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


'''Herpes simplex''' is a [[viral disease]] caused by [[herpes simplex virus]]es that primarily infect [[mucosal tissue]]s. Infection of the [[genital]]s is commonly known as ''herpes'' and is predominantly caused by the type 2 strain of herpes simplex virus (HSV-2) that is usually sexually transmitted. The type 1 strain of herpes simplex virus (HSV-1) is the usual cause oral herpes, colloquially called ''[[cold sores]]''. HSV-1 and HSV-2 are transmitted by direct contact with an infected sore or body fluid of an infected individual, and can cause painful fluid-filled blisters, containing millions of infectious [[virus]] particles. Following initial infection, these viruses travel from cells in the skin to [[Sensory neuron|sensory nerves]], where they reside as life-long, latent viruses. HSV-1 lies dormant in [[Trigeminal ganglion|trigeminal ganglia]] that provide sensation to the lips, lower mouth and neck; HSV-2 resides in [[sacral ganglia]] that supply sensation to the genitals, [[perineum]] and upper legs. Following reactivation, the viruses travel down the same nerves to reinfecte the same area of skin initially infected.
'''Herpes simplex''' is a [[viral disease]] caused by chelsea,johnny,and michael [[herpes simplex virus]]es that primarily infect [[mucosal tissue]]s. Infection of the [[genital]]s is commonly known as ''herpes'' and is predominantly caused by the type 2 strain of herpes simplex virus (HSV-2) that is usually sexually transmitted. The type 1 strain of herpes simplex virus (HSV-1) is the usual cause oral herpes, colloquially called ''[[cold sores]]''. HSV-1 and HSV-2 are transmitted by direct contact with an infected sore or body fluid of an infected individual, and can cause painful fluid-filled blisters, containing millions of infectious [[virus]] particles. Following initial infection, these viruses travel from cells in the skin to [[Sensory neuron|sensory nerves]], where they reside as life-long, latent viruses. HSV-1 lies dormant in [[Trigeminal ganglion|trigeminal ganglia]] that provide sensation to the lips, lower mouth and neck; HSV-2 resides in [[sacral ganglia]] that supply sensation to the genitals, [[perineum]] and upper legs. Following reactivation, the viruses travel down the same nerves to reinfecte the same area of skin initially infected.


HSV-1 genital herpes is more infectious during primary episodes than HSV-2, but reoccurs less frequently than genital HSV-2. Both herpes infections have periods of active disease lasting 2-21 days and then [[remission]] when the sores disappear. The majority of cases are asymptomatic, however, although [[viral shedding|shedding]] may still occur. Over time, periods of remission generally increase in length, and the duration of [[lesion]]s and viral shedding also decreases leading to reduced episodes of active disease. The frequency of recurrences is regulated by [[Adaptive immune system|specific immunity]] developed against the virus. Previous HSV-1 infection tends to ameliorate the symptoms of a subsequent HSV-2 infection.
HSV-1 genital herpes is more infectious during primary episodes than HSV-2, but reoccurs less frequently than genital HSV-2. Both herpes infections have periods of active disease lasting 2-21 days and then [[remission]] when the sores disappear. The majority of cases are asymptomatic, however, although [[viral shedding|shedding]] may still occur. Over time, periods of remission generally increase in length, and the duration of [[lesion]]s and viral shedding also decreases leading to reduced episodes of active disease. The frequency of recurrences is regulated by [[Adaptive immune system|specific immunity]] developed against the virus. Previous HSV-1 infection tends to ameliorate the symptoms of a subsequent HSV-2 infection.

Revision as of 16:38, 19 February 2008

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

Herpes simplex is a viral disease caused by chelsea,johnny,and michael herpes simplex viruses that primarily infect mucosal tissues. Infection of the genitals is commonly known as herpes and is predominantly caused by the type 2 strain of herpes simplex virus (HSV-2) that is usually sexually transmitted. The type 1 strain of herpes simplex virus (HSV-1) is the usual cause oral herpes, colloquially called cold sores. HSV-1 and HSV-2 are transmitted by direct contact with an infected sore or body fluid of an infected individual, and can cause painful fluid-filled blisters, containing millions of infectious virus particles. Following initial infection, these viruses travel from cells in the skin to sensory nerves, where they reside as life-long, latent viruses. HSV-1 lies dormant in trigeminal ganglia that provide sensation to the lips, lower mouth and neck; HSV-2 resides in sacral ganglia that supply sensation to the genitals, perineum and upper legs. Following reactivation, the viruses travel down the same nerves to reinfecte the same area of skin initially infected.

HSV-1 genital herpes is more infectious during primary episodes than HSV-2, but reoccurs less frequently than genital HSV-2. Both herpes infections have periods of active disease lasting 2-21 days and then remission when the sores disappear. The majority of cases are asymptomatic, however, although shedding may still occur. Over time, periods of remission generally increase in length, and the duration of lesions and viral shedding also decreases leading to reduced episodes of active disease. The frequency of recurrences is regulated by specific immunity developed against the virus. Previous HSV-1 infection tends to ameliorate the symptoms of a subsequent HSV-2 infection.

