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{{అనువాదం}}
{{Infobox Disease |
Image = Herpes(PHIL 1573 lores).jpg|
Line 38 ⟶ 37:
ఆహారంలో పోషక విలువల సమతుల్యత సరిగా ఉండేలా చూసుకోవాలి, ఇంటి పరిసరాలు పరిశుభ్రంగా ఉంచుకోవాలి.
 
== మూలాలు==
erpes 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 become [[Virus latency|latent]] and reside life-long. Causes of recurrence are uncertain, though some potential triggers have been identified. Over time, episodes of active disease reduce in frequency and severity.
 
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 method of preventing transmission of herpes, but they merely reduce rather than eliminate risk. 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.
 
A cure for herpes has not yet been developed. Once infected, the virus remains in the body for life. However, after several years, some people will become perpetually [[asymptomatic]] and will no longer experience outbreaks, though they may still be contagious to others. Treatments with [[antivirals]] can reduce viral shedding and alleviate the severity of symptomatic episodes. Vaccines are in [[clinical trials]] but have not demonstrated effectiveness. It should not be confused with conditions caused by other viruses in the ''[[herpesviridae]]'' family such as [[herpes zoster]], which is caused by [[varicella zoster virus]]. The differential diagnosis includes [[hand, foot and mouth disease]] due to similar lesions on the skin.
 
== Classification==
Herpes simplex is divided into two types: HSV type 1 and HSV type 2.<ref name=Peds09/> HSV1 primarily causes mouth, throat, face, eye, and [[central nervous system]] infections, while HSV2 primarily causes anogenital infections.<ref name=Peds09/> However, each may cause infections in all areas.<ref name=Peds09/>
 
== Signs and symptoms ==
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 newborns, transplant recipients, or AIDS patients are prone to severe complications from HSV infections. HSV infection has also been associated with cognitive deficits of [[bipolar disorder]],<ref name="Dickerson2004 Mar 15">{{cite journal
|author=Dickerson FB, Boronow JJ, Stallings C, ''et al.'' |title=Infection with herpes simplex virus type 1 is associated with cognitive deficits in bipolar disorder |journal=Biol. Psychiatry |volume=55 |issue=6 |pages=588–93 |year=2004 |month=March |pmid=15013827 |doi=10.1016/j.biopsych.2003.10.008
}}</ref> and [[Alzheimer's disease]],<ref name="Itzhaki1997 Jan 25">{{cite journal
|author=Itzhaki RF, Lin WR, Shang D, Wilcock GK, Faragher B, Jamieson GA |title=Herpes simplex virus type 1 in brain and risk of Alzheimer's disease |journal=Lancet |volume=349 |issue=9047 |pages=241–4 |year=1997 |month=January |pmid=9014911 |doi=10.1016/S0140-6736(96)10149-5
}}</ref> although this is often dependent on the [[genetics]] of the infected person.
 
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">{{cite journal |author=Gupta R, Warren T, Wald A |title=Genital herpes |journal=Lancet |volume=370 |issue=9605 |pages=2127–37 |year=2007 |month=December |pmid=18156035 |doi=10.1016/S0140-6736(07)61908-4 |url=http://linkinghub.elsevier.com/retrieve/pii/S0140-6736(07)61908-4}}</ref> 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 reduce the symptoms of a later HSV-2 infection, although HSV-2 can still be contracted. Most indications are that an HSV-2 infection contracted prior to HSV-1 seroconversion will also immunize that person against HSV-1 infection.{{Citation needed|date=May 2010}}
 
Many people infected with HSV-2 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=10.1007/s11908-000-0084-y}}</ref>
 
