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Herpes
Herpes
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Herpes simplex is a viral disease caused by Herpes simplex viruses; both herpes simplex virus 1 (HSV-1) and herpes simplex virus 2 (HSV-2) cause herpes simplex. Infection with the herpes virus is categorized into one of several distinct disorders based on the site of infection. Oral herpes, the visible symptoms of which are colloquially called cold sores, infects the face and mouth. Oral herpes is the most common form of infection. Infection of the genitals, commonly known as herpes, is the second most common form of herpes. Other disorders such as herpetic whitlow, herpes gladiatorum, ocular herpes (keratitis), cerebral herpes infection encephalitis, Mollaret's meningitis, neonatal herpes, and possibly Bell's palsy are all caused by herpes simplex viruses.

Herpes viruses cycle between periods of active disease—presenting as blisters containing infectious virus particles—that last 2–21 days, followed by a 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 nerves, where they reside as life-long, latent viruses. Causes of recurrence are uncertain, though some potential triggers have been identified. Over time episodes of active disease reduce in frequency.

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

There is currently no cure for herpes; no vaccine is currently available to prevent or eliminate herpes, although vaccines of varying effectiveness are currently in phase III trials. Also, treatments are available to reduce viral reproduction and shedding, prevent the virus from entering the skin, and alleviate the severity of symptomatic episodes.

Disorders

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 (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,^[1] and Alzheimer's disease,^[2] 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.^[3] As a result of primary infection, the body produces antibodies to the particular type of HSV involved, preventing a subsequent infection of that type at a different site. In HSV-1 infected individuals, seroconversion after an oral infection will prevent additional HSV-1 infections such as whitlow, genital herpes, and keratitis. Prior HSV-1 seroconversion seems to ameliorate the symptoms of a later HSV-2 infection, however HSV-2 can still be contracted. Most indications are that an HSV-2 infection contracted prior to HSV-1 seroconversion will immunize that person against HSV-1 infection. ^[4] This is not necessarily good, as prior HSV-1 infection has the tendency to ameliorate the effects of symptomatic HSV-2 reoccurrences.

Condition	Description	Illustration
Herpes labialis	Infection occurs when the virus comes into contact with oral mucosa or abraded skin.
Herpes genitalis	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.
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.
Herpes gladiatorum	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 provides an area of entry for HSV-1. Symptoms present within 2 weeks of direct skin-to-skin contact with an infected person. They include skin ulceration on the face, ears, and neck, fever, headache, sore throat and swollen glands. It occasionally affects the eyes or eyelids.
Herpetic keratitis	Primary infection typically presents as swelling of the conjunctiva and eye-lids (blepharoconjunctivitis), accompanied by small white itchy lesions on the surface of the cornea.	File:Herpes2.JPG
Herpesviral encephalitis	HSE is thought to be caused by the retrograde transmission of virus from a peripheral site on the face following HSV-1 reactivation, along a nerve axon, to the brain.
Herpesviral meningitis	HSV-2 is the most common cause of Mollaret's meningitis, a type of recurrent viral meningitis.
Neonatal herpes simplex	Neonatal HSV infection is a rare but serious condition, usually caused by vertical transmission of HSV from mother to newborn.	File:SOA-Herpes-neonatorum.jpg
Bell's palsy	In a mouse model a type of facial paralysis called Bell's palsy has been linked to the presence and reactivation of latent HSV-1 inside the sensory nerves of the face (geniculate ganglia).^[5]^[6] This is supported by findings that show the presence of HSV-1 DNA in saliva at a higher frequency in patients with Bell's palsy relative to those without the condition.^[7] However, since HSV can also be detected in these ganglia in large numbers of individuals that have never experienced facial paralysis, and high titers of antibodies for HSV are not found in HSV-infected individuals with Bell's palsy relative to those without, this theory has been contested.^[8] In other studies HSV-1 DNA was not detected in the cerebrospinal fluid of Bell's palsy sufferers, raising questions whether HSV-1 is the causative agent in this type of facial paralysis.^[9]^[10] The potential effect of HSV-1 in the etiology of Bell's palsy has prompted the use of antiviral medication to treat the condition. The benefits of acyclovir and valacyclovir have been studied.^[11] But the effect appears small, if at all detectable.
Herpes simplex in the immunocompromised host	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.^[12]
Alzheimer’s disease	Scientists discovered a link between HSV-1 and Alzheimer’s disease in 1979.^[13] In the presence of a certain gene variation (APOE-epsilon4 allele carriers), HSV-1 appears to be particularly damaging to the nervous system and increases one’s risk of developing Alzheimer’s disease. The virus interacts with the components and receptors of lipoproteins, which may lead to the development of Alzheimer's disease.^[14] This research identifies HSVs as the pathogen most clearly linked to the establishment of Alzheimer’s.^[15] Without the presence of the gene allele, HSV type 1 does not appear to cause any neurological damage and thus increase the risk of Alzheimer’s.^[16] A study published in The Journal of Pathology,^[17] has shown a striking localization of herpes simplex virus type 1 DNA within the beta-amyloid plaques that characterize Alzheimer's disease, and suggests that this virus is a major cause of the plaques and hence probably a significant aetiological factor in Alzheimer's disease.