HSV-1 and HSV-2 belong to a family of herpes viruses called herpesviridae. Eight members of herpesviridae infect humans to cause a variety of illnesses including cold sores, chickenpox or varicella, shingles or herpes zoster (VZV), cytomeglovirus (CMV), and various cancers, and can cause brain inflammation (encephalitis). All viruses in the herpes family produce life-long infections. Recurrences can be triggered in some individuals by specific events, such as sunburn, ultraviolet light, wind, trauma, surgery, stress or other infections. Since viral reactivation is controlled by the immune system, in immunocompetent persons, oral and genital herpes are not typically life-threatening. However, individuals with HIV or transplant patients, with compromised immune systems, can develop serious HSV infections such as keratitis or encephalitis. Additionally, immuno-incompetent newborns, infected by genital herpes at birth or shortly thereafter, are at highest risk if they acquire CNS (central nervous system) HSV infection that can cause brain damage or disseminated HSV which often results in liver failure and death. SEM (Skin eyes mouth) HSV infection usually involves only external lesions but can progress to CNS or diseminated if untreated. The risk of neonatal HSV occurring is higher when the mother has a primary infection just prior to birth and lacks protective antibodies that would otherwise reduce viable virus shedding. While great strides have been made in the treatment of neonatal herpes with the advancement of acyclovir antiviral therapy, the major impediment to it's irradication remains late diagnosis with lesions appearing late in the course of the disease, or not at all. Infection is asymptomatic in up 40% of cases.

Oral herpes (HSV-1) affects 50-80% of the U.S. population by the time they are in their 40s, and genital herpes caused by HSV-2 affects approximately 20-30%. In recent years, a decline in adolescent HSV-1 seroprevalence by a few percent per decade has been observed in the US and other industrialized countries. [1] However, the incidence of HSV-1 genital herpes is increasing as result of more women entering their child bearing years while seronegative for HSV-1.[1] Despite the apparent declines in HSV seroprevalence, the American Social Health Association (ASHA) predict that since up to 90% of HSV infected people are unaware of their infection due to mild or misdiagnosed symptoms up to 40% of all men and 50% of all women could be infected with genital herpes by 2025.[2]


Orofacial infection

Herpes
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  1. Prodromal symptoms
  2. Skin appears irritated and red
  3. Sore or cluster of fluid-filled blisters appear
  4. Lesion begins to heal, usually without scarring [3]

In the absence of a coldsore one may also transmit the virus through the skin. Oral herpes lesions occur on the lips, on the fixed mucosa inside the mouth, including the hard palate (roof of the mouth), and gingiva (gums)[citation needed], but can occur almost anywhere on the face. Oral herpes and cold sores can sometimes be confused with canker sores.

Genital infection

Herpes
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  1. Prodromal symptoms
  2. Itching in affected area
  3. Sore appears
  4. Lesion begins to heal, usually without scarring.

In males, the lesions may occur on the shaft of the penis, in the genital region, on the inner thigh, buttocks, or anus. In females, lesions may occur on or near the pubis, labia, clitoris, vulva, buttocks or anus. Symptoms can be confused with those of cystitis, chlamydia or gonorrhea, so careful observation by a doctor is important.

The appearance of herpes lesions and the experience of outbreaks in these areas varies tremendously among individuals. Herpes lesions on or near the genitals may look like cold sores. An outbreak may look like a paper cut, or chafing, or appear to be a yeast infection. Symptoms of a genital outbreak may include aches and pains in the area, discharge from the penis or vagina, and severe discomfort and burning when urinating.

Initial outbreaks (Primary infection) are usually more severe than subsequent ones, and generally also involve flu-like symptoms and swollen glands for a week or so. Subsequent outbreaks tend to be periodic or episodic, occur on average four to five times a year, and can be triggered by stress, illness, fatigue, menstruation, and other changes. The virus lies dormant in the nerve ganglia that serve the infected dermatome between outbreaks, from where the body's immune system cannot remove it. HSV-2 is widespread, affecting an estimated 1 in 4 females and 1 in 5 males in the United States. Although certain therapies can prevent outbreaks or reduce the risk of transmission to partners, no cure is yet available.[4]

Herpes simplex encephalitis

Herpes
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Herpes simplex encephalitis is a very serious disorder, thought to be caused by the retrograde transmission of the virus from a peripheral site on the face to the central nervous system along a nerve axon. It is known that the virus lies dormant in the ganglion of the trigeminal or fifth cranial nerve. The reason for reactivation remains unclear. It has also been proposed that the olfactory nerve may be involved.[5] Without treatment, it results in rapid death in around 70% of cases. Even with the best modern treatment, it is fatal in around 20% of cases treated, and causes serious long-term neurological damage in over half the survivors. For unknown reasons the virus seems to target the temporal lobes of the brain. A small population of survivors, perhaps 20%, show little long-term damage. It is most common in children and middle-aged adults. Although herpes simplex is by no means the most common cause of viral encephalitis (accounting for about 10% of cases in the US), because of the high risk of damage if it is not treated, as well as being one of the few encephalitis for which definitive treatment is available, patients presenting with encephalitis symptoms are likely to be treated against this disorder without waiting for a positive diagnosis. A positive diagnosis can be obtained by CSF PCR for herpes simplex DNA, CSF viral culture or a rising titre for antibodies. The fact that the electroencephalogram is abnormal in >90% of the patients with herpes simplex encephalitis further aids the diagnosis.