{| class="wikitable"
|-
! Condition
! Description
! Illustration
|-
|[[Gingivostomatitis|Herpetic gingivostomatitis]]
| Herpetic gingivostomatitis is often the initial presentation during the first herpes infection. It is of greater severity than herpes labialis which is often the subsequent presentations. Around 90% of the U.S. population is affected with this disease.<ref>{{cite web |url=http://www.dent.ucla.edu/pic/visitors/herpes/page1.html#primar |title=PRIMARY INFECTION OR PRIMARY HERPETIC GINGIVOSTOMATITIS (PHG ) |format= |work= |accessdate=|archiveurl=https://archive.is/9305|archivedate=2012-08-05}}</ref>
|[[దస్త్రం:Herpesgingiva.JPG|center|150px]]
|-
| [[Herpes labialis]]
| Infection occurs when the virus comes into contact with oral mucosa or abraded skin.
| [[దస్త్రం:Cold sore.jpg|center|150px]]
|-
| [[Herpes genitalis]]
| When symptomatic, the typical manifestation of a primary HSV-1 or HSV-2 genital infection is clusters of inflamed [[papule]]s and [[Vesicle (dermatology)|vesicles]] on the outer surface of the genitals resembling cold sores.
| [[దస్త్రం:SOA-Herpes-genitalis-female.jpg|center|150px]]
|-
| [[Herpetic whitlow]]
| Herpes whitlow is a painful infection that typically affects the fingers or thumbs. Occasionally infection occurs on the toes or on the nail cuticle.
| [[దస్త్రం:Herpetic whitlow in young child.jpg|center|150px]]
|-
| [[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'', which presents as skin ulceration on the face, ears, and neck. Symptoms include fever, headache, sore throat and swollen glands. It occasionally affects the eyes or eyelids.
|
|-
| [[Herpetic keratoconjunctivitis]]
| Primary infection typically presents as swelling of the [[conjunctiva]] and eyelids ([[blepharoconjunctivitis]]), accompanied by small white itchy lesions on the surface of the [[cornea]].
|
|-
| [[Herpesviral encephalitis]]
| A herpetic infection of the brain that 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 the [[trigeminal nerve]] [[axon]], to the brain. HSV is the most common cause of viral encephalitis. When infecting the brain, the virus shows a preference for the [[temporal lobe]].<ref>{{cite web |url=http://emedicine.medscape.com/article/341142-overview |title=Herpes Encephalitis: eMedicine Radiology |format= |work= |accessdate=}}</ref>.
| [[దస్త్రం:Hsv encephalitis.jpg|center|150px]]
|-
| [[Herpesviral meningitis]]
| HSV-2 is the most common cause of Mollaret's meningitis, a type of recurrent viral meningitis.
|
|-
| [[Neonatal herpes simplex]]
| [[Infant|Neonatal]] HSV infection is a rare but serious condition, usually caused by [[vertical transmission]] of HSV (type 1 or 2) from mother to newborn.
|
|-
|-
| During [[immunodeficiency]]
| In patients with a weakened immune system, herpes simplex can cause unusual lesions in the skin. One of the most striking is the appearance of clean linear erosions in skin creases, with the appearance of a knife cut.<ref>{{cite journal|title=Linear erosive Herpes Simplex Virus infection in immunocompromised patients: the “Knife-Cut Sign”|journal=Clin Infect Dis|year=2008|volume=47|pages=1440–1441|doi=10.1086/592976|author=Jocelyn A. Lieb, Stacey Brisman, Sara Herman, Jennifer MacGregor, Marc E. Grossman|pmid=18937574|issue=11}}</ref>
|-
| [[Herpetic sycosis]]
| Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicle.<ref name="Andrews">{{cite book |author=James, William D.; Berger, Timothy G.; et al. |title=Andrews' Diseases of the Skin: clinical Dermatology |publisher=Saunders Elsevier |location= |year=2006 |pages= |isbn=0-7216-2921-0 |oclc= |doi= |accessdate=}}</ref>{{rp|369}}
|-
| [[Eczema herpeticum]]
| Infection with herpesvirus in patients with chronic [[atopic dermatitis]] may result in spread of herpes simples throughout the eczematous areas.<ref name="Andrews" />{{rp|373}}
|-
| [[Herpes esophagitis]]
| Symptoms may include painful swallowing ([[odynophagia]]) and difficulty swallowing ([[dysphagia]]). It is often associated with impaired immune function (e.g. [[HIV]]/[[AIDS]], [[immunosuppression]] in solid [[organ transplants]]).
| [[దస్త్రం:Herpes esophagitis.JPG|center|150px]]
|}
 
== Pathophysiology ==
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 |work= |archiveurl = http://web.archive.org/web/20080121164311/http://www.ahmf.com.au/health_professionals/guidelines/preventing_gh_transmission.htm |archivedate = January 21, 2008}}</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. The only way to contract Herpes simplex virus 2 is through direct skin-to-skin contact with an infected individual.{{Citation needed|date=January 2010}} 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"/> Virus enters into susceptible cells via entry receptors<ref>
{{cite journal
| title = Viral entry mechanisms: cellular and viral mediators of herpes simplex virus entry
| last = Akhtar
| first = Jihan
| last2 = Shukla
| first2 = Deepak
| journal = FEBS Journal
| volume = 2009
| issue = 276
| url = http://www3.interscience.wiley.com/cgi-bin/fulltext/122668866/PDFSTART
}}</ref>
such as nectin-1, HVEM and 3-O sulfated heparan sulfate.<ref>
{{cite journal
| title = A Novel Role for 3-O-Sulfated Heparan Sulfate in Herpes Simplex Virus 1 Entry
| journal = Cell
| volume = 99
| issue = 1
| pages = 13–22
| last = Shukla
| first = Deepak
| last2 = Liu
| first2 = Jian
| last3 = Blaiklock
| first3 = Peter
| last4 = Shworak
| first4 = Nicholas W.
| last5 = Bai
| first5 = Xiaomei
| last6 = Esko
| first6 = Jeffrey D.
| last7 = Cohen
| first7 = Gary H.
| last8 = Eisenberg
| first8 = Roselyn
| last9 = Rosenberg
| first9 = Robert D.
| url = http://www.cell.com/retrieve/pii/S0092867400800586
| doi = 10.1016/S0092-8674(00)80058-6
| pmid = 10520990
| year = 1999
}}</ref>
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 one to twelve annual recurrences to those who 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 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
| pmid = 8106731}}</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.
 
