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Herpes simplex (
Greek: ἕρπης
herpēs, "creeping" or "latent") is a
viral disease from the
herpesviridae family caused by both
Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2). 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 or
fever blisters, is an infection of the face or mouth. Oral herpes is the most common form of infection.
Genital herpes, known simply as
herpes, is the second most common form of herpes. Other disorders such as
herpetic whitlow,
herpes gladiatorum,
ocular herpes, cerebral herpes infection
encephalitis,
Mollaret's meningitis,
neonatal herpes, and possibly
Bell's palsy are all caused by herpes simplex viruses.
Herpes viruses cycle between periods of active diseasepresenting as blisters containing infectious
virus particlesthat last 221 days, followed by a
remission period. Genital herpes, however, is often
asymptomatic, though
viral shedding may still occur. After initial infection, the viruses are transported along
sensory nerves to the sensory nerve cell bodies, where they become
latent and reside lifelong. Causes of recurrence are uncertain, though some potential triggers have been identified, including immunosuppressant drugs. The previously latent virus then multiplies new virus particles in the nerve cell and these are transported along the
axon of each
neuron to the nerve terminals in the skin, where they are released. 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. Recurrent infections (outbreaks) may occur from time to time, especially in times of
immune impairment such as
HIV and
cancer-related immune suppression.[SUP]
[1][/SUP] However, after several years, outbreaks become less severe and more sporadic, and 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. 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.
[h=2]Classification[/h] Herpes simplex is divided into two types: HSV type 1 and HSV type 2. HSV1 causes primarily mouth, throat, face, eye, and
central nervous system infections, whereas HSV2 causes primarily anogenital infections. However, each may cause infections in all areas.[SUP]
[2][/SUP]
[h=2]Signs and symptoms[/h] HSV infection causes several distinct medical
disorders. Common infection of the skin or mucosa may affect the face and mouth (orofacial herpes), genitalia (genital herpes), or hands (
herpetic 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). People with immature or suppressed immune systems, such as newborns, transplant recipients, or people with AIDS are prone to severe complications from HSV infections. HSV infection has also been associated with cognitive deficits of
bipolar disorder,[SUP]
[3][/SUP] and
Alzheimer's disease, 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.[SUP]
[4][/SUP] 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
herpes of the eye. Prior HSV-1 seroconversion seems to reduce the symptoms of a later HSV-2 infection, although HSV-2 can still be contracted.
Many people infected with HSV-2 display no physical symptomsindividuals with no symptoms are described as asymptomatic or as having
subclinical herpes.[SUP]
[5][/SUP]
[TABLE="class: wikitable"]
[TR]
[TH]Condition[/TH]
[TH]Description[/TH]
[TH]Illustration[/TH]
[/TR]
[TR]
[TD]
Herpetic gingivostomatitis[/TD]
[TD]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.[/TD]
[TD]
[/TD]
[/TR]
[TR]
[TD]
Herpes labialis[/TD]
[TD]Infection occurs when the virus comes into contact with oral mucosa or abraded skin.[/TD]
[TD]
[/TD]
[/TR]
[TR]
[TD]
Herpes genitalis[/TD]
[TD]When symptomatic, the typical manifestation of a primary HSV-1 or HSV-2 genital infection is clusters of inflamed
papules and
vesicles on the outer surface of the genitals resembling cold sores.[/TD]
[TD]
[/TD]
[/TR]
[TR]
[TD]
Herpetic whitlow and
Herpes gladiatorum[/TD]
[TD]Herpes whitlow is a painful infection that typically affects the fingers or thumbs. On occasion, infection occurs on the toes or on the nail cuticle. Individuals that participate in
contact sports such as
wrestling,
rugby, and
soccer sometimes acquire a condition caused by HSV-1 known as
herpes gladiatorum,
scrumpox,
wrestlers 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.[/TD]
[/TR]
[/TABLE]
[h=2]Prevention[/h]
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.[SUP]
[28][/SUP] On an annual basis, without the use of antivirals or condoms, the transmission risk of HSV-2 from infected male to female is approximately 811%.[SUP]
[23][/SUP][SUP]
[29][/SUP] 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 45% annually.[SUP]
[29][/SUP] Suppressive antiviral therapy reduces these risks by 50%.[SUP]
[30][/SUP] Antivirals also help prevent the development of symptomatic HSV in infection scenariosmeaning the infected partner will be seropositive but symptom freeby about 50%. Condom use also reduces the transmission risk significantly.[SUP]
[31][/SUP][SUP]
[32][/SUP] Condom use is much more effective at preventing male to female transmission than vice-versa.[SUP]
[31][/SUP] The effects of combining antiviral and condom use is roughly additive, thus resulting in approximately a 75% combined reduction in annual transmission risk.[SUP][
citation needed][/SUP] 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.[SUP][
citation needed][/SUP] Previous HSV-1 infection appears to reduce the risk for acquisition of HSV-2 infection among women by a factor of 3.[SUP]
[33][/SUP]
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.[SUP][
citation needed][/SUP]
In October 2011, it was reported that the anti-HIV drug
tenofovir, when used topically in a microbicidal vaginal gel, reduced herpes virus sexual transmission by 51%.[SUP]
[34][/SUP]
[h=3]Barrier methods[/h]
Condoms offer moderate protection against HSV-2 in both men and women, with consistent condom users having a 30% lower risk of HSV-2 acquisition compared with those that never use condoms.[SUP]
