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==Overview==
==Overview==
'''Herpes simplex''' is a [[viral disease]] caused by [[Herpes simplex virus]]es. Infection of the [[genital]]s is commonly known as ''herpes'' and predominantly occurs following sexual transmission of the type 2 strain of the virus (HSV-2).<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> Oral herpes, colloquially called ''cold sores'', is usually caused by the type 1 strain of herpes simplex virus (HSV-1).<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>  Both viruses cause periods of active disease—presenting as painful blisters containing infectious [[virus]] particles—that lasts 2-21 days and is followed by [[remission]] when the sores disappear. Most cases of genital herpes are [[asymptomatic]], although [[viral shedding]] may still occur.<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> HSV-1 and HSV-2 are transmitted by direct contact with a sore or body fluid of an infected individual.  After initial infection, these viruses move to [[Sensory neuron|sensory nerves]], where they reside as life-long, [[Virus latency|latent]] viruses. The viruses lie dormant in [[Trigeminal ganglion|trigeminal ganglia]] that provide sensation to the lips, lower mouth and neck, or in [[sacral ganglia|lumbrosacral]] that supply sensation to the genitals, [[perineum]] and upper legs.<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>  Occasionally, these viruses reactivate and return to the area of skin infected during the primary infection.  Triggers for recurrences are uncertain but may include sunburn, [[ultraviolet light]], wind, trauma, surgery, and stress. Over time, episodes of active disease reduce and the frequency of recurrences is regulated by [[Adaptive immune system|specific immunity]] developed against the virus.<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>
'''Herpes simplex''' is a [[viral disease]] caused by [[Herpes simplex virus]]es. Infection of the [[genital]]s is commonly known as ''herpes'' and predominantly occurs following sexual transmission of the type 2 strain of the virus (HSV-2).<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> Oral herpes, colloquially called ''cold sores'', is usually caused by the type 1 strain of herpes simplex virus (HSV-1).<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>  Both viruses cause periods of active disease—presenting as painful blisters containing infectious [[virus]] particles—that lasts 2-21 days and is followed by [[remission]] when the sores disappear. Most cases of genital herpes are [[asymptomatic]], although [[viral shedding]] may still occur.<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> HSV-1 and HSV-2 are transmitted by direct contact with a sore or body fluid of an infected individual.  After initial infection, these viruses move to [[Sensory neuron|sensory nerves]], where they reside as life-long, [[Virus latency|latent]] viruses. The viruses lie dormant in [[Trigeminal ganglion|trigeminal ganglia]] that provide sensation to the lips, lower mouth and neck, or in [[sacral ganglia|lumbrosacral]] that supply sensation to the genitals, [[perineum]] and upper legs.<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>  Occasionally, these viruses reactivate and return to the area of skin infected during the primary infection.  Triggers for recurrences are uncertain but may include sunburn, [[ultraviolet light]], wind, trauma, surgery, and stress. Over time, episodes of active disease reduce and the frequency of recurrences is regulated by [[Adaptive immune system|specific immunity]] developed against the virus.<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>
 