== 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 [[Vesicle (dermatology)|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 [[fungal infection]], [[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"/>
 
Until recently, [[Serology|serological]] tests for antibodies to HSV were rarely useful to diagnosis and not routinely used in clinical practice<ref name="pmid17939933"/>. The older IgM serologic assay could not differentiate between antibodies generated in response to HSV-1 or HSV-2 infection. However, the new Immunodot glycoprotein G-specific (IgG) HSV test is more that 98% specific at discriminating HSV-1 from HSV-2.
<ref name="ClinMicro1988;26:662-667">{{cite journal |author=Ashley RL, et. al. |title=Comparison of wester blod (immunoblot) and glycoprotein G-specific immunodot enzyme assay for detecting antibodies to herpes simplex virus type 1 and type 2 in human era |journal=J. Clin. Microbiol. |volume=26 |issue=4 |pages=662–667 |year=1988 |url=http://jcm.asm.org/cgi/content/abstract/26/4/662?ijkey=e6b5d2fe810a92d0353f5a1649d94014839a0663&keytype2=tf_ipsecsha |pmid=2835389 |pmc=266403}}</ref>
It is the opinion of some modern medical professionals that the new IgG test should always be clinically preferred to the old IgM test, however not all doctors appear to be informed of the availability of the newer, reliable IgG tests.
<ref name="GoodNewsAboutBadNews">
{{Cite book
| last = Warren
| first = Terri
| authorlink = Terri Warren
| title = The Good News About The Bad News
| url = http://books.google.com/?id=PoRB5qQXW70C&printsec=frontcover&dq=%22good+news+about+the+bad+news%22&q
| year = 2009
| page = 209
| isbn = 1572246189
| publisher = New Harbinger Publications }}
</ref>
 
== Prevention ==
[[దస్త్రం:Kondom.jpg|thumb|Barrier protection, such as a [[condom]], can reduce the risk of herpes transmission.]]
 
As with almost all sexually transmitted infections, women are more susceptible to acquiring genital HSV-2 than men.<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%.<ref name=Mertz1993>{{cite journal
|author=Mertz GJ |title=Epidemiology of genital herpes infections |journal=Infect Dis Clin North Am. |volume=7 |issue=4 |pages=825–39 |year=1993 |month=December |pmid=8106731
}}</ref><ref name=Kulhanjian1992>{{cite journal
|doi=10.1056/NEJM199204023261403
|author=Kulhanjian JA, Soroush V, Au DS, ''et al.'' |title=Identification of women at unsuspected risk of primary infection with herpes simplex virus type 2 during pregnancy |journal=N. Engl. J. Med. |volume=326 |issue=14 |pages=916–20 |pmid=1311799 |url=http://content.nejm.org/cgi/content/abstract/326/14/916
|date= April 2, 1992 }}</ref>
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.<ref name=Kulhanjian1992/> Suppressive antiviral therapy reduces these risks by 50%.<ref name=Corey2004>{{cite journal
|author=Corey L, Wald A, Patel R, ''et al.'' |title=Once-daily valacyclovir to reduce the risk of transmission of genital herpes |journal=N Engl J Med. |volume=350 |issue=1 |pages=11–20 |year=2004 |month=January |pmid=14702423 |doi=10.1056/NEJMoa035144 |url=http://content.nejm.org/cgi/reprint/350/1/11.pdf
|format=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%.<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 | url=http://jama.ama-assn.org/cgi/content/full/285/24/3100 | 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 | url=http://www.ihmf.org/journal/download/91casper(10)vol910.pdf|format=PDF}}</ref><ref name=Wald2005>{{cite journal
|author=Wald A, Langenberg AG, Krantz E, ''et al.'' |title=The relationship between condom use and herpes simplex virus acquisition |journal=Ann Intern Med. |volume=143 |issue=10 |pages=707–13 |year=2005 |month=November |pmid=16287791 |url=http://www.annals.org/cgi/reprint/143/10/707
}}</ref> 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.{{Citation needed|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.{{Citation needed|date=May 2008}}
 
However, asymptomatic carriers of the HSV-2 virus are still contagious. In many infections, the first symptom a person will have of their own infection is the horizontal transmission to a sexual partner or the vertical transmission of neonatal herpes to a newborn at term. Since most asymptomatic individuals are unaware of their infection, they are considered at high risk for spreading HSV.{{Citation needed|date=May 2010}}
 
