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Herpes

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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 simplex is a viral infection caused by one of two Herpes Simplex Viruses (HSV), members of the Herpesviridae family. Manifestations of herpes infections vary significantly between individuals. Most cases of genital herpes are caused by HSV-2. It 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.[1]

HSV disease

There are two types of Herpes Simplex Virus: HSV Type 1 and HSV Type 2. The ways in which herpes infections manifest themselves vary tremendously among individuals. The following are general descriptions of the courses outbreaks may take in the oral and genital regions.

Infectious fluid-filled blister on lower lip (herpes labialis)

Herpes is also formed on the tongue as bumps or white dots

Orofacial infection (generally HSV-1)

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


It is estimated that 50% of adults in the United Kingdom are carriers of the Herpes Simplex Virus,[2] many of which will never exhibit any symptoms of infection. Similarly, 50% of Americans have HSV-1 antibodies in their blood by the time they're teenagers or young adults and 80-90% of Americans have HSV-1 antibodies by the time they are over age 50.[3] It is also possible for the virus to be transmitted across the skin in the absence of a coldsore. Oral herpes lesions typically occur on the lips, but can occur almost anywhere on the face. They can also occur on the fixed mucosa inside the mouth, including the hard palate (roof of the mouth), and gingiva (gums). Oral herpes and cold sores can sometimes be confused with canker sores.

Genital infection (generally HSV-2)

  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. This may require a very careful examination; for example, during delivery, examination by use of a flashlight may be necessary. Symptoms can be confused with that of 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/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 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, typically occur four to five times a year, and can be triggered by stress, illness, fatigue, menstruation, and other changes. The virus sequesters in the nerve ganglia that serve the infected dermatome during non-eruptive periods, where it cannot be conventionally eliminated by the body's immune system.

Herpes simplex encephalitis (generally HSV-1)

Herpes
SpecialtyInfectious diseases, dermatology Edit this on Wikidata

Herpes simplex encephalitis is a very serious disorder, thought to be caused by the retrograde transmission of the virus from a peripheral site 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.[4] 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, and causes serious long-term neurological damage in over half the survivors. Again, 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 associated with it if it is not treated as well as being one of the few encephalitis to 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.

The virus usually infects through the mouth and enters the nucleus during the first 7 days, and will remain latent for 10 days to 100 years, and will then reactivate from common stress, fever, or a sunburn. The virus will soon be contagious through more cold sores, and the disease will start to attack the brain.

Neonatal herpes simplex

Herpes
SpecialtyInfectious diseases, dermatology Edit this on Wikidata
File:SOA-Herpes-neonatorum.jpg
HSV at newborn child.

Neonatal HSV disease is a rare, but serious, consequence of vertical HSV transmission from mother to newborn child. Prospective active surveillance data indicate an incidence rate of 3.61 per 100,000 live births in Australia, with similar rates in the UK; but much lower than the USA. [5][6] Preliminary studies indicate the epidemiology in Canada is closer to Europe than to the United States. The mortality rate from neonatal HSV disease is high (up to 25%) despite current interventions with antiviral therapies. Death results from disseminated HSV disease and/or HSV encephalitis in the newborn children.

Ocular herpes

Ocular herpes (generally HSV-1) is a special case of herpes infection (herpes viral keratitis) that affects the nerves serving the cornea of the eye. 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. Research is ongoing for a vaccine against ocular herpes.[citation needed]

Ocular herpes is the leading cause of infectious blindness in the developed world.[citation needed] As with orofacial or genital herpes, trauma to the eye increases the chance of a recurrence. 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.

A common cause of infection of the eye is the handling of contact lenses with hands infected by active sores at other sites, notably the mouth; thus the common practice of wetting lenses with saliva when no proprietary solution is available (such as for reinsertion after accidental dislodging) is extremely dangerous and should always be avoided.[citation needed]

Outbreak triggers

Oral herpes

Physical or psychological stress can trigger an outbreak. Local injury to the face, lips, eyes or mouth, as through trauma, surgery, or sunburns are well established triggers of recurrent orolabial herpes due to herpes simplex virus type 1 (HSV-1). Similarly, intercurrent infections, such as upper respiratory viral infections or other febrile diseases, can cause outbreaks, hence the historic terms "cold sore" and "fever blister". Generalized psychological stress and anxiety are also triggers.

Genital herpes

Controversy exists about triggers of recurrent outbreaks of genital herpes, typically due to HSV-2. It is often stated that stress, menstruation, diet (such as foods high in arginine, like chocolate, peanuts and walnuts) or sexual activity may increase the chance and severity of outbreaks.[citation needed] However, 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 is virtually never effective in controlling symptomatic oubreaks of genital herpes. Similarly, neither objective data nor biological plausibility support the notion that excessive usage of antibiotics affect 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.

Symptoms

Herpes infections, whether initial or recurring, are usually first felt as a tingling and/or itching sensation in the affected location. 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 is contracted through direct skin contact (not necessarily in the genital area) with an infected person. There are no documented cases of infection via an inanimate object (e.g. a towel, toilet seat etc.) Such infection is theoretically possible but highly unlikely due to the fragility of the virus itself. The virus travels through tiny breaks in the skin (or mucous membranes in the mouth and genital areas), so, 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 splices 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).

Symptoms usually appear within 2 weeks. The sores usually heal within 2 - 4 weeks. [7]

Transmission was thought to be most common during an active outbreak; however, in the early 1980s, it was found that the virus can be shed from the skin, saliva and genital secretions in the absence of symptoms.

Recurrence

Herpes recurs only at a site of previous infection. The periodicity (frequency) and amplitude (severity) of recurrence varies greatly depending on the individual and various environmental factors including stress (both physical and mental). Often, for a given site, the infection will recur only two or three times, with severity attenuating (decreasing) each time. The mechanism by which the body seems to gain the upper-hand for a given recurrence site is poorly understood by the medical community.