==Classification==
===Anogenital Infection===
HSV-2 is widespread, affecting an estimated 1 in 4 females and 1 in 5 males in the United States. Most young, sexually active patients who have genital, anal, or perianal ulcers have either genital [[Herpes simplex|herpes]] or [[syphilis]]. The frequency of each condition differs by geographic area and population; however, genital herpes is the most prevalent of these diseases.
===Ocular Infection===
Ocular herpes is generally caused by HSV-1 and is a special case of facial herpes infection known as herpes keratitis.  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>
===Herpes Encephalitis===
Herpes simplex [[encephalitis]] (HSE) is a very serious disorder and one of the most severe viral infections of the human [[central nervous system]].
===Herpes Simplex Neonatorum===
[[Infant|Neonatal]] HSV disease is a rare but serious condition, usually as a consequence of [[vertical transmission]] of the virus from the mother to the newborn child, although an estimated 10% of cases may be acquired [[postnatal|postnatally]] from a parent, caretaker, or sibling. From 1/3,000 to 1/20,000 of live births are infected with neonatal herpes. Approximately 22% of pregnant women have had a previous exposure HSV-2, and a further 2% or more women acquire the virus during pregnancy.<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}}</ref> Particularly among young adults, genital herpes infections are increasing caused by HSV-1.<ref name="pmid17197885">{{cite journal |author=Baker DA |title=Consequences of herpes simplex virus in pregnancy and their prevention |journal=Curr. Opin. Infect. Dis. |volume=20 |issue=1 |pages=73–6 |year=2007 |pmid=17197885 |doi=10.1097/QCO.0b013e328013cb19}}</ref>
===Herpetic Whitlow===
A herpetic whitlow is a lesion on a [[finger]] or [[thumb]] caused by the [[herpes simplex virus]].  In children the primary source of infection is the orofacial area, and it is commonly inferred that the [[virus]] (in this case commonly [[HSV-1]]) is transferred by the chewing or sucking of [[finger]]s or [[thumbs]].  In adults it is more common for the primary source to be the [[genital]] region, with a corresponding preponderance of [[HSV-2]]. It is also seen in adult health care workers such as dentists because increased exposure to the herpes virus.
===Herpes Gladiotorum===
Individuals that participate in contact sports such as wrestling, rugby, and soccer sometimes acquire a condition caused by HSV-1 known as herpes gladiatorum, ''[[scrumpox]]'', ''wrestler’s herpes'' or ''mat herpes''. Abraded skin caused by contacts sports provides an area of entry for HSV-1. Symptoms present within 2 weeks of direct skin-to-skin contact with an infected person, and include skin ulceration on the face, ears, and neck. This disorder may cause fever, headache, sore throat and swollen glands, and occasionally affects the eyes. Physical symptoms sometimes recur in the skin.<ref name="pmid17939933">Fatahzadeh M, Schwartz RA (2007) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=17939933 Human herpes simplex virus infections: epidemiology, pathogenesis, symptomatology, diagnosis, and management.] ''J Am Acad Dermatol'' 57 (5):737-63; quiz 764-6. [http://dx.doi.org/10.1016/j.jaad.2007.06.027 DOI:10.1016/j.jaad.2007.06.027] PMID: [http://pubmed.gov/17939933 17939933]</ref>
===Mollaret's Meningitis===
Mollaret's meningitis is a recurrent [[inflammation]] of the protective membranes covering the [[brain]] and [[spinal cord]], known collectively as the [[meninges]]. Mollaret's meningitis is caused by [[herpes simplex virus]]. It is a recurrent, benign, [[aseptic meningitis]].
==Epidemiology and Demographics==
==Epidemiology and Demographics==
Prevalence of HSV-1 and HSV-2 infections varies throughout the world.<ref name="pmid17939933"/>  Socioeconomic status appears to be an important factor associated with HSV-1 infection levels with developing countries, such as those in Sub-Saharan Africa, showing higher levels of HSV-1 and younger acquisition rates than industrialized countries like the [[United States]] and countries in Northern Europe. The risk of infection for HSV-1 is associated with lower income and a more crowded living environment. Levels of HSV-2 infections are much lower in the U.S. (20-30%), Australia (12%), the United Kingdom (4%) and Germany (14%).<ref name="pmid16926356">{{cite journal |author=Xu F, Sternberg MR, Kottiri BJ, ''et al'' |title=Trends in herpes simplex virus type 1 and type 2 seroprevalence in the United States |journal=JAMA |volume=296 |issue=8 |pages=964–73 |year=2006 |pmid=16926356 |doi=10.1001/jama.296.8.964}}</ref> Risk Factors for acquiring HSV-2 include: Female sex; black race; commencement of sexual activity at a younger age; higher number of sexual partners; and lower socioeconomic status.
Prevalence of HSV-1 and HSV-2 infections varies throughout the world.<ref name="pmid17939933"/>  Socioeconomic status appears to be an important factor associated with HSV-1 infection levels with developing countries, such as those in Sub-Saharan Africa, showing higher levels of HSV-1 and younger acquisition rates than industrialized countries like the [[United States]] and countries in Northern Europe. The risk of infection for HSV-1 is associated with lower income and a more crowded living environment. Levels of HSV-2 infections are much lower in the U.S. (20-30%), Australia (12%), the United Kingdom (4%) and Germany (14%).<ref name="pmid16926356">{{cite journal |author=Xu F, Sternberg MR, Kottiri BJ, ''et al'' |title=Trends in herpes simplex virus type 1 and type 2 seroprevalence in the United States |journal=JAMA |volume=296 |issue=8 |pages=964–73 |year=2006 |pmid=16926356 |doi=10.1001/jama.296.8.964}}</ref> Risk Factors for acquiring HSV-2 include: Female sex; black race; commencement of sexual activity at a younger age; higher number of sexual partners; and lower socioeconomic status.