Recurrence

Following active infection herpes viruses establish a latent infection in sensory and autonomic ganglia of the nervous system. The double-stranded DNA of the virus is incorporated into the cell physiology by infection of the nucleus of a nerve's cell body. HSV latency is static—no virus is produced—and is controlled by a number of viral genes, including Latency Associated Transcript (LAT).^[18]

Many HSV infected people experience recurrence within the first year of infection.^[3] Prodrome precedes development of lesions. Prodromal symptoms include tingling (paresthesia), itching, and pain where lumbosacral nerves innervate the skin. Prodrome may occur as long as several days or as short as a few hours before lesions develop. Beginning antiviral treatment when prodrome is experienced can reduce the appearance and duration of lesions in some individuals. During recurrence fewer lesions are likely to develop, lesions are less painful, and lesions heal faster (within 5–10 days without antiviral treatment), than those occurring during the primary infection.^[3] Subsequent outbreaks tend to be periodic or episodic, occurring on average four to five times a year when not using antiviral therapy.

The causes of reactivation are uncertain, but several potential triggers have been documented. Physical or psychological stress can trigger an outbreak of herpes.^[19] Changes in the immune system during menstruation may play a role in HSV-1 reactivation.^[20]^[21] 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.^[22]^[23]^[24]^[25]^[26]

The frequency and severity of recurrent outbreaks may vary greatly between patients. An immunity to the virus is built over time; immunocompromised individuals may experience episodes that are longer, more frequent and more severe. Antiviral medication has been proven to shorten the frequency and duration of outbreaks.^[27] Outbreaks may occur at the original site of the infection or in close proximity to nerve endings that reach out from the infected ganglia. In the case of a genital infection, sores can appear at the original site of infection or near the base of the spine, the buttocks, back of the thighs.

Transmission and prevention

Herpes is contracted through direct contact with an active lesion or body fluid of an infected person.^[28] Herpes transmission occurs between discordant partners; a person with a history of infection (HSV seropositive) can pass the virus to an HSV seronegative person.^[3] While herpes virus type 2 has been demonstrated to remain viable on toilet seats for 2 to 4 hours after contact and on dry gauze for up to 72 hours, as of the submission of those findings (1984) there were no documented cases of infection via an inanimate object (e.g. a towel, toilet seat, drinking vessels).^[29] 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 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.^[30] 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.^[30] Asymptomatic shedding is more frequent within the first 12 months of acquiring HSV. Concurrent infection with HIV increases the frequency and duration of asymptomatic shedding.^[31] There are indications that some individuals may have much lower patterns of shedding, but evidence supporting this is not fully verified; no significant differences are seen in the frequency of asymptomatic shedding when comparing persons with 1 to 12 annual recurrences to those that have no recurrences.^[30]

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 monogamous couple, a seronegative female runs a greater than 30% per year risk of contracting an HSV infection from a seropositive male partner.^[32] 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.

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

For genital herpes, condoms are highly effective in limiting transmission of herpes simplex infection.^[33]^[34] The virus cannot pass through latex, but a condom's effectiveness is somewhat limited on a public health scale by their limited use in the community,^[35] and on an individual scale because the condom may not completely cover blisters on the penis of an infected male, or the base of the penis or testicles not covered by the condom may come into contact with free virus in vaginal fluid of an infected female. In such cases, abstinence from sexual activity or washing of the genitals after sex is recommended. The use of condoms or dental dams also limits the transmission of herpes from the genitals of one partner to the mouth of the other (or vice versa) during oral sex. When one partner has a herpes simplex infection and the other does not, the use of antiviral medication, such as valaciclovir, in conjunction with a condom, further decreases the chances of transmission to the uninfected partner.^[3] Topical microbicides which contain chemicals that directly inactivate the virus and block viral entry are currently being investigated.^[3] Vaccines for HSV are currently undergoing trials. Once developed, they may be used to help with prevention or minimize initial infections as well as treatment for existing infections.^[36]

As with almost all sexually transmitted infections, women are more susceptible to acquiring genital HSV-2 than men.^[37] 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%.^[38]^[32] 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.^[38] Suppressive antiviral therapy reduces these risks by 50%.^[39] 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%.^[33]^[34]^[40] Condom use is much more effective at preventing male to female transmission than vice-versa.^[33] 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]} 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]}

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.^[41]^[42] 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.^[3] The use of antiviral treatments, such as aciclovir, given from the 36th week of pregnancy limits HSV recurrence and shedding during childbirth, thereby reducing the need for caesarean section.^[3]

HSV-2 infected individuals are at higher risk for acquiring HIV when practicing unprotected sex with HIV positive persons, particularly during an outbreak with active lesions.^[43]

