral diseases}}

[[Category:Sexually transmitted diseases and infections]]
[[Category:Viral diseases]]

[[ar:هربس بسيط]]
[[cs:Jednoduchý opar]]
[[da:Herpes]]
[[de:Herpes simplex]]
[[es:Herpes]]
[[eo:Herpeto]]
[[fr:Herpès]]
[[ko:단순 포진]]
[[id:Herpes simpleks]]
[[it:Herpes]]
[[he:הרפס]]
[[ms:Herpes]]
[[nl:Genitale herpes]]
[[ja:性器ヘルペス]]
[[no:Herpesvirusinfeksjon]]
[[pl:Zakażenia opryszczkowe]]
[[pt:Herpes]]
[[ru:Герпес]]
[[sk:Jednoduchý opar]]
[[sr:Херпес]]
[[zh:單純疱疹病毒]]

Revision as of 06:48, 7 August 2008

Herpes
SpecialtyInfectious diseases, dermatology Edit this on Wikidata
This article is about the disease. For information about the specific virus, see Herpes simplex virus.
"herpes" redirects here. For all types of herpes viruses, see Herpesviridae.


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