Cold sore virus (herpes simplex) usually infects through the mouth and enters the nucleus of the nerve cell during the first 7 days, and will remain latent for 10 days to 20 years, and will then reactivate due to common stress, fever, trauma, or sunburn. The virus will soon be contagious through more cold sores. In a few people with a genetic susceptibiliy, the virus may attack the brain encephalitis.

Neonatal herpes simplex

Herpes
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Neonatal HSV disease is rare but serious, usually the consequence of vertical HSV transmission from mother to newborn child, although an estimated 10% of cases are thought to be acquired postnatally from a parent, caretaker, or sibling. Primary infection of a seronegative mother in the third trimester has a 30-57% transmission rate, whereas recurring infection in a mother seropositive for both HSV 1 and 2 has 1-3% transmission rate. This in part is due to the protective nature of maternal antibodies which develop in the baby from about the seventh month of pregnancy. HSV-1 neonatal herpes is extremely rare in underdeveloped countries because seroconversion to HSV-1 usually occurs in childhood or adolescence, precluding a genital HSV-1 infection. HSV-2 infections are much more common. In industrialized nations the adolescent HSV-1 seroprevalance has been steadily dropping for the last 5 decades as a result of better hygiene, less over-crowding, and smaller family size. The resulting increase of young women entering the child bearing years HSV-1 seronegative, has been a harbinger of increased HSV-1 genital herpes and as a result, neonatal herpes in developed nations. HSV-1 Genital infection is now thought to be about 50% in the U.S. and as high as 70% in Japan. Prospective active surveillance data indicate a low incidence rate of 3.61 per 100,000 live births in Australia, with similar rates in the UK; in the USA the rate is somewhat higher, estimated to be 6 to 20 per 100,000 live births depending on region and demographics. [6][7] A recent three year study in Canada revealed a NHSV rate of 5.9 per 100,000 live births. Among the surprises in the study, 62.5 percent of cases were HSV-1 and 98.7% of transmission was asymptomatic. [8]

Neonatal herpes manifests itself in three forms. Skin, eyes, mouth, herpes (SEM) which is characterized by external lesions but no internal organ involvement, and has the best prognosis. Lesions are likely to appear on trauma sites such as the attachment site of fetal scalp electrodes, the location of forceps or vacuum extractors, the margin of the eyes, the circumcision, trauma, or surgey locations. Disseminated Herpes, (DIS) which involves internal organ infection noteably the liver; and Central Nervous System herpes (CNS) which involves the nervous system and the brain, possibly leading to encephalitis. CNS has the highest morbidity when treated because disseminated herpes has a higher mortality rate. SEM herpes untreated, may spread to internal organs and result in mortality or morbidity due to disseminated HSV disease and/or HSV encephalitis due to CNS Herpes. The mortality rate from neonatal HSV disease in the US is down to about 25% from as high as 85% a few decades ago, due to the advent of vidarabine, and later acyclovir antiviral therapy. The morbidity and mortality still remain high due to DIS and CNS herpes are not diagnosed early enough for antiviral therapies to be administered, in part because 20-40% of infected neonates to not have lesions, making early diagnosis difficult.

Ocular herpes

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Ocular herpes (generally HSV-1) is a special case of facial herpes infection (herpes viral keratitis) that affects the nerves serving the cornea of the eye. It is unilateral, affecting one eye at a time. It usually manifests as small white itchy lesions on the surface of the cornea, known as dendritic ulcers because they show a branching pattern. Additional symptoms include dull pain deep inside the eye, mild to acute dryness and sinusitis. Most first infections resolve spontaneously in a few weeks or with the use of oral and topical antivirals. However, the virus continues to inhabit the neurons of the eye and to multiply. Subsequent symptoms (with or without visible lesions) include chronic dry eye, low grade intermittent conjunctivitis or chronic unexplained sinusitis. When the patient is immunocompromised or the concentration of viral DNA reaches a critical limit, the presence of the virus can trigger a massive autoimmune response in the eye, resulting in the patient's own system destroying the corneal stroma. This usually results in loss of vision due to opacification of the cornea. Treatment with corneal transplants may be ineffective, as reinfection of the transplant is common; however, with concurrent use of antivirals the chance of graft acceptance is higher.

As with orofacial or genital herpes, trauma to the eye increases the chance of a recurrence.[citation needed] Thus herpes viral keratitis can produce complications in the case of patients undergoing radial keratotomy by laser (lasik) to correct vision defects, and patients undergoing this procedure should be carefully screened.

Bell's Palsy

Up to 70% of the cases of Bell's palsy can be linked to the presence of HSV-1. The virus seems to cause an inflammation of the facial nerve CN-VII that controls the muscles of the face, causing paralysis of the face and inability to blink an eye. Bell's palsy is also linked to Lyme disease, chickenpox (shingles), brain tumor, or just physical trauma. In the case of an infection by HSV-1, treatment with an anti-viral and a steroid-based anti-inflammatory are recommended and improvement should be expected in 2 to 4 weeks, and full recovery within 3 to 6 months in 90% of the cases[1].

Herpes Whitlow

Herpes whitlow (herpetic whitlow) is typically contracted by healthcare workers that come in contact with the virus. The most common are dental workers who contract Herpes Whitlow at the rate of about 2% a year in the U.S.[citation needed] Again it is the seronegative person who is at risk. It will typically manifest itself on fingers, cuticle, and is usually associated with HSV-1 in the health care field. Amongst the general public herpetic whitlow is more commonly HSV-2. A person who has already seroconverted cannot get a herpetic whitlow of the HSV type for which they are seropositive.