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.^[44] 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 allergic stomatitis. When lesions do not appear inside the mouth primary orofacial herpes is sometimes mistaken for impetigo, a bacterial infection. Common mouth ulcers (aphthous ulcer) also resemble intraoral herpes, but do not present a vesicular stage.^[44]

Genital herpes can be more difficult to diagnose than oral herpes since most HSV-2-infected persons have no classical symptoms.^[44] Further confusing diagnosis, several other conditions resemble genital herpes, including lichen planus, atopic dermatitis, and urethritis.^[44] 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.^[44]

Serological tests for antibodies to HSV are rarely useful to diagnosis and not routinely used in clinical practice^[44], but are important in epidemiological studies. Serologic assays cannot differentiate between antibodies generated in response to a genital versus an oral HSV infection, and as such cannot confirm the site of infection. Absence of antibody to HSV-2 does not exclude genital infection because of the increasing incidence of genital infections caused by HSV-1.

Epidemiology

Although many people infected with HSV develop labial or genital lesions, the majority are either undiagnosed or display no physical symptoms—individuals with no symptoms are described as asymptomatic or as having subclinical herpes.^[45] 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. Many studies have been performed around the world to estimate the numbers of individuals infected with HSV-1 and HSV-2 by determining if they have developed antibodies against either viral species.^[46] This information provides population prevalence of HSV viral infections in individuals with or without active disease.

Seroprevalence estimates for HSV-1 and HSV-2^[46]
Location	Year(s)	Prevalence (%)
		HSV-1	HSV-2
		Total	Female	Male
Africa
Benin	1997-8	-	30	12
Cameroon	1997-8	-	46-51	24-27
Central African Republic	1998-9	99	82	-
Eritrea	1995	84-97	23	24-27
The Gambia	1998-9	-	29-32	5
Kenya	1997-8	-	68	35
Mali^[47]	1991-7	93	43	-
Morocco^[47]	1991-7	99	26	-
South Africa	1999	-	53	17
Tanzania	1992	-	42	19
Uganda	1989-93	91	71	36
Zambia	1997-8	-	55	36
Zimbabwe	1993-8	-	67	36-53
Asia
Bangladesh	1996-8	46^#	8-14	-
China	1987-95	-	18-29	17
Israel	1998-9	70	5	4
Japan	1985-93	50-60	1-17	2
Jordan	<2000	-	41	53
South Korea^[48]	2004	-	28	22
Philippines	1991-3	-	9	-
Syria	1995-8	80-100	0	0-1
Thailand^[47]^[46]	1991-7	51	35	15
Turkey	1991-2	97	42	-
Australasia
Australia	<1992-8	79-80	11-15	-
New Zealand	1993-8	-	4-15	3-7
Central/South America
Brazil	1990-7	-	23-42	-
Colombia^[47]	1985-97	89	57	-
Costa Rica	1984-5	-	39	-
Haiti	<1992	-	54	-
Mexico	1992-7	-	30	-
Peru^[47]	1991-7	92	36	-
Europe
Bulgaria^[49]	1999	84	15->40	15-30
Denmark	1986	76	31	-
Finland	1966-89	-	26-31	-
Germany	1996-7	87	15	11
Greenland	1986	98	68	-
Italy	1981-8	81-93	1-5	0-5
Norway	1992-4	79	27	-
Spain	1992-3	79	4	4
Sweden	1989-93	41^#	21-33	-
Switzerland	1997	65-87	22	11
UK	1984-95	69-78	5	3
North America
Canada	1999	57	13	-
USA	1988-94	68	26	18
^# in children

Europe

Large differences in HSV-1 seroprevalence are seen in different European countries. HSV-1 seroprevalence is high in Bulgaria (83.9%) and The Czech Republic (80.6%), and lower in Belgium (67.4%), The Netherlands (56.7%), and Finland (52.4%).^[49] The typical age at which HSV-1 infection is acquired ranges from 5 to 9 years in Central and Eastern European countries like Bulgaria and the Czech Republic, to over 25 years of age in Northern European countries such as Finland, The Netherlands, Germany, and England and Wales. Young adults in Northern European countries are less likely to be infected with HSV-1. European women are more likely to be HSV-1 seropositive than men.^[49]

HSV-2 seropositivity is widely distributed in Europeans older than 12, although there are large differences in the percentage of the population exposed to HSV-2. Bulgaria has a high (23.9%) HSV-2 seroprevalence relative to other European countries: Germany (13.9%), Finland (13.4%), Belgium (11.1%), The Netherlands (8.8%), the Czech Republic (6.0%), and England and Wales (4.2%).^[49] Women are more likely to be seropositive than men, and likely acquire the virus at an earlier age. In each country of Europe, HSV-2 seropositivity becomes more common from adolescence onwards and increases in the population with age, with a decline in the older age groups in some countries.^[49]