=== Barrier methods ===
[[Condom]]s offer moderate protection against HSV-2 in both men and women, with consistent condom users having a 30% lower risk of HSV-2 acquisition compared with those who never use condoms<ref name=Martin>{{cite journal | author=Emily T. Martin, MPH; Elizabeth Krantz, MS; Sami L. Gottlieb, MD, MSPH; Amalia S. Magaret, PhD; Andria Langenberg, MD; Lawrence Stanberry, MD, PhD; Mary Kamb, MD, MPH; Anna Wald, MD, MPH | title=A Pooled Analysis of the Effect of Condoms in Preventing HSV-2 Acquisition | journal=Archives of Internal Medicine | year=2009 | pages=1233–1240 | volume=169 | issue=13 | pmid= 19597073| url=http://archinte.ama-assn.org/cgi/content/abstract/169/13/1233 | doi=10.1001/archinternmed.2009.177 | pmc=2860381}}</ref> The virus cannot pass through a latex condom, but a condom's effectiveness is limited because it does not prevent skin contact or bodily fluid contact with the scrotum, anus, buttocks, upper thighs or area immediately surrounding the penis, all of which are susceptible to infection with and transmission of the virus. Preventing contact with these areas during sex, in addition to wearing a condom, should theoretically provide enhanced protection against herpes. Wearing clothing or [[undergarments]] such as [[boxer shorts]] that cover these susceptible areas but still allow access to the genitals through a small opening (such as a fly) should help prevent transmission and infection.
 
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 being investigated.<ref name="pmid18156035"/>
 
=== Antivirals ===
Antivirals may reduce asymptomatic shedding; it is believed asymptomatic genital HSV-2 viral shedding occurs on 20% of days per year in patients not undergoing antiviral treatment, versus 10% of days while on antiviral therapy.<ref name="pmid16238897"/>
 
=== Pregnancy ===
The risk of transmission from mother to baby is highest if the mother becomes infected at around the time of delivery (30% to 60%),<ref>{{cit journal|author=Brown ZA, Selke S, Zeh J ''et al.''|title=The acquisition of herpes simplex virus during pregnancy|journal=N Engl J Med|volume=337|pages=509–515|year=1997}}</ref><ref>{{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|pages=203–209|year=2003|doi=10.1001/jama.289.2.203|pmid=12517231|issue=2}}</ref> but the risk falls to 3% if it is a recurrent infection, and is less than 1% if there are no visible lesions.<ref>{{cite journal|author=Brown ZA, Benedetti J, Ashley R ''et al.''|title=Neonatal herpes simplex virus infection in relation to asymptomatic maternal infection at the time of labor|journal=N Engl J Med|volume=324|page=1247|year=1991}}</ref> 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. A seronegative mother that contracts HSV at this time has up to a 57% chance of conveying the infection to her baby during childbirth, since insufficient time will have occurred for the generation and transfer of protective maternal antibodies before the birth of the child, 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= 10.1086/514600|url=http://www.journals.uchicago.edu/doi/pdf/10.1086/514600
}}</ref><ref name="pmid1849612">{{cite journal |author=Brown ZA, Benedetti J, Ashley R, ''et al.'' |title=Neonatal herpes simplex virus infection in relation to asymptomatic maternal infection at the time of labor |journal=N. Engl. J. Med. |volume=324 |issue=18 |pages=1247–52 |year=1991 |month=May |pmid=1849612 |doi= 10.1056/NEJM199105023241804|url=}}</ref> Women that are seropositive for only one type of HSV are only half as likely to transmit HSV as infected seronegative mothers. 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 acyclovir, given from the 36th week of pregnancy, limits HSV recurrence and shedding during childbirth, thereby reducing the need for caesarean section.<ref name="pmid18156035"/>
 
Acyclovir is the recommended antiviral for herpes suppressive therapy during the last months of pregnancy. The use of valaciclovir and famciclovir, while potentially improving compliance have less well determined safety in pregnancy.
 
== Treatment ==
There is no method to eradicate herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks. [[Analgesic]]s such as [[ibuprofen]] and [[acetaminophen]] can reduce pain and fever. Topical anesthetic treatments such as [[prilocaine]], [[lidocaine]], [[benzocaine]] 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 |month=December |pmid=3147021 |pmc=1835116 |doi= |url=}}</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 |month=December |pmid=10570387 |doi= 10.1016/S0190-9622(99)70260-4|url=}}</ref><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 |volume=4 |issue=10 |pages=1809–19 |year=2003 |month=October |pmid=14521490 |doi=10.1517/14656566.4.10.1809 |url=}}</ref>
 
=== Antiviral ===
 
[[దస్త్రం:Acyclovir pills.jpg|thumb|The antiviral medication acyclovir]]
 
There are several [[Antiviral drug|antivirals]] that are effective for treating herpes including: [[aciclovir]] (acyclovir), [[valaciclovir]] (valacyclovir), [[famciclovir]], and [[penciclovir]]. Aciclovir was the first discovered and is now available in [[generic medications|generic]].
 