Outbreak triggers

Oral herpes (cold sores)

Physical or psychological stress can trigger an outbreak. Local injury to the face, lips, eyes or mouth, as through trauma, surgery, wind, ultraviolet light, or sunburns are well established triggers. Similarly, concurrent infections, such as upper respiratory viral infections or other febrile diseases, can cause outbreaks, hence the historic terms "cold sore" and "fever blister".

Genital herpes

Controversy exists about triggers of recurrent outbreaks of genital herpes, historically due to HSV-2 but increasingly due to HSV-1. No scientific studies have clearly documented such triggers, and the objective data available suggest that outbreaks are not influenced by stressful events, anxiety, depression, or similar influences. The clinical experience of most experts involved in clinical care is that attempts by infected persons to modify external triggers are virtually never effective in controlling symptomatic outbreaks of genital herpes. Similarly, neither objective data nor biological plausibility support the notion that excessive usage of antibiotics affects the immune system's ability to keep the disease within the nerve ganglia (particularly as antibiotics are useless against viruses of any type) or otherwise affect herpes recurrences, nor the occasional assertion that "chronic" genital herpes is in any way related to low-level food allergy. Despite "theories" to the contrary, herpes outbreaks have not been medically documented to be triggered by menstrual cycles. Sores usually heal within 2 - 4 weeks. This varies greatly on the individual however, as some may not exhibit any symptoms for years, and some may not show symptoms at all. [9]

Symptoms

Herpes infections, whether initial or recurring, are usually first felt as a tingling and/or itching sensation (like chicken pox) in the affected location. The very first outbreak is usually more severe than any recurrence. [citation needed] These initial feelings are usually followed, depending on how severe the infection is, by the emergence of a raised or swollen area on the skin. This swollen area then becomes painful in general, but acutely sore when touched, stretched or moved. Eventually the sore area will abscess, and emit a virus-laden clear fluid for several days before scabbing over. Once scabbed over the lesion will usually heal completely within a period of a week to ten days. In immuno-compromised individuals this cycle can be significantly protracted.

From the onset of infection/outbreak, many patients experience headaches, fatigue (sometimes extreme), and peculiar twitching sensations in the nerves that lead to the area of the outbreak. The fatigue associated with herpes infections can concatenate with depression brought on by the cosmetic or sexually compromising nature of the infection, to yield a deeply gloomy overall mental state that some believe can contribute to increasing the length and severity of an infection.

Transmission

Herpes can be contracted through direct skin contact with an infected person. There are no documented cases of infection via an inanimate object (e.g. a towel, toilet seat, drinking vessels) although such infection is theoretically possible but highly unlikely due to the fragility of the virus itself.[verification needed] The virus travels through tiny breaks in the skin or mucous membranes in the mouth (HSV-1) and genital areas (HSV-2), though healthy skin and mucous membranes are normally an effective barrier to infection. However, in the case of mucous membranes, even microscopic abrasions are sufficient to expose the nerve endings into which the virus inserts itself. This is why most herpes transmission happens in mucous membranes or in areas of the body where mucous membranes and normal skin merge (e.g., the corners of the mouth). Herpes could also be transmitted by using a razor on the genital area that has previously been used on the genital area of an infected person during an outbreak. If the razor is kept at body heat (over 90 degrees Farenheit) and the area between razor blades remains moist, then the virus can survive and can be transmitted to a person who uses the razor. Herpes transmission (types 1 & 2) occurs between discordant partners, i.e. a person with a history of infection (seropositive), having relations with a seronegative partner. Following the initial infection with one type, the patient develops antibodies (seroconversion) and cannot get a herpes infection with this type elsewhere, so a person with a cold sore cannot contract a herpes whitlow or genital HSV-1 infection. In a monogamous couple, where the female is seronegative with a seropositive partner, she runs a 30% per year risk of contracting an HSV-1 infection. If she contracts an oral HSV-1 infection first, after seroconversion, which takes around 6 weeks, she cannot get a genital HSV-1 infection.

Recurrence

The herpes virus establishes a latent state in sensory and autonomic ganglia. Although the frequency and severity of recurrent outbreaks may vary greatly depending upon the individual, physical and/or mental stress have been commonly noted as contributors to an outbreak. However more recent research suggests that stress may be a symptom and not a cause.

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 near the base of the spine, the buttocks, back of the thighs, or they may appear at the original site of infection.

The human body is able to build up an immunity to the virus over time. Suppressive drugs may interfere with the immune system's ability to fight the virus; however, antiviral medication has been proven to shorten the duration and/or frequency of the outbreaks in the first year or so.

Studies have been conducted by major pharmaceutical companies to determine therapy results, however, the resultant claims are vague, and there hasn't been an objective governing body to determine the exact nature of the disease or its cure.

Autoinoculation

Self-reinfection, known medically as autoinoculation, is possible during intensely virulent initial (primary) infection with either HSV-1 or HSV-2 in a given infection site. The most common manifestations in children are HSV-1 herpetic whitlow, a pustular lesion typically of a finger, and herpes of the eye (keratitis, keratoconjunctivitis). Once seroconversion has occurred and antibodies established (about 6 weeks) it is unlikely that a person will reinfect themself.