North America

United States

African Americans and immigrants from developing countries typically have an HSV-1 seroprevalance in their adolescent population that is two or three times higher than that of Caucasian Americans.^[44] Many white Americans become sexually active while seronegative for HSV-1. The absence of antibodies from a prior oral HSV-1 infection leaves these individuals susceptible to herpes whitlow, herpes gladiatorium, and HSV-1 genital infection. Primary genital infection brings with it the risk of vertical transmission to the neonate, and is highest if the mother contracts a primary infection during the third trimester of pregnancy. In the U.S. the number of genital infections caused by HSV-1 is now thought to be about 50% of first episodes of genital infection.^[50]^[51] In healthy adults, HSV-2 infection occurs more frequently in the USA than in Europe, and infection rates appear to be increasing. In individuals over 12 years old, HSV-2 seroprevalence has increased from 16.4% in 1976 to 21.8% in 1994 and is still rising.^[52] The current incidence of genital herpes caused by HSV-2 in the U.S. is roughly one in four or five adults, with approximately 50 million people infected with genital herpes and an estimated 0.5 million new genital herpes infections occurring each year.^[44] African Americans appear more susceptible to HSV-2, although the presence of active genital symptoms is more likely in Caucasian Americans. The largest increase in HSV-2 acquisition during the past few years is in white adolescents. People with many lifetime sexual partners and those who are sexually active from a young age are also at higher-risk for the transmission of HSV-2 in the U.S.^[53]^[54]^[55]^[56] Women are at higher risk than men for acquiring HSV-2 infection, and the chance of being infected increases with age.^[44]

Canada

According to a study in Ontario, up to 55% of Canadians age of 15 to 16, and 89% of individuals in their early forties have antibodies to HSV-1.^[57] Teenagers are less likely to be seropositive for HSV-2—antibodies against this virus are only found in 0–3.8% of 15-16 year olds. However, 21% of individuals in their early forties have antibodies against HSV-2, reflecting the sexually transmitted nature of this virus. When standardising for age, HSV-2 seroprevalence in Ontario for individuals between the ages of 15 to 44 was 9.1%. This is much lower than estimated levels of HSV-2 seroprevalence in people of a similar age range in the United States.^[57] HSV-2 seroprevalence in pregnant women between the ages of 15-44 in British Columbia is similar, with 57% having antibodies for HSV-1 and 13% having antibodies for HSV-2.^[46] In British Columbia in 1999, the seroprevalence of HSV-2 antibody in leftover serum submitted for antenatal testing revealed a prevalence of 17.3%, ranging from 7.1% in women 15-19 years old to 28.2% in those 40-44 years.^[58] • In attendees at an Alberta sexually transmitted infection (STI) clinic in 1994 and 1995, the seroprevalence of HSV-1 and -2 in leftover sera was 56% and 19%, respectively.^[59] In Nova Scotia, 58.1% of 1,790 HSV isolates from genital lesion cultures in women were HSV-1; in men, 36.7% of 468 isolates were HSV-1^[60]

Africa

Sub-Saharan Africa

HSV-2 is more common in Sub-Saharan Africa than in Europe or the North America. Up to 82% of women and 53% of men in Sub-Saharan Africa are seropositive for HSV-2. These are the highest levels of HSV-2 infection in the world, although exact levels vary from country to country in this continent.^[61] In most African countries, HSV-2 prevalence increases with age. However, age-associated decreases in HSV-2 seroprevalence has been observed for women in Uganda and Zambia, and in men in Ethiopia, Benin, and Uganda.^[46]

Northern Africa

Genital herpes appears less common in Northern Africa compared to Sub-Saharan Africa. For example, only 26% of middle-aged women have antibodies for HSV-2 in Morocco.^[47] Women are more likely to be infected with HSV-2 once they are over the age of 40.^[47] Children in Egypt are often infected with HSV from a young age—HSV-1 or HSV-2 antibodies are present in an estimated 54% of children under the age of 5, and 77% in children over 10 years of age.^[62] Algerian children are also likely to acquire HSV-1 infection at a young age (under 6) and 81.25% of the population has antibodies to HSV-1 by the age of 15.^[63]

Central and South America

Relative to rates in Europe and North America, HSV-2 seroprevalency is high in Central and South America. Infection levels are estimated at 20% to 60%.^[46]^[61] During the mid 1980s, HSV-2 prevalence was 33% in 25–29 year old women and 45% in those aged 40 and over in Costa Rica. In the early 1990s HSV-2 prevalence was approximately 45% among women over 60 in Mexico.^[46] The highest HSV-2 prevalence in Central or South America—60%—has been found in Colombian middle-aged women, although similar HSV-2 prevalence has been observed in younger women in Haiti (54%).^[46] HSV-2 infects about 30% of women over 30 years old in Colombia, Costa Rica, Mexico, and Panama. HSV-2 antibodies were found in more than 41% of women of childbearing age in Brazil.^[46] However, no increase in seroprevalence was associated with age in women over 40 years old in Brazil—HSV-2 prevalence was estimated at 50% among women aged 40–49, 33% among women 50–59, and 42% among women over 60. Women in Brazil are more likely to acquire an HSV-2 infection if their male partners had history of anal sex and had many sexual partners in his lifetime.^[47] In Peru, HSV-2 prevalence is also high among women in their 30s but is lower in men.^[46]