Revision as of 20:03, 6 March 2013

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Lakshmi Gopalakrishnan, M.B.B.S.

Overview

Herpes simplex is a viral disease caused by Herpes simplex viruses. Infection of the genitals is commonly known as herpes and predominantly occurs following sexual transmission of the type 2 strain of the virus (HSV-2).[1] Oral herpes, colloquially called cold sores, is usually caused by the type 1 strain of herpes simplex virus (HSV-1).[2] Both viruses cause periods of active disease—presenting as painful blisters containing infectious virus particles—that lasts 2-21 days and is followed by remission when the sores disappear. Most cases of genital herpes are asymptomatic, although viral shedding may still occur.[3] HSV-1 and HSV-2 are transmitted by direct contact with a sore or body fluid of an infected individual. After initial infection, these viruses move to sensory nerves, where they reside as life-long, latent viruses. The viruses lie dormant in trigeminal ganglia that provide sensation to the lips, lower mouth and neck, or in lumbrosacral that supply sensation to the genitals, perineum and upper legs.[4] Occasionally, these viruses reactivate and return to the area of skin infected during the primary infection. Triggers for recurrences are uncertain but may include sunburn, ultraviolet light, wind, trauma, surgery, and stress. Over time, episodes of active disease reduce and the frequency of recurrences is regulated by specific immunity developed against the virus.[5]

Classification

Anogenital Infection

HSV-2 is widespread, affecting an estimated 1 in 4 females and 1 in 5 males in the United States. Most young, sexually active patients who have genital, anal, or perianal ulcers have either genital herpes or syphilis. The frequency of each condition differs by geographic area and population; however, genital herpes is the most prevalent of these diseases.

Ocular Infection

Ocular herpes is generally caused by HSV-1 and is a special case of facial herpes infection known as herpes keratitis. It begins with infection of epithelial cells on the surface of the eye and retrograde infection of nerves serving the cornea.[6]

Herpes Encephalitis

Herpes simplex encephalitis (HSE) is a very serious disorder and one of the most severe viral infections of the human central nervous system.

Herpes Simplex Neonatorum

Neonatal HSV disease is a rare but serious condition, usually as a consequence of vertical transmission of the virus from the mother to the newborn child, although an estimated 10% of cases may be acquired postnatally from a parent, caretaker, or sibling. From 1/3,000 to 1/20,000 of live births are infected with neonatal herpes. Approximately 22% of pregnant women have had a previous exposure HSV-2, and a further 2% or more women acquire the virus during pregnancy.[7] Particularly among young adults, genital herpes infections are increasing caused by HSV-1.[8]

Herpetic Whitlow

A herpetic whitlow is a lesion on a finger or thumb caused by the herpes simplex virus. In children the primary source of infection is the orofacial area, and it is commonly inferred that the virus (in this case commonly HSV-1) is transferred by the chewing or sucking of fingers or thumbs. In adults it is more common for the primary source to be the genital region, with a corresponding preponderance of HSV-2. It is also seen in adult health care workers such as dentists because increased exposure to the herpes virus.