General hygiene principles suggest that persons with outbreaks should wash their hands immediately before touching the area of an oral or genital lesion to prevent introducing bacteria, and afterwards to further limit the low risk of autoinoculation.

In cases where herpes is present in an area where the dermis is subject to high abrasive forces (such as the often irritated shaved beard region, or the surfaces of the penis and vulva during vigorous sexual activity), it is quite common to spread an initial lesion to other sites during the first infection.

Asymptomatic shedding

HSV asymptomatic shedding is believed to occur on 2.9% of days while on antiviral therapy, versus 10.8% of days without. Shedding is known to be more frequent within the first 12 months of acquiring HSV-2, and concurrent infection with HIV also increases the frequency and duration of asymptomatic shedding.[10] There are some indications that some individuals may have much lower patterns of shedding, but evidence supporting this is not fully verified. Sex should always be avoided in the presence of symptomic lesions. Oral sex performed by someone with oral lesions or other symptoms should be avoided, to avoid transmission of HSV-1 to the partner's genitals. Even without symptoms it is possible for transmission to occur. Many people still believe herpes cannot be transmitted through oral sex. This is a dangerous myth. [citation needed]

Women are more susceptible to acquiring genital HSV-2 than men; in the US, 11% of men and 23% of women carry HSV-2.[11] 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%. 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. Suppressive antiviral therapy reduces these risks by 50%. Antivirals also help prevent the development of symptomatic HSV in infection scenarios by about 50%, meaning the infected partner will be seropositive but symptom free. Condom use also reduces the transmission risk by 50%. Condom use is much more effective at preventing male to female transmission than vice-versa. [12] The effects of combining antiviral and condom use is roughly additive, thus resulting in approximately a 75% combined reduction in annual transmission risk. 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.

A 2004 study of 1484 couples showed condom usage reduced transmission by 96% and suppressive therapy with valacyclovir further reduced transmission by 50% resulting in a 98% reduction in transmission over an eight month period.[citation needed]

Prevention

For genital herpes, condoms are a highly recommended way to limit transmission of herpes simplex infection, as demonstrated in research. [12][13] However, condoms are by no means completely effective. The virus cannot get through latex. But their effectiveness is somewhat limited on a public health scale by the limited use of condoms in the community [14]; and on an individual scale because some blisters may not be covered by the condom, or free virus in female vaginal fluid may enable infection around the base of the penis or testicles not covered by the condom.

The use of condoms or dental dams can limit 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 herpes simplex infection and the other does not, the use of valaciclovir, in conjunction with a condom, has been demonstrated to decrease further the chances of transmission to the uninfected partner, and the Food and Drug Administration (FDA) approved this as a new indication for the drug in August 2003.

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. [15]

Other measures that have been suggested include:

  • Abstinence from sexual activity while HSV blisters are present
  • Gentle and well lubricated as opposed to vigorous, abrasive sex - use the new silicone lubricants
  • Thorough washing of the genitals after sex in cool water
  • Not ejaculating inside a partner during sex (if herpes lesions have appeared inside the urethra)
  • Management of stress
  • Adequate sleep and nutrition
  • Use of a lip protectant or lip gloss to avoid cracks and abrasions through which the virus may infect
  • Treatment using ascorbate-Cu(II) [16]

Epidemiology

African-Americans and immigrants from undeveloped countries typically have HSV-1 rates in adolescence that are two or three times higher than that of caucasians. As a result of lower HSV-1 seroprevalence, more white Americans are entering marriage/sexual activity/child bearing years seronegative for HSV-1. The absence of antibodies to HSV-1 from a prior oral HSV-1 infection leaves them susceptible to primary HSV-1 genital infections. This brings with it a risk of vertical transmission to the neonate if the mother contracts a primary infection in the third trimester, due to lack of time for full seroconversion before childbirth. The seronegative mother (who lacks antibodies) has up to a 57% chance of conveying the infection to her baby during childbirth; whereas a recurrent infection in a woman seropositive for both HSV-1 and HSV-2 is thought to be around 1-3%.

The incidence of genital herpes (HSV-2) in the US is estimated to be between 25 and 30 percent or about one in four adults. "Although African Americans are more likely to test positively for HSV-2, Caucasians have a higher risk for active genital symptoms, and over the past few years the greatest increase in HSV-2 has been observed in white adolescents." People with multiple sexual partners and those who become sexually active at a young age are also higher-risk populations for the transmission of HSV-2. [17][2][18][19]

Future vaccines

The National Institutes of Health (NIH) in the United States is currently in the midst of phase III trials of a vaccine against HSV-2, called Herpevac. 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. Assuming FDA approval, a commercial version of the vaccine is estimated to become available around 2008. During initial trials, the vaccine did not exhibit any evidence in preventing HSV-2 in males. 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. 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.

Treatment

Currently, there is no treatment that can eradicate any of the herpes viruses from the body. Non-prescription analgesics can reduce pain and fever during initial outbreaks. Topical anesthetic treatment (lidocaine - or lignociane - ointment) can relieve itching and pain. Many claim that a combination of DMSO and hydrogen peroxide, used properly can kill the virus.