Asia

Eastern and South East Asia

HSV-1 seroprevalence in some Asian countries is low, relative to other countries worldwide, with only 51% women in Thailand, and between 50-60% in Japan possessing antibodies.^[47]^[46] HSV-2 seroprevalence in developing Asian countries is comparable (10-30%) to that observed in North America and Northern Europe.^[61] However, estimates of HSV-2 infectivity in Thailand are higher than observed in other Eastern Asian countries; total HSV-2 seroprevalence is approximately 37% in this country.^[47] HSV-2 seroprevalence is low in women in the Philippines (9%), although commencing activity while young is associated with an increase risk of acquiring HSV-2 infection; woman starting sexual activity by the time they reach 17 are seven times more likely to be HSV-2 seropositive than those starting sexual activity when over 21.^[64] In South Korea, incidence of HSV-2 infection in those under the age of 20 is low, only 2.7% in men and 3.0% in women.^[48] Seroprevalence levels increase in older South Koreans however, such that the population over 20 that has antibodies against HSV-2 is 21.7% of men and 28% of women.^[48]

Southern Asia

In India 33.3% of individuals are seropositive for HSV-1 and 16.6% are seropositive for HSV-2. Those with both HSV-1 and HSV-2 antibodies are estimated at 13.3% of the population. Indian men are more likely to be infected with HSV-2 than women, and increasing seroprevalence of this virus is associated with an increasing age.^[65]

Middle East

Turkey- High levels of HSV-1 (97%) and HSV-2 (42%) were found amongst pregnant women in the city of Erzurum in Eastern Anatolia Region, Turkey.^[46] In Istanbul however, lower HSV-2 seroprevalence was observed; HSV-2 antibodies were found in 4.8% of sexually active adults, while HSV-1 antibodies were found in 85.3%.^[66] Only 5% of pregnant women were infected with HSV-2, and 98% were infected with HSV-1. Prevalence of these viruses was higher in sex workers of Istanbul, reaching levels of 99% and 60% for HSV-1 and HSV-2 prevalence respectively.^[66]

Jordan- The prevalence of HSV-2 in Jordan is 52.8% for men and 41.5% for women.^[67]

Israel- HSV-1 seroprevalence is 59.8% in the population of Israel and increases with age in both genders but the adolescent seroprevalence has been declining as in most industrialized nations. ^[68]An estimated 9.2% of Israeli adults are infected with HSV-2. Infection of either HSV-1 or HSV-2 is higher in females; HSV-2 seroprevalence reaches 20.5% in females in their 40s. These values are similar to levels in HSV infection in Europe.^[69] Antibodies for HSV-1 or HSV-2 are also more likely to be found individuals born outside of Israel, and individuals residing in Jerusalem and Southern Israel; people of Jewish origin living in Israel are less likely to possess antibodies against herpes.^[69] Among pregnant women in Israel a small scale cross sectional study found the prevalence of HSV-2 infection was 13.3% and that of HSV-1 was 94.9%. The HSV-2 infection rate was 3-fold higher among immigrants from the former Soviet Union (27.5%) than among Israeli-born Jewish and Arab women (9%). ^[70] Approximately 78% of HSV-2 infections in Israel are asymptomatic.^[71]HSV-1 causes 66.3% of genital herpes in the Tel Aviv area.^[72]

Syria- Genital herpes infection from HSV-2 is predicted to be low in Syria although HSV-1 levels are high. HSV-1 infections is common (95%) among healthy Syrians over the age of 30, while HSV-2 prevalence is low in healthy individuals (0.15%), and persons infected with other sexually transmitted diseases (9.5%). High risk groups for acquiring HSV-2 in Syria, include prostitutes and bar girls; they have 34% and 20% seroprevalence respectively.^[73]

Oceania

In Australia the seroprevalence of HSV-1 is 76%, with differences associated with age, gender and Indigenous status.^[74] An estimated 12% of Australian adults are seropositive for HSV-2, with higher prevalence in women (16%) than in men (8%).^[74] Larger cities have higher HSV-2 seroprevalence (13%) than rural populations (9%). Higher prevalence is found in Indigenous Australians (18%) than non-Indigenous Australians (12%) but is lower than HSV-2 prevalence observed in the United States.^[74] As in the U.S., HSV-1 is increasingly identified as the cause of genital herpes in Australians; HSV-1 was identified in the anogenital area of only 3% of the population in 1980, but had risen to 41% in 2001.^[75] This was most common in females and persons under 25.^[75] The number of genital herpes infections appears to be rising in New Zealand with three times more cases in 1993 compared to 1977.^[76] In this country, HSV-2 affects 60% more women than men of similar age.^[46]