[35][/SUP] A
female condom can provide greater protection than the male condom, as it covers the labia.[SUP]
[36][/SUP] The virus cannot pass through a synthetic condom, but a male condom's effectiveness is limited[SUP]
[37][/SUP] because herpes ulcers may appear on areas not covered by the male condom. Neither type of condom prevents contact with the scrotum, anus, buttocks, or upper thighs, areas that may come in contact with ulcers or genital secretions during sexual activity. Protection against herpes simplex depends on the site of the ulcer; therefore if ulcers appear on areas not covered by condoms, abstaining from sexual activity until the ulcers are fully healed is one way to limit risk of transmission.[SUP]
[38][/SUP] The risk is not eliminated, however, as viral shedding capable of transmitting infection may still occur while the infected partner is asymptomatic.[SUP]
[39][/SUP] 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.[SUP]
[4][/SUP] Topical
microbicides that contain chemicals that directly inactivate the virus and block viral entry are being investigated.[SUP]
[4][/SUP]
[h=3]Antivirals[/h] 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.[SUP]
[19][/SUP]
[h=3]Pregnancy[/h] The risk of transmission from mother to baby is highest if the mother becomes infected at around the time of delivery (30% to 60%),[SUP]
[40][/SUP][SUP]
[41][/SUP] since insufficient time will have occurred for the generation and transfer of protective maternal antibodies before the birth of the child. In contrast, the risk falls to 3% if it is a recurrent infection,[SUP]
[42][/SUP] and is 13% is the woman seropositive for both HSV-1 and HSV-2,[SUP]
[42][/SUP][SUP]
[43][/SUP] and is less than 1% if there are no visible lesions.[SUP]
[42][/SUP] Women seropositive for only one type of HSV are only half as likely to transmit HSV as infected seronegative mothers. To prevent neonatal infections, seronegative women are recommended to avoid unprotected oral-genital contact with an HSV-1 seropositive partner and conventional sex with a partner having a genital infection during the last trimester of pregnancy. Mothers infected with HSV are advised to avoid procedures that would cause trauma to the infant during birth (e.g. fetal scalp electrodes, forceps, and vacuum extractors) and, should lesions be present, to elect
caesarean section to reduce exposure of the child to infected secretions in the birth canal.[SUP]
[4][/SUP] 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.[SUP]
[4][/SUP]
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.
[h=2]Treatment[/h] There is no method to eradicate herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks.
Analgesics 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.[SUP]
[44][/SUP][SUP]
[45][/SUP][SUP]
[46][/SUP]
[h=3]Antiviral[/h]
The antiviral medication acyclovir
There are several
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.[SUP]
[47][/SUP] Valacyclovir is also available as a generic.[SUP]
[48][/SUP]
Evidence supports the use of aciclovir and valaciclovir in the treatment of herpes labialis[SUP]
[49][/SUP] as well as herpes infections in people with
cancer.[SUP]
[50][/SUP] The evidence to support the use of acyclovir in primary herpetic gingivostomatitis is less strong.[SUP]
[51][/SUP]
[h=3]Topical[/h] A number of
topical antivirals are effective for herpes labialis including acyclovir, penciclovir, and
docosanol.[SUP]
[49][/SUP][SUP]
[52][/SUP]
[h=3]Alternative medicine[/h] Certain
dietary supplements and
alternative remedies are claimed to be beneficial in the treatment of herpes.[SUP]
[53][/SUP] There is however insufficient evidence to support use of many of these compounds including
echinacea,
eleuthero,
L-lysine,
zinc,
monolaurin bee products and
aloe vera.[SUP]
[54][/SUP] While there are a number of small studies showing possible benefit from monolaurin, L-lysine, aspirin, lemon balm, topical zinc or licorice root cream in treatment, these are preliminary studies that have not been confirmed by higher quality
randomized controlled studies.[SUP]
[55][/SUP]
[h=2]Prognosis[/h] 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
nucleus of a nerve's
cell body. HSV latency is staticno virus is producedand is controlled by a number of viral genes, including
Latency Associated Transcript (LAT).[SUP]
[56][/SUP]
Many HSV-infected people experience recurrence within the first year of infection.[SUP]
[4][/SUP]
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 510 days without antiviral treatment) than those occurring during the primary infection.[SUP]
[4][/SUP] 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 the protein
VP16 plays a key role in reactivation of the dormant virus.[SUP]
[57][/SUP] Changes in the immune system during
menstruation may play a role in HSV-1 reactivation.[SUP]
[58][/SUP][SUP]
[59][/SUP] 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.[SUP]
[60][/SUP][SUP]
[61][/SUP][SUP]
[62][/SUP][SUP]
[63][/SUP][SUP]
[64][/SUP]
The frequency and severity of recurrent outbreaks vary greatly between people. Some individuals' outbreaks can be quite debilitating with large, painful lesions persisting for several weeks, while others 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.[SUP]
[65][/SUP] Outbreaks may occur at the original site of the infection or in proximity to nerve endings that reach out from the infected ganglia. In the case of a genital infection, sores can appear at the original site of infection or near the base of the spine, the buttocks, or the back of the thighs. HSV-2 infected individuals are at higher risk for acquiring
HIV when practicing unprotected sex with HIV-positive persons, in particular during an outbreak with active lesions.[SUP]
[66][/SUP]