Antiviral Medication

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 class and generic brands are now available at a greatly reduced cost. Some prescription drugs to treat herpes can cause diarrhea several times a day so patients are advised to take over the counter diarrhea tablets as required in these cases along with the medication. It has been claimed that the evidence for the effectiveness of topically applied cream for recurrent labial outbreaks is weak.[20] Likewise oral therapy for episodes is inappropriate for most non-immunocompromised patients, whilst there is evidence for oral prophylactic role in preventing recurrences.[21]

Valaciclovir and famciclovir are prodrugs of aciclovir and penciclovir respectively, with improved oral bioavailability (55% vs 20% and 75% vs 5% respectively).

Antiviral medications 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 thymidine kinase to convert the drug to a monophosphate form and subsequently interfere with viral DNA replication. Penciclovir's primary advantage over aciclovir cream is that it has a far longer cellular half-life – 10 hours (HSV-1)/20 hours (HSV-2) for penciclovir versus 3 hours (HSV-1/2) for aciclovir.

Aciclovir is the recommended antiviral for suppressive therapy in the last months of pregnancy to prevent transmission of herpes simplex to the neonate. The use of valaciclovir and famciclovir, while potentially improving treatment compliance and efficacy, are still undergoing safety evaluation in this context. [22] There is evidence in mice that treatment with famciclovir, rather than aciclovir, during an initial outbreak can help lower the incidence of future outbreaks by reducing the amount of latent virus in the neural ganglia. This potential effect on latency over aciclovir drops to zero a few months post-infection. [23]

Topical treatments

Docosanol (Abreva) is available as a cream for direct application to the affected area of skin. Docosanol prevents the virus 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.[24] Marketed by Avanir Pharmaceuticals under the brand name Abreva, it was the first over-the-counter antiviral drug approved for sale in the United States and Canada. In March, 2007 it was the subject of a US nationwide class-action suit against Avanir and GlaxoSmithKline as the claim that it cut recovery times in half was found to have been misleading in a California court.[25]

Tromantadine is available as a gel that inhibits entry and spreading 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. It forms a "shield" at the area of application that prevents a sore from increasing in size and stops spreading of the virus by breakage or oozing during the healing process.

Aloe Vera is available as cream or gel which makes affected area heal faster, and may even prevent recurrences.[26]

Other drugs

Cimetidine, a common component of heartburn medication, has been shown to lessen the severity of herpes zoster outbreaks in several different instances, and offered some relief from herpes simplex [27] [28] [29] . This is an off-label use of the drug.

It and probenecid have been shown to reduce the renal clearance of aciclovir. [30] The study showed these compounds reduce the rate, but not the extent, at which valaciclovir is converted into aciclovir. Renal clearance of aciclovir was reduced by approximately 24% and 33% respectively. In addition, respective increases in the peak plasma concentration of acyclovir of 8% and 22% were observed. The authors concluded that these effects were "not expected to have clinical consequences regarding the safety of valaciclovir". Due to the tendency of aciclovir to precipitate in renal tubules, combining these drugs should only occur under the supervision of a physician.

Availability of non-generic prescriptions

Availability of generic prescriptions

  • Acyclovir (aciclovir) is no longer under US or UK patent protection, available in generic form.

Drugs in development

  • BILS 179 BS, BILS 45 BS, BILS 22 BS, also inhibitors of helicase-primase enzyme, researched in Ridgefield, Connecticut, by James Crute's team at Boehringer Ingelheim Pharmaceuticals. [33][34]

Natural compounds

Despite numerous testimonials, no controlled trials of acceptable scientific design, and few if any other types of objective data, support a clinically significant benefit of treatment of genital or oral herpes with compounds other than the antiviral drugs discussed above. For most if not all "natural" or "alternative" agents, the biological basis for presumptive therapeutic benefit is poorly documented or, in some cases, overtly specious. To the extent that anecdotal reports suggest occasional individual benefit or that hypothetical benefit can be anticipated from laboratory research, the quantitative effects - in reduction of recurrence frequency, speed of healing of lesions, and similar outcomes - are trivial compared with antiviral therapy. In addition, only antiviral therapy has been shown to reduce subclinical shedding of HSV or to reduce the frequency of sexual transmission to uninfected partners, perhaps the greatest concern of most persons with genital herpes. Natural and alternative remedies should be considered minor adjunts to routine management, if used at all.

Lactoferrin

Lactoferrin, a component of whey protein, has been shown to have a synergistic effect with aciclovir against HSV in vitro.[38] The concentration of lactoferrin which achieved 50% of maximum effectiveness observed (that is, the EC50) also acted in synergy with aciclovir; the concentration required to achieve EC50 for each substance was reduced "two- to sevenfold."

Lysine

Lysine supplementation has been proposed as a complementary therapy for the prophylaxis and treatment of herpes simplex. Lysine supplementation is highly dose-dependent, with beneficial effects apparent only at doses exceeding 1000 mg per day. A small randomised controlled trial indicated a decrease in recurrence rates in nonimmunocompromised patients at a dose of 1248 mg of lysine monohydrochloride, but no effect at 624 mg daily. This study did not show any evidence of shortening the healing time compared to placebo. [39] Another small randomised controlled trial indicated the benefit of 3000 mg lysine daily for the reduction of occurrence, severity and healing time for recurrent HSV infection. [40]

Tissue culture studies have shown the suppression of viral replication when the lysine to arginine ratio in vitro favours lysine. The therapeutic consequence of this finding is unclear, but dietary arginine may affect the effectiveness of lysine supplementation. [41]