Treatment

There is currently no cure that can eradicate herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks. Antiviral drugs also reduce asymptomatic shedding; it is believed asymptomatic HSV-2 viral shedding occurs on 10.8% of days per year in patients not undergoing antiviral treatment, versus 2.9% of days while on antiviral therapy.^[30] Non-prescription analgesics can reduce pain and fever during initial outbreaks. Topical anesthetic treatments such as prilocaine, lidocaine or tetracaine can also relieve itching and pain.^[77]^[78]

History

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,^[79] keratitis,^[80] in immunocompromised (transplant) patients,^[81] or disseminated herpes zoster.^[82] The original compounds used were 5-iodo-2'-deoxyuridine, AKA idoxuridine, IUdR, or(IDU) and 1-β-D-arabinofuranosylcytosine or ara-C,^[83] later marketed under the name cytosar or cytorabine. The usage expanded to include topical treatment of herpes simplex,^[84] zoster, and varicella.^[85] Some trials combined different antivirals with differing results.^[79] 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 ^[86], trifluorothymidine (TFT)^[87], Ribivarin,^[88] interferon,^[89] Virazole,^[90] and 5-methoxymethyl-2'-deoxyuridine (MMUdR).^[91] The introduction of 9-(2-hydroxyethoxymethyl)guanine, AKA acyclovir, in the late 1970s^[92] raised antiviral treatment another notch and led to vidarabine vs. acyclovir trials in the late 1980s.^[93] 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.^[94] 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.^[94] 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.^[94]

Antiviral medication

Antiviral medications used against herpes viruses work by interfering with viral replication, effectively slowing the replication rate of the virus and providing a greater opportunity for the immune response to intervene. All drugs in this class depend on the activity of the viral enzyme thymidine kinase to convert the drug sequentially from its prodrug form to monophosphate (with one phosphate group), diphosphate (with two phosphate groups), and finally to the triphosphate (with three phosphate groups) form which interferes with viral DNA replication.^[95]

There are several prescription antiviral medications for controlling herpes simplex outbreaks, including aciclovir (Zovirax), valaciclovir (Valtrex), famciclovir (Famvir), and penciclovir. Aciclovir was the original, and prototypical, member of this drug class; it is now available in generic brands at a greatly reduced cost. Valaciclovir and famciclovir—prodrugs of aciclovir and penciclovir, respectively—have improved solubility in water and better bioavailability when taken orally.^[95] Aciclovir is the recommended antiviral for suppressive therapy for use during the last months of pregnancy to prevent transmission of herpes simplex to the neonate in cases of maternal recurrent herpes.^[96] The use of valaciclovir and famciclovir, while potentially improving treatment compliance and efficacy, are still undergoing safety evaluation in this context.

Several studies in humans and mice provide evidence that early treatment with famciclovir soon after the first infection with herpes can significantly lower the chance of future outbreaks of herpes. Early use of famciclovir has been shown to reduce the amount of latent virus in the neural ganglia.^[97]^[98]^[99] A review of human subjects treated for five days with famciclovir 250 mg three times daily during their first herpes episode found that only 4.2 percent experienced a recurrence within six months after the first outbreak, a fivefold decrease compared to the 19 percent recurrence in acyclovir-treated patients.^[100] Despite these promising results, early famciclovir treatment for herpes in this or similar dosage regimes has yet to find mainstream adoption. As a result, some doctors and patients have opted for off-label use. One suggested regime is famciclovir at 10-20 mg/kg per day for 5-10 days, with treatment to commence as soon as possible after the first herpes infection(not the first symptoms or outbreak), and the most effective time for initiating treatment to be five days or less after the first herpes infection. However, the window of opportunity for this treatment is only a few months after first infection with the virus, following this the potential effect on latency drops to zero.^[101]

Antiviral medications are also available as topical creams for treating recurrent outbreaks on the lips, although their effectiveness is disputed.^[102] Penciclovir cream has a 7-17 hour longer cellular half-life than aciclovir cream, increasing its effectiveness relative to aciclovir when topically applied.^[103]

Topical treatments

Docosanol is available as a cream for direct application to the affected area of skin. It prevents HSV from fusing to cell membranes, thus barring the entry of the virus into the skin. Docosanol was approved for use after clinical trials by the FDA in July 2000.^[104] Docosanol is marketed by Avanir Pharmaceuticals under the name Abreva. It was the first over-the-counter antiviral drug approved for sale in the United States and Canada. Avanir Pharmaceuticals and GlaxoSmithKline Consumer Healthcare were the subject of a U.S. nationwide class-action suit in March, 2007 due to the misleading claim that it cut recovery times in half.^[105]

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

Lipactin by Novartis is another over-the-counter topical gel which has been clinically shown to reduce sympotms and healing duration of a Herpes Simplex infection.

There is some limited research that has shown that tea tree oil may have topical anti-viral activity, especially with the Herpes virus^[106]

Other drugs

Cimetidine, a common component of heartburn medication, has been shown to lessen the severity of herpes zoster outbreaks in several different instances.^[107]^[108]^[109] This is an off-label use of the drug. It and probenecid have been shown to reduce the renal clearance of aciclovir.^[110] These compounds also reduce the rate, but not the extent, at which valaciclovir is converted into aciclovir.