Evidence supports the use of aciclovir and valaciclovir in the treatment of herpes labialis<ref name=Best07>{{cite journal |author=Chon T, Nguyen L, Elliott TC |title=Clinical inquiries. What are the best treatments for herpes labialis? |journal=J Fam Pract |volume=56 |issue=7 |pages=576–8 |year=2007 |month=July |pmid=17605952 |doi= |url=}}</ref> as well as herpes infections in people with [[cancer]].<ref>{{cite journal|author=Glenny AM, Fernandez Mauleffinch LM, Pavitt S, Walsh T |title=Interventions for the prevention and treatment of herpes simplex virus in patients being treated for cancer|journal=Cochrane Database Syst Rev |volume= |issue=1 |pages=CD006706 |year=2009 |pmid=19160295|doi=10.1002/14651858.CD006706.pub2 |url=}}</ref> The evidence to support the use of acyclovir in primary herpetic gingivostomatitis is less strong.<ref>{{cite journal |author=Nasser M, Fedorowicz Z, Khoshnevisan MH, Shahiri Tabarestani M |title=Acyclovir for treating primary herpetic gingivostomatitis |journal=Cochrane Database Syst Rev |volume= |issue=4 |pages=CD006700 |year=2008 |pmid=18843726 |doi=10.1002/14651858.CD006700.pub2 |url=}}</ref>
 
=== Topical ===
 
A number of [[topical]] antivirals are effective for herpes labialis including acyclovir, penciclovir, and [[docosanol]].<ref name=Best07/><ref>{{cite journal |author=Treister NS, Woo SB |title=Topical n-docosanol for management of recurrent herpes labialis |journal=Expert Opin Pharmacother |volume=11 |issue=5 |pages=853–60 |year=2010 |month=April |pmid=20210688 |doi=10.1517/14656561003691847 |url=}}</ref> Docosanol can be purchased [[over the counter]] in Canada and the USA.
 
=== Alternative medicine ===
Certain [[dietary supplement]]s and [[Complementary and alternative medicine|alternative remedies]] are claimed to be beneficial in the treatment of herpes. There is however insufficient evidence to support use of many of these compounds including [[echinacea]], [[eleuthero]], [[L-lysine]], [[zinc]], bee products and [[aloe vera]].<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 |month=October |pmid=16209859 |doi= |url=}}</ref>
 
A single study indicates possible benefit from [[laser]] treatment.<ref>{{cite journal |author=Hargate G |title=A randomised double-blind study comparing the effect of 1072-nm light against placebo for the treatment of herpes labialis |journal=Clin. Exp. Dermatol. |volume=31 |issue=5 |pages=638–41 |year=2006 |month=September |pmid=16780494 |doi=10.1111/j.1365-2230.2006.02191.x |url=}}</ref>
 
== Prognosis ==
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 |url=http://www.pnas.org/content/99/23/15234 |doi=10.1073/pnas.232546899 |pmc=137573}}</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 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. A recent study (2009) showed that a protein [[VP16]] plays a key role in reactivation of the dormant virus.<ref>{{cite web |url=http://www.sciencenews.org/view/generic/id/42223/title/How_herpes_re-rears_its_ugly_head_ |title=How Herpes Re-rears Its Ugly Head - Science News |format= |work= |accessdate=}}</ref><!--PMID: 19321615 and PMID: 19325890 possible sources, --> 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=10.1016/S0190-9622(87)70232-1}}</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=10.1016/S1079-2104(97)90342-5}}</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 vary greatly between patients. Some individuals' outbreaks can be quite debilitating with large, painful lesions persisting for several weeks, while others will experience only minor itching or burning for a few days. There is some evidence that genetics plays a role in the frequency of cold sore outbreaks. An area of human chromosome 21 that includes 6 genes has been linked to frequent oral herpes outbreaks. An immunity to the virus is built over time. Most infected individuals will experience fewer outbreaks and outbreak symptoms will often become less severe. After several years, some people will become perpetually [[asymptomatic]] and will no longer experience outbreaks, though they may still be contagious to others. Immuno-compromised 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}}</ref> Outbreaks may occur at the original site of the infection or in proximity to nerve endings that reach out from the infected ganglia. In the case of a genital infection, sores can appear at the original site of infection or near the base of the spine, the buttocks, or the back of the thighs.
HSV-2 infected individuals are at higher risk for acquiring [[HIV]] when practicing unprotected sex with HIV-positive persons,<ref>{{cite journal
|author=Sobngwi‐Tambekou J, Taljaard D, Lissouba P, ''et al.''
|title=Effect of HSV‐2 Serostatus on Acquisition of HIV by Young Men: Results of a Longitudinal Study in Orange Farm, South Africa
|journal=J Infect Dis
|volume=199
|pages=958–964
|doi=10.1086/597208
|year=2009
|pmid=19220143
|issue=7
|pmc=2868899}}</ref> 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>
 