Self reinfection

Self reinfection, known medically as autoinoculation, is more likely during intensely virulent initial infection with either HSV-1 or HSV-2 in a given infection site. The most common manifestations are herpetic whitlow, a pustular lesion typically of a finger, and herpes of the eye (keratitis, keratoconjunctivitis).

General hygiene principles suggest that persons with recurrent oral or genital herpes should avoid direct contact with active lesions and should wash their hands immediately after using the toilet or touching the area of an oral lesion, 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 vagina during vigorous sexual activity), it is quite common to spread an initial lesion to other sites, which then become highly virulent initial infections, and so on. The medical community has failed to make this very obvious fact clear to patients and this has resulted in great amplification of their general misery, not to mention the much higher likelihood that a person infected in multiple sites (whether genital, or otherwise) will spread this disease to friends, family and sexual partners.

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.[8] 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.

Women are more susceptible to acquiring genital HSV-2 than men; in the US, 11% of men and 23% of women carry HSV-2.[9] On an annual basis, without the use of antivirals or condoms, the transmission risk 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. [10] 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.

Prevention

For genital herpes, condoms are a highly recommended way to limit transmission of herpes simplex infection, as demonstrated in research. [10][11] However, condoms are by no means completely effective. The effectiveness of this method is somewhat limited on a public health scale by the limited use of condoms in the community [12]; 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.

Condoms do not prevent the condom wearer from spreading the infection to new sites either on himself through abrasion (if he is already infected and suffering an outbreak), or on the female partner if she is suffering from an outbreak and the sexual activity spreads this infection from one site to another on her own body (see "Self Reinfection" above).

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. [13]

Other measures that have been suggested include:

  • Abstinence from sexual activity while HSV blisters are present
  • Avoidance of cross-infecting new sites on the body if HSV blisters are present
  • Gentle and well lubricated as opposed to vigorous, abrasive sex
  • Thorough washing of the genitals after sex
  • 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) [14]

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-1 infection at the time they got the vaccine. Because about 50% of persons in the United States have HSV-1 infection, this further reduces the population for whom this vaccine might be appropriate.

Treatment

Currently, there is no cure for herpes. There is no treatment that can eradicate herpes virus from the body at reactivations of the virus. Non-prescription analgesics can reduce pain and fever during initial outbreaks.

Anti-viral Medication

There are several prescription antiviral medications for controlling herpes 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 diarrohea several times a day so patients are advised to take non prescribed diarrohea 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.[15] Likewise oral therapy for episodes is inappropriate for most non-immunocompromised patients, whilst there is evidence for oral prophylactic role in preventing recurrences.[16]

Valaciclovir and famciclovir are prodrugs of aciclovir and penciclovir respectively, with improved oral bioavailability (55% vs 20% and 75% vs 5% respectively). These 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 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 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. [17] 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. [18]

Other drugs exhibiting anti-viral activity

Docosanol (Abreva) is another treatment that may be effective. Docosanol works by preventing the virus from fusing to cell membranes, thus barring entry into the cell for the virus. This may keep an outbreak contained to a smaller area than would otherwise be observed.

Zilactin is an early relief cold sore/fever blister gel that works by applying the gel, which when dry forms a "shield" to prevent the sore from increasing in size and prevents spreading by breakage or oozing during the healing process.

Tromantadine is another antiviral drug effective against herpes.

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 [19] [20] [21] . This is an off-label use of the drug.

It and probenecid have been shown to reduce the renal clearance of aciclovir. [22] 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 is no longer under US 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. [25][26]

Natural compounds

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. [30] 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. [31]

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. [32]

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 cheese may slow the spread of lesions, and reduce virus shedding and self-reinfection. Eating 100g (~4oz) 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. [31] 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. [33]

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.[34] 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.[35]

Lactoferrin

Lactoferrin, a component of whey protein, has been shown to have a synergistic effect with aciclovir against HSV in vitro.[36] 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 seven-fold."

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.[37] A more recent in vivo study in mice showed the efficacy of topical resveratrol cream in preventing cutaneous HSV lesion formation.[38] Research on a much more potent derivative of resveratol, 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. 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. [39] A recent animal study found that aspirin inhibited thermal stress-induced ocular viral shedding of HSV-1, and a possible benefit in reducing recurrences. [40] 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 anti-viral effects of aspirin.

Other

The evidence for the effectiveness of zinc and Vitamin C supplementation is poor. [41] 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 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.[42] In-vivo studies in animals confirmed the anti-viral activity of BHT against genital herpes.[43] 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 are not well known, but the blisters may leave scars, and historically 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 with herpes 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.

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. [44] 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 very significant obstetrical/neonatal risks associated with it, and probably may merit treatment with acyclovir as an independent problem. [45]

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). [46]

Psychological and social effects

Herpes can have a dramatic effect on an individual's mental well-being and sexual behaviour.

Quality of life issues

Upon diagnosis of genital herpes, people can experience a number of negative feelings related to the condition. Though these feelings lessen over time, they can include:[47]

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

The impact of genital herpes included:

  • partial or complete cessation of sexual activity
  • total or partial loss of interest in sex
  • decreased sexual pleasure
  • sex life more inhibited and less spontaneous
  • anxiety related to sexual desirability
  • increased depression

In order to improve the well-being of people with herpes, a number of support groups [48], communities [49] and dating sites [50][51] have formed a presence on the Internet.

Media portrayal

Media portrayals of genital herpes - which might help to destigmatise the condition - remain few and, when they occur, are often negative.[52]

Examples of such portrayals in the main types of media include:

  • in the mainstream press, a 