Limited evidence suggests that low dose aspirin (125 mg daily) might be beneficial in patients with recurrent HSV infections. Aspirin (acetylsalicylic acid) is an non-steroidal anti-inflammatory drug which reduces the level of prostaglandins—naturally occurring lipid compounds—that are essential in creating inflammation.^[111] A recent study in animals showed inhibition of thermal (heat) stress induced viral shedding of HSV-1 in the eye by aspirin, and a possible benefit in reducing the frequency of recurrences.^[112]

Another treatment is the use of petroleum jelly. Healing of cold sores is sped by barring water or saliva from reaching the sore.

Vaccines

Zostavax is a live vaccine developed by Merck & Co. (September, 2008) which has been shown to reduce the incidence of herpes zoster (known as Shingles) by 51.3% in a pivotal phase III study of 38,000 adults aged 60 and older who received the vaccine.

The National Institutes of Health (NIH) in the United States is currently conducting phase III trials of Herpevac, a vaccine against HSV-2.^[113] The vaccine has only been shown to be effective for women who have never been exposed to HSV-1. Overall, the vaccine is approximately 48% effective in preventing HSV-2 seropositivity and about 78% effective in preventing symptomatic HSV-2.^[113] During initial trials, the vaccine did not exhibit any evidence of preventing HSV-2 in males.^[113] Additionally, the vaccine only reduced the acquisition of HSV-2 and symptoms due to newly acquired HSV-2 among women who did not have HSV-2 infection at the time they got the vaccine.^[113] Because about 20% of persons in the United States have HSV-2 infection, this further reduces the population for whom this vaccine might be appropriate.^[113]

Researchers at the University of Florida have made a hammerhead ribozyme that targets and cleaves the mRNA of essential genes in HSV-1. The hammerhead which targets the mRNA of the UL20 gene greatly reduced the level of HSV-1 ocular infection in rabbits and reduced the viral yield in vivo.^[114]

Natural compounds

File:RedoxonVitaminC.jpg

Many people seek benefits in natural products and dietary supplements for treatment of herpes

Certain dietary adjustments, dietary supplements, and alternative remedies are believed to be beneficial in the treatment of herpes, either alone, or in conjunction with prescribed antiviral therapy. There is currently insufficient scientific and clinical evidence to support the effective use of many of these compounds to treat herpes in humans.^[115]

Lysine supplementation has been used for the prophylaxis and treatment of herpes simplex although doses smaller than 1 gram per day appear to be ineffective.^[116]^[117]^[118]

Aloe vera, available as a cream or gel, makes an affected area heal faster and may prevent recurrences.^[119]

Lemon balm (Melissa officinalis) has antiviral activity against HSV-2 in cell culture and may reduce HSV symptoms in herpes infected people.^[120]^[121]^[121]

Carrageenans—linear sulphated polysaccharides extracted from red seaweeds—have been shown to have antiviral effects in HSV-infected cells and in mice.^[122] ^[123]

There is conflicting evidence on a possible benefit from extracts from the plant echinacea in treating oral^[124], but not genital, herpes.^[125]

Resveratrol, a compound naturally produced by plants and a component of red wine, prevents HSV replication in cultured cells and reduces cutaneous HSV lesion formation in mice. It is not considered potent enough to be an effective treatment on its own.^[126]^[127]

Extracts from garlic have shown antiviral activity against HSV in cell culture experiments, although the extremely high concentrations of the extracts required to produce an antiviral effect was also toxic to the cells.^[128]

The plant Prunella vulgaris, commonly known as selfheal, also prevents expression of both type 1 and type 2 herpes in cultured cells.^[129]

Lactoferrin, a component of whey protein, has been shown to have a synergistic effect with aciclovir against HSV in vitro.^[130]

Some dietary supplements have been suggested to positively treat herpes. These include vitamin C, vitamin A, vitamin E, and zinc.^[131]^[132]

Butylated hydroxytoluene (BHT), commonly available as a food preservative, has been shown in cell culture and animal studies to inactivate herpes virus.^[133]^[134] However, BHT has not been clinically tested and approved to treat herpes infections in humans.

Psychological and social effects

Some people experience negative feelings related to the condition following diagnosis, particularly if they have acquired the genital form of the disease. Feelings can include depression, fear of rejection, feelings of isolation, fear of being found out, self-destructive feelings, and fear of masturbation.^[135] These feelings usually lessen over time. Herpes support groups have been formed in the United States and the UK, providing information about herpes and running message forums and dating websites for sufferers.^[136]^[137]^[138]^[139]^[140]^[141]^[142]^[143]

People with the herpes virus are often hesitant to divulge to other people, including friends and family, that they are infected. This is especially true of new or potential sexual partners that they consider casual.^[144] A perceived reaction is sometimes taken into account before making a decision about whether to inform new partners and at what point in the relationship. Many people choose not to disclose their herpes status when they first begin dating someone, but wait until it later becomes clear that they are moving towards a sexual relationship. Other people disclose their herpes status upfront. Still others choose only to date other people who already have herpes.