== Epidemiology ==
Worldwide rates of HSV infection are between 65% and 90%.<ref name=Peds09>{{cite journal |author=Chayavichitsilp P, Buckwalter JV, Krakowski AC, Friedlander SF |title=Herpes simplex |journal=Pediatr Rev |volume=30 |issue=4 |pages=119–29; quiz 130 |year=2009 |month=April |pmid=19339385 |doi=10.1542/pir.30-4-119 |url=}}</ref> HSV1 is more common than HSV2 with rates of both increasing as people age.<ref name=Peds09/> Rates of infection are determined by the presence of [[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 |url=http://www.journals.uchicago.edu/doi/full/10.1086/343739 |doi=10.1086/343739}}</ref>
 
In the US 17.2% of the population is HSV-2 seropositive with only 14.5% of the seropositive population aware that they are infected.<ref name="JAMA. 2006;296:964-973. ">{{cite journal|last=Xu|first=Fujie|coauthors=Fujie Xu, MD, PhD; Maya R. Sternberg, PhD; Benny J. Kottiri, PhD; Geraldine M. McQuillan, PhD; Francis K. Lee, PhD; Andre J. Nahmias, MD; Stuart M. Berman, MD, ScM; Lauri E. Markowitz, MD |date=2006-10-23|title=Trends in Herpes Simplex Virus Type 1 and Type 2 Seroprevalence in the United States|journal=JAMA|publisher=AMA|volume=296|issue=8|url=http://jama.ama-assn.org/cgi/content/full/296/8/964|pmid=16926356|doi=10.1001/jama.296.8.964|pages=964–73}}</ref>
 
== History ==
Herpes has been known for at least 2,000 years. It is said that Emperor [[Tiberius]] banned kissing in Rome for a time due to so many people having cold sores. In the 16th century ''[[Romeo and Juliet]]'', it is mentioned that there are blisters "o'er ladies' lips." In 18th century it was so common among prostitutes that it was called "a vocational disease of women."<ref name=scarlet />
 
The term ''Herpes Simplex'' appeared in [[Richard Boulton]]'s A System of Rational and Practical Chirurgery in 1713, where the terms ''[[Herpes miliaris]]'' and ''[[Herpes exedens]]'' also appeared.
 
Herpes was not found to be a virus until the 1940s.<ref name=scarlet />
 
Herpes antiviral therapy began in the early 1960s with the experimental use of medication that interfered with viral replication called [[deoxyribonucleic acid]] (DNA) inhibitors. The original use was against normally fatal or disabilitating illness such as adult encephalitis,<ref name="pmid4790599">{{cite journal
|author=Chow AW, Roland A, Fiala M, ''et al.''
|title=Cytosine arabinoside therapy for herpes simplex encephalitis--clinical experience with six patients
|journal=Antimicrob. Agents Chemother.
|volume=3
|issue=3
|pages=412–7
|year=1973
|month=March
|pmid=4790599
|pmc=444424
|doi=
|url=http://aac.asm.org/cgi/pmidlookup?view=long&pmid=4790599
}}</ref> keratitis,<ref name="pmid14454441">{{cite journal
|author=Kaufman HE, Howard GM
|title=Therapy of experimental herpes simplex keratitis
|journal=Invest Ophthalmol
|volume=1
|issue=
|pages=561–4
|year=1962
|month=August
|pmid=14454441
|doi=
|url=http://www.iovs.org/cgi/pmidlookup?view=long&pmid=14454441
}}</ref> in immunocompromised (transplant) patients,<ref name="pmid180198">{{cite journal
|author=Ch'ien LT, Whitley RJ, Alford CA, Galasso GJ
|title=Adenine arabinoside for therapy of herpes zoster in immunosuppressed patients: preliminary results of a collaborative study
|journal=J. Infect. Dis.
|volume=133 Suppl
|issue=
|pages=A184–91
|year=1976
|month=June
|pmid=180198
|doi=
|url=
}}</ref> or disseminated herpes zoster.<ref name="pmid5352659">{{cite journal
|author=McKelvey EM, Kwaan HC
|title=Cytosine arabinoside therapy for disseminated herpes zoster in a patient with IgG pyroglobulinemia
|journal=Blood
|volume=34
|issue=5
|pages=706–11
|year=1969
|month=November
|pmid=5352659
|doi=
|url=http://www.bloodjournal.org/cgi/pmidlookup?view=long&pmid=5352659
}}</ref> The original compounds used were 5-iodo-2'-deoxyuridine, AKA idoxuridine, IUdR, or(IDU) and 1-β-D-arabinofuranosylcytosine or ara-C,<ref name="pmid4364937">{{cite journal
|author=Fiala M, Chow A, Guze LB
|title=Susceptibility of herpesviruses to cytosine arabinoside: standardization of susceptibility test procedure and relative resistance of herpes simplex type 2 strains
|journal=Antimicrob. Agents Chemother.
|volume=1
|issue=4
|pages=354–7
|year=1972
|month=April
|pmid=4364937
|pmc=444221
|doi=
|url=http://aac.asm.org/cgi/pmidlookup?view=long&pmid=4364937
}}</ref> later marketed under the name cytosar or cytorabine. The usage expanded to include topical treatment of herpes simplex,<ref name="pmid6598">{{cite journal
|author=Allen LB, Hintz OJ, Wolf SM, ''et al.''
|title=Effect of 9-beta-D-arabinofuranosylhypoxanthine 5'-monophosphate on genital lesions and encephalitis induced by Herpesvirus hominis type 2 in female mice
|journal=J. Infect. Dis.
|volume=133 Suppl
|issue=
|pages=A178–83
|year=1976
|month=June
|pmid=6598
|doi=
|url=
}}</ref> zoster, and varicella.<ref name="pmid4190397">{{cite journal
|author=Juel-Jensen BE
|title=Varicella and cytosine arabinoside
|journal=Lancet
|volume=1
|issue=7646
|page=572
|year=1970
|month=March
|pmid=4190397
|doi=10.1016/S0140-6736(70)90815-9
|url=
}}</ref> Some trials combined different antivirals with differing results.<ref name="pmid4790599"/> The introduction of 9-β-D-arabinofuranosyladenine, AKA ara-A or vidarabine, considerably less toxic than Ara-C, in the mid 1970s, heralded the way for the beginning of regular neonatal antiviral treatment. Vidarabine was the first systemically administered antiviral medication with activity against HSV for which therapeutic efficacy outweighed toxicity for the management of life-threatening HSV disease. Intravenous vidarabine was licensed for use by the [[U.S. Food and Drug Administration]] (FDA) in 1977. Other experimental antivirals of that period included: Heparin <ref name="pmid4289440">{{cite journal
|author=Nahmias AJ, Kibrick S
|title=Inhibitory effect of heparin on herpes simplex virus
|journal=J. Bacteriol.
|volume=87
|issue=5
|pages=1060–6
|year=1964
|month=May
|pmid=4289440
|pmc=277146
|doi=
|url=http://jb.asm.org/cgi/pmidlookup?view=long&pmid=4289440
}}</ref>,
trifluorothymidine (TFT)<ref name="pmid4790562">{{cite journal
|author=Allen LB, Sidwell RW
|title=Target-organ treatment of neurotropic virus diseases: efficacy as a chemotherapy tool and comparison of activity of adenine arabinoside, cytosine arabinoside, idoxuridine, and trifluorothymidine
|journal=Antimicrob. Agents Chemother.
|volume=2
|issue=3
|pages=229–33
|year=1972
|month=September
|pmid=4790562
|pmc=444296
|doi=
|url=http://aac.asm.org/cgi/pmidlookup?view=long&pmid=4790562
}}</ref>, Ribivarin,<ref name="pmid212976">{{cite journal
|author=Allen LB, Wolf SM, Hintz CJ, Huffman JH, Sidwell RW
|title=Effect of ribavirin on Type 2 Herpesvirus hominis (HVH/2) in vitro and in vivo
|journal=Ann. N. Y. Acad. Sci.
|volume=284
|issue=
|pages=247–53
|year=1977
|month=March
|pmid=212976
|doi=10.1111/j.1749-6632.1977.tb21957.x
|url=
}}</ref> interferon,<ref name="pmid4404669">{{cite journal
|author=Allen LB, Cochran KW
|title=Target-organ treatment of neurotropic virus disease with interferon inducers
|journal=Infect. Immun.
|volume=6
|issue=5
|pages=819–23
|year=1972
|month=November
|pmid=4404669
|pmc=422616
|doi=
|url=http://iai.asm.org/cgi/pmidlookup?view=long&pmid=4404669
}}</ref> Virazole,<ref name="pmid4340949">{{cite journal
|author=Sidwell RW, Huffman JH, Khare GP, Allen LB, Witkowski JT, Robins RK
|title=Broad-spectrum antiviral activity of Virazole: 1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide
|journal=Science (journal)
|volume=177
|issue=50
|pages=705–6
|year=1972
|month=August
|pmid=4340949
|doi=
|url=http://www.sciencemag.org/cgi/pmidlookup?view=long&pmid=4340949
}}</ref> and 5-methoxymethyl-2'-deoxyuridine (MMUdR).<ref name="pmid1239978">{{cite journal
|author=Babiuk LA, Meldrum B, Gupta VS, Rouse BT
|title=Comparison of the antiviral effects of 5-methoxymethyl-deoxyuridine with 5-iododeoxyuridine, cytosine arabinoside, and adenine arabinoside
|journal=Antimicrob. Agents Chemother.
|volume=8
|issue=6
|pages=643–50
|year=1975
|month=December
|pmid=1239978
|pmc=429441
|doi=
|url=http://aac.asm.org/cgi/pmidlookup?view=long&pmid=1239978
}}</ref> The introduction of 9-(2-hydroxyethoxymethyl)guanine, AKA acyclovir, in the late 1970s<ref name="pmid91931">{{cite journal
|author=O'Meara A, Deasy PF, Hillary IB, Bridgen WD
|title=Acyclovir for treatment of mucocutaneous herpes infection in a child with leukaemia
|journal=Lancet
|volume=2
|issue=8153
|page=1196
|year=1979
|month=December
|pmid=91931
|doi=10.1016/S0140-6736(79)92428-0
|url=
}}</ref> raised antiviral treatment another notch and led to vidarabine vs. acyclovir trials in the late 1980s.<ref name="pmid1988829">{{cite journal
|author=Whitley R, Arvin A, Prober C, ''et al.''
|title=A controlled trial comparing vidarabine with acyclovir in neonatal herpes simplex virus infection. Infectious Diseases Collaborative Antiviral Study Group
|journal=N. Engl. J. Med.
|volume=324
|issue=7
|pages=444–9
|year=1991
|month=February
|pmid=1988829
|doi=
10.1056/NEJM199102143240703|url=http://content.nejm.org/cgi/content/abstract/324/7/444
}}</ref> The lower toxicity and ease of administration over vidarabine has led to acyclovir becoming the drug of choice for herpes treatment after it was licensed by the FDA in 1998.<ref name="pmid11483782">{{cite journal
|author=Kimberlin DW, Lin CY, Jacobs RF, ''et al.''
|title=Safety and efficacy of high-dose intravenous acyclovir in the management of neonatal herpes simplex virus infections
|journal=Pediatrics
|volume=108
|issue=2
|pages=230–8
|year=2001
|month=August
|pmid=11483782
|doi=10.1542/peds.108.2.230
|url=http://pediatrics.aappublications.org/cgi/pmidlookup?view=long&pmid=11483782
}}</ref> Another advantage in the treatment of neonatal herpes included greater reductions in mortality and morbidity with increased dosages, something that did not occur when compared with increased dosages of vidarabine.<ref name="pmid11483782"/> On the other side of the equation, acyclovir seems to inhibit antibody response and newborns on acyclovir antiviral treatment experienced a slower rise in antibody titer than those on vidarabine.<ref name="pmid11483782"/>
 
== Society and culture ==
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 (mood)|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=125–34
| issue=June
| url=http://www.stacommunications.com/journals/cme/images/cmepdf/june01/hsv.pdf|format=PDF}}</ref> These feelings usually lessen over time. Much of the hysteria and stigma surrounding herpes stems from a media campaign beginning in the late 1970s and peaking in the early 1980s. There were multiple articles worded in fear-mongering and anxiety-provoking terminology, such as the now ubiquitous "attacks," "outbreaks," "victims," and "sufferers." At one point the term "herpetic" even entered the popular lexicon. The articles were published by ''Reader's Digest'', ''U.S. News'', and ''Time'' magazine, among others. A made-for-TV movie was named ''Intimate Agony.'' The peak was when ''Time'' magazine had 'Herpes: The New Scarlet Letter' on the cover in August 1982, forever stigmatizing the word in the public mind.<ref name=scarlet>{{cite news |title= The New Scarlet Letter |work= [[Time (magazine)|Time]] |author= John Leo |date= 1982-08-02 |url= http://www.time.com/time/magazine/article/0,9171,1715020,00.html}}</ref> The scientific reality is that most people are asymptomatic, the virus causes no real health problems for a vast majority of people, and a vast majority (around 90%) of the Earth's population carries HSV-1, 2, or both.<ref>Herpes FAQ {{cite web |url=http://www.herpesonline.org/faq.html |title=Herpes FAQ }}</ref><ref>{{cite web |url=http://www.webmd.com/genital-herpes/guide/genital-herpes-living-managing |title=WebMD Genital Herpes: Living and Managing }}</ref> [[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>Lists of support groups and events:
* {{cite web
|url=http://www.herpesaz.com/html/groups.html
|title=A to Z Herpes Support Groups }}
* {{cite web
|url=http://www.herpes-coldsores.com/support/herpes.htm
|title=Herpes Support Groups }}
* {{cite web
|url=http://www.NationalHClub.com
|title=NationalHClub.com Local and National Herpes Events }}
</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 whom 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
| url=http://sti.bmj.com/cgi/content/full/79/1/42
| doi=10.1136/sti.79.1.42
| pmc=1744583}}</ref>
 
== References ==
{{Reflist|colwidth=30em}}
 
== బయటి లింకులు ==
== External links ==
'''General'''
* [http://cdc.gov/std/Herpes/STDFact-Herpes.htm Genital Herpes Fact Sheet] at [[The Centers for Disease Control and Prevention]]
"https://te.wikipedia.org/wiki/సర్పి" నుండి వెలికితీశారు