Lysine intake may be supplemented by varying the diet. Dairy products offer the highest ratio of lysine to arginine amino-acid content. Contrarily, nuts (and peanuts, even though they aren't true nuts), deliver a large dose of arginine. To help forestall outbreaks, you might avoid nuts during stressful periods, and eat cheese any time you do eat nuts. During an outbreak, eating apples may slow the spread of lesions, and reduce virus shedding and self-reinfection. Eating 100g (~3.5oz) of Parmesan cheese supplies 3.3g of lysine, vs. 1.3g of arginine. The same amount of almonds provides 0.7g of lysine, but 2.4g of arginine. (Cf. the Danish Food Composition Databank, http://www.foodcomp.dk/fcdb_alphlist.asp)

High doses of lysine (greater than 10 grams daily) are known to cause gastrointestinal adverse effects. Dyspepsia was reported in 3 of 114 subjects treated with L-lysine in one study. [40] Prolonged and/or very high lysine doses may also have adverse effects on renal function, indeed lysine is contraindicated in lysine hypersensitivity and kidney or liver disease. (Anon., 2005) One patient, with a history of risk factors for renal impairment, developed tubulointerstitial nephritis (Fanconi's Syndrome) after taking lysine 3000 mg daily for approximately 5 years. [42]

Arginine

Tissues culture studies have shown the suppression of viral replication when the lysine to arginine ratio in vitro favors lysine. The therapeutic consequence of this finding is unclear, but dietary arginine may affect the effectiveness of lysine supplementation. Some rich sources of Arginine include peanuts, peanut butter and other nuts, chocolate and raw grains.

Melissa officinalis L. (Lemon Balm)

Of the many practical applications for Melissa officinalis L. (Lemon balm), one is antiviral activity against HSV-2.[43] The tincture may be taken orally and used topically. A cream made with lemon balm extract is a popular treatment for cold sores and genital herpes in Germany (Lomaherpan) and UK (Lomabrit)

Polysaccharides

Carrageenans, linear sulphated polysaccharides extracted from red seaweeds, have been shown to have antiviral effects in HSV-infected cells.

  • There are indications that a carrageenan based gel may offer some protection against HSV-2 transmission by binding to the receptors on the herpes virus thus preventing the virus from binding to cells. Researchers have shown that a carrageenan-based gel effectively prevented HSV-2 infection at a rate of 85% in a mouse model.[44] There is an ongoing large-scale trial of the efficacy of a similar formulation on humans results are expected to be published in 2007.
  • The natural carrageenans 1T1, 1C1, 1C3 isolated from Gigartina skottsbergii seaweed inhibited the replication activity of HSV-1 and HSV-2 in infected mouse astrocyte nerve cells and vero cells.[45]

Resveratrol

Resveratrol, a compound in red wine, has been shown by researchers to prevent HSV replication in vitro by inhibiting a protein needed by the virus to replicate. Resveratrol alone was not considered potent enough by the researchers to be an effective treatment.[46] A more recent in vivo study in mice showed the efficacy of topical resveratrol cream in preventing cutaneous HSV lesion formation.[47] Research on a much more potent derivative of resveratrol, named stil-5, is ongoing. There is no evidence that red wine consumption provides any similar benefits.

Unproven

Limited evidence suggests that low dose aspirin (125 mg daily) might be beneficial in patients with recurrent HSV infections. It reduces the level of prostaglandins which are essential in creating an inflammation. A small study of 21 volunteers with recurrent HSV indicated a significant reduction in duration of active HSV infections, milder symptoms, and longer symptom-free periods as compared to a control group. [48] A recent animal study found that aspirin inhibited thermal stress-induced ocular viral shedding of HSV-1, and a possible benefit in reducing recurrences. [49] Aspirin is not recommended in persons under 18 years of age with herpes simplex due to the increased risk of Reye's syndrome. Long term daily doses of aspirin have a side effect of reduced blood coagulation, facilitating bruising. A single 81 mg "daily dose" aspirin is a safer regimen given that there are no studies of the correlation between dosage and antiviral effects of aspirin.

Other

The evidence for the effectiveness of zinc and Vitamin C supplementation is poor. [50] Other supplements with anecdotal evidence of benefits include monolaurin, vitamin A, vitamin B12, garlic, and echinacea. Daily multivitamin intake may be beneficial through maintenance of immune system health. High doses of synthetic vitamin A should not be taken in early pregnancy due to linkage with birth defects. In addition, some anecdotal reports indicate that placing ice in contact with an emerging cold sore for 5-10 minutes throughout the day can help shorten the duration of the outbreak, or prevent it from developing further.

Butylated Hydroxytoluene (BHT), commonly available as a food preservative, has been shown in in-vitro laboratory studies to inactivate the herpes virus.[51] In-vivo studies in animals confirmed the antiviral activity of BHT against genital herpes.[52] However BHT has not been clinically tested and approved to treat herpes infections in humans.

Latent infection and biology

The herpes virus is a double-stranded DNA (dsDNA)-type virus. Herpes establishes a latent infection in cells of the nervous system. Double-stranded DNA is incorporated into the cell physiology by infection of the cell nucleus, where a loop of dsDNA is maintained. During inactive, or latent, periods of the infection, a subset of the Herpes genome termed LAT or Latency Associated Transcript is active and may be involved in maintenance of latency.

Long-term effects

The long-term effects of herpes simplex are not well known, but the blisters may leave scars, and during the 1980s it was thought to contribute to the risk of cervical cancer in women. Subsequently, another virus, human papillomavirus (HPV), has been shown to be a primary cause of cervical cancer in women. Additionally, people who have unprotected sex with an HIV positve person when they have active sores are at a higher risk of HIV transmission because of open blisters. In newborns, however, herpes can cause serious damage: death, neurological damage, mental retardation, and blindness. Fortunately this is extremely rare.

The immune system is able to destroy active herpes virus particles but the herpes virus has the ability to hide from the immune system in an inactive (or latent) state. Current research suggests that this ability to hide may be achieved via modification to cellular enzyme histone deacetylases (HDACs), namely HDAC1 and HDAC2. [53] Hypothetically, by interfering with the HDAC enzymes' effectiveness, it may be possible to block the virus's ability to hide from the immune system, leading to a complete elimination of the virus by the immune system. Studies on the impact of HDAC inhibitors on viral latency are ongoing in the HIV arena.

Obstetric/neonatal risks

Recurrent genital herpes has a slight obstetrical/neonatal risks associated with it, and may merit treatment with acyclovir to prevent an outbreak at term. [54]

Viral Meningitis

It is reasonably well-established in the last few years that herpes simplex virus 2 (HSV-2) is the most common cause of recurrent viral meningitis (Mollaret's meningitis). [55]

Alzheimer's Risk

It has recently been reported that there is a possible link between the HSV-1 virus and Alzheimer's in people who carry a particular gene. http://news.bbc.co.uk/1/hi/health/7071576.stm. However this BBC news report also cites other research quoting that 70% of suffers of Alzheimer's carry HSV1, which is entirely consistent with the HSV1 infection rate of the general population (50-80% as quoted on this page)

Psychological and social effects

Due to the social stigma attached to having genital herpes, it can be difficult for an individual to initially come to terms with the changes that carrying the virus may present. Negative attitudes towards the virus have developed within society through mis-information and ignorance thus causing the many anxieties felt by those diagnosed. Initial diagnosis can cause dramatic psychological and emotional stress, due to fears about future relationships and loss of self-confidence. The fears and anxieties born out of contracting genital herpes are themselves a result of poor education on the subject and prejudices surrounding STI's. Genital herpes (HSV2) is medically a condition no different to that of facial herpes (HSV1) yet both evoke such contrasting attitudes. People are generally very accepting of facial coldsores but are horrified at the thought of genital coldsores. With more education and openly discussing herpes simplex it is hoped that modern society (in the UK at least) will come to accept the two equally for what they are; no more than minor skin conditions. Only then can we begin to eliminate the unnecessary psychological and emotional stress felt by so many who come in to contact with the virus.

Quality of life issues

Upon diagnosis of the herpes virus, people can experience a number of negative feelings related to the condition. Though these feelings lessen over time, they can include:[56]

  • depression 81%
  • fear of rejection 75%
  • feeling of isolation 69%
  • fear of being found out 55%
  • self-destructive feelings 28%
  • fear of masturbation 13%

In order to improve the well-being of people with herpes, a number of support groups in the US [57] and the UK, [58] communities [59] and dating sites [60][61] have formed a presence on the Internet.


Disclosure to new partners

People with the herpes virus are often hesitant to divulge to other people that they have the virus, including friends and family but especially new or potential sexual partners. People may be less likely to inform what they consider to be 'casual' partners.[62]

In addition, the perception of the likely 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.

It is found that reactions from sexual partners are more commonly positive than not, even though negative reactions are greatly feared and this fear is usually what constitutes the 'problem' of having herpes; rather than the physical implications it causes. However, rejection can happen, usually through mis-information and/or false notions on how herpes simplex will affect ones life. Negative reactions can be prevented through education and the spreading of correct information.

Whether the law can help a person who catches herpes depends on the jurisdiction where it was contracted as legal jurisdictions define their own rules regarding the transmission of STIs such as herpes.[63] There can be both criminal and civil possibilities. For example, in the criminal case of R. v. Sullivan heard in England and Wales, an attempt was made to prosecute Sullivan for sexual assault after his partner experienced a primary outbreak of genital herpes, on the basis that he had failed to reveal the fact that he had herpes. The presiding judge dismissed the prosecution case during preliminary hearings, citing inability to prove prior knowledge and the trial did not take place. Civil claims for transmission of herpes are, for their part, usually based on negligence if transmission was accidental and battery if deliberate. The first successful case to allow such a claim in the United States was Kathleen K. v. Robert B., decided by the California Court of Appeals.


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  57. ^ Herpes Support Groups & Clinics
  58. ^ Herpes Viruses Association - a patient run group
  59. ^ Herpes message forum with over 4000 members
  60. ^ H-Date, a dating site for persons with either or both of HSV-1 or HSV-2
  61. ^ MPwH - Meeting People with Herpes, a dating site with over 65000 members
  62. ^ Green J, Ferrier S, Kocsis A, Shadrick J, Ukoumunne OC, Murphy S, Hetherton J. (2003). "Determinants of disclosure of genital herpes to partners". Sex. Transm. Infect. 79 (1): 42–44. PMID 12576613.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  63. ^ Webpage on social aspects of genital herpes

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