Herpes Gladiotorum

Individuals that participate in contact sports such as wrestling, rugby, and soccer sometimes acquire a condition caused by HSV-1 known as herpes gladiatorum, scrumpox, wrestler’s herpes or mat herpes. Abraded skin caused by contacts sports provides an area of entry for HSV-1. Symptoms present within 2 weeks of direct skin-to-skin contact with an infected person, and include skin ulceration on the face, ears, and neck. This disorder may cause fever, headache, sore throat and swollen glands, and occasionally affects the eyes. Physical symptoms sometimes recur in the skin.[4]

Mollaret's Meningitis

Mollaret's meningitis is a recurrent inflammation of the protective membranes covering the brain and spinal cord, known collectively as the meninges. Mollaret's meningitis is caused by herpes simplex virus. It is a recurrent, benign, aseptic meningitis.

Epidemiology and Demographics

Prevalence of HSV-1 and HSV-2 infections varies throughout the world.[4] Socioeconomic status appears to be an important factor associated with HSV-1 infection levels with developing countries, such as those in Sub-Saharan Africa, showing higher levels of HSV-1 and younger acquisition rates than industrialized countries like the United States and countries in Northern Europe. The risk of infection for HSV-1 is associated with lower income and a more crowded living environment. Levels of HSV-2 infections are much lower in the U.S. (20-30%), Australia (12%), the United Kingdom (4%) and Germany (14%).[9] Risk Factors for acquiring HSV-2 include: Female sex; black race; commencement of sexual activity at a younger age; higher number of sexual partners; and lower socioeconomic status.

Clinical Presentation

Disorders such as herpetic whitlow, herpes gladiatorum, and ocular herpes are caused by herpes simplex viruses. Infection of the central nervous system causes serious disorders - these include herpes encephalitis, Mollaret's meningitis, and possibly Bell's palsy.[10][11] In newborn babies, infection by herpes viruses (neonatal herpes) can be highly serious, resulting in brain damage or even death.[12] In immunocompetent people, herpes simplex is not typically life-threatening. However, individuals with compromised immune systems can develop serious HSV infections such as encephalitis.

Diagnosis

The clinical diagnosis of genital herpes is both nonsensitive and nonspecific. The classical painful multiple vesicular or ulcerative lesions are absent in many infected persons. HSV-1 is causing an increasing proportion of first episodes of anogenital herpes in some populations (such as young women and MSM) and might now account for most of genital herpes infections.[13][14] Recurrences and subclinical shedding are less frequent for genital HSV-1 infection than for genital HSV-2 infection.[15][16] A patient’s prognosis and the type of counseling needed depends on the type of genital herpes (HSV-1 or HSV-2) causing the infection; therefore, the clinical diagnosis of genital herpes should be confirmed by laboratory testing.[17] Both virologic and type-specific serologic tests for HSV should be performed to diagnose patients with or at risk for STDs.

Treatment

Treatments are available to reduce the symptoms and speed up the healing process of herpes infections but there is currently no cure.[5] Antiviral medications can shorten and prevent outbreaks during the period of time the person takes the medication. In addition, daily suppressive therapy for symptomatic herpes can reduce transmission to partners. Antiviral drugs, such as aciclovir and valaciclovir, taken orally, reduce viral reproduction and shedding, and some topical creams, such as Docosanol and Tromantadine prevent the virus from entering the skin. Some other drugs reduce herpetic symptoms by synergising with oral antiviral medication; Cimetidine and probenecid can reduce aciclovir clearance and aspirin can reduce inflammation associated with viral infection. Some natural remedies may have potential benefits in reducing herpes outbreaks or their symptoms. No vaccine is currently available to prevent or treat herpes.[5]