References

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External links

General

Images

Links to genital herpes pictures (Hardin MD/University of Iowa)
Herpes photo library at Dermnet
Pictures of Orofacial Herpes (Coldsores) (VisualDxHealth)
Clinical Pictures of Genital Herpes (VisualDxHealth)
Genital Herpes Pictures
Atlas of Ophthalmology (UoIowa), annotations under "herpes simplex"

Other

[Dickerson2004_Mar_15-1] Dickerson FB, Boronow JJ, Stallings C; et al. (2004). "Infection with herpes simplex virus type 1 is associated with cognitive deficits in bipolar disorder". Biol. Psychiatry. 55 (6): 588–93. doi:10.1016/j.biopsych.2003.10.008. PMID 15013827. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[Itzhaki1997_Jan_25-2] Itzhaki RF, Lin WR, Shang D, Wilcock GK, Faragher B, Jamieson GA (1997). "Herpes simplex virus type 1 in brain and risk of Alzheimer's disease". Lancet. 349 (9047): 241–4. doi:10.1016/S0140-6736(96)10149-5. PMID 9014911. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[pmid18156035-3] ^ ^a ^b ^c ^d ^e ^f ^g ^h Gupta R, Warren T, Wald A (2007). "Genital herpes". Lancet. 370 (9605): 2127–37. doi:10.1016/S0140-6736(07)61908-4. PMID 18156035. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[Brown1997_Aug_21-4] Brown ZA, Selke S, Zeh J; et al. (1997). "The acquisition of herpes simplex virus during pregnancy". N Engl J Med. 337 (8): 509–15. doi:10.1056/NEJM199708213370801. PMID 9262493. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[pmid1336296-5] Takasu T, Furuta Y, Sato KC, Fukuda S, Inuyama Y, Nagashima K (1992). "Detection of latent herpes simplex virus DNA and RNA in human geniculate ganglia by the polymerase chain reaction". Acta Otolaryngol. 112 (6): 1004–11. doi:10.3109/00016489209137502. PMID 1336296.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid7598372-6] Sugita T, Murakami S, Yanagihara N, Fujiwara Y, Hirata Y, Kurata T (1995). "Facial nerve paralysis induced by herpes simplex virus in mice: an animal model of acute and transient facial paralysis". Ann. Otol. Rhinol. Laryngol. 104 (7): 574–81. PMID 7598372.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid16917546-7] Lazarini PR, Vianna MF, Alcantara MP, Scalia RA, Caiaffa Filho HH (2006). "Herpes simplex virus in the saliva of peripheral Bell's palsy patients". Rev Bras Otorrinolaringol (Engl Ed) (in Portuguese). 72 (1): 7–11. PMID 16917546.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid15699730-8] Linder T, Bossart W, Bodmer D (2005). "Bell's palsy and Herpes simplex virus: fact or mystery?". Otol. Neurotol. 26 (1): 109–13. doi:10.1097/00129492-200501000-00020. PMID 15699730.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid17573575-9] Kanerva M, Mannonen L, Piiparinen H, Peltomaa M, Vaheri A, Pitkäranta A (2007). "Search for Herpesviruses in cerebrospinal fluid of facial palsy patients by PCR". Acta Otolaryngol. 127 (7): 775–9. doi:10.1080/00016480601011444. PMID 17573575.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid16676828-10] Stjernquist-Desatnik A, Skoog E, Aurelius E (2006). "Detection of herpes simplex and varicella-zoster viruses in patients with Bell's palsy by the polymerase chain reaction technique". Ann. Otol. Rhinol. Laryngol. 115 (4): 306–11. PMID 16676828.{{cite journal}}: CS1 maint: multiple names: authors list (link)

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v t e Sexually transmitted infections (STI)
Bacterial	Chancroid (Haemophilus ducreyi) Chlamydia, lymphogranuloma venereum (Chlamydia trachomatis) Donovanosis (Klebsiella granulomatis) Gonorrhea (Neisseria gonorrhoeae) Mycoplasma hominis infection (Mycoplasma hominis) Syphilis (Treponema pallidum) Ureaplasma infection (Ureaplasma urealyticum)
Protozoal	Trichomoniasis (Trichomonas vaginalis)
Parasitic	Crab louse Scabies
Viral	AIDS (HIV-1/HIV-2) Cancer cervical vulvar penile anal Human papillomavirus (HPV) Genital warts (condyloma) Hepatitis B (Hepatitis B virus) Herpes simplex HSV-1 & HSV-2 Molluscum contagiosum (MCV) Zika fever (Zika virus)
General inflammation	female Cervicitis Pelvic inflammatory disease (PID) male Epididymitis Prostatitis either Proctitis Urethritis/Non-gonococcal urethritis (NGU)