References

  1. Gupta R, Warren T, Wald A (2007). "Genital herpes". Lancet. 370 (9605): 2127–37. doi:10.1016/S0140-6736(07)61908-4. PMID 18156035.
  2. Bruce AJ, Rogers RS (2004). "Oral manifestations of sexually transmitted diseases". Clin. Dermatol. 22 (6): 520–7. doi:10.1016/j.clindermatol.2004.07.005. PMID 15596324.
  3. Leone P (2005). "Reducing the risk of transmitting genital herpes: advances in understanding and therapy". Curr Med Res Opin. 21 (10): 1577–82. doi:10.1185/030079905X61901. PMID 16238897.
  4. 4.0 4.1 4.2 Fatahzadeh M, Schwartz RA (2007). "Human herpes simplex virus infections: epidemiology, pathogenesis, symptomatology, diagnosis, and management". J. Am. Acad. Dermatol. 57 (5): 737–63, quiz 764–6. doi:10.1016/j.jaad.2007.06.027. PMID 17939933.
  5. 5.0 5.1 5.2 Koelle DM, Corey L (2008). "Herpes Simplex: Insights on Pathogenesis and Possible Vaccines". Annu Rev Med. 59: 381–395. doi:10.1146/annurev.med.59.061606.095540. PMID 18186706.
  6. Carr DJ, Härle P, Gebhardt BM (2001). "The immune response to ocular herpes simplex virus type 1 infection". Exp. Biol. Med. (Maywood). 226 (5): 353–66. PMID 11393165.
  7. Brown ZA, Gardella C, Wald A, Morrow RA, Corey L (2005). "Genital herpes complicating pregnancy". Obstet Gynecol. 106 (4): 845–56. doi:10.1097/01.AOG.0000180779.35572.3a. PMID 16199646.
  8. Baker DA (2007). "Consequences of herpes simplex virus in pregnancy and their prevention". Curr. Opin. Infect. Dis. 20 (1): 73–6. doi:10.1097/QCO.0b013e328013cb19. PMID 17197885.
  9. Xu F, Sternberg MR, Kottiri BJ; et al. (2006). "Trends in herpes simplex virus type 1 and type 2 seroprevalence in the United States". JAMA. 296 (8): 964–73. doi:10.1001/jama.296.8.964. PMID 16926356.
  10. Tyler KL (2004). "Herpes simplex virus infections of the central nervous system: encephalitis and meningitis, including Mollaret's". Herpes. 11 Suppl 2: 57A–64A. PMID 15319091.
  11. Schirm J, Mulkens PS (1997). "Bell's palsy and herpes simplex virus". APMIS. 105 (11): 815–23. PMID 9393551.
  12. Kimberlin DW, Whitley RJ (2005). "Neonatal herpes: what have we learned". Semin Pediatr Infect Dis. 16 (1): 7–16. doi:10.1053/j.spid.2004.09.006. PMID 15685144.
  13. Ryder N, Jin F, McNulty AM, Grulich AE, Donovan B (2009) Increasing role of herpes simplex virus type 1 in first-episode anogenital herpes in heterosexual women and younger men who have sex with men, 1992-2006. Sex Transm Infect 85 (6):416-9. DOI:10.1136/sti.2008.033902 PMID: 19273479
  14. Roberts CM, Pfister JR, Spear SJ (2003) Increasing proportion of herpes simplex virus type 1 as a cause of genital herpes infection in college students. Sex Transm Dis 30 (10):797-800. DOI:10.1097/01.OLQ.0000092387.58746.C7 PMID: 14520181
  15. Benedetti J, Corey L, Ashley R (1994) Recurrence rates in genital herpes after symptomatic first-episode infection. Ann Intern Med 121 (11):847-54. PMID: 7978697
  16. Engelberg R, Carrell D, Krantz E, Corey L, Wald A (2003) Natural history of genital herpes simplex virus type 1 infection. Sex Transm Dis 30 (2):174-7. PMID: 12567178
  17. Scoular A (2002) Using the evidence base on genital herpes: optimising the use of diagnostic tests and information provision. Sex Transm Infect 78 (3):160-5. PMID: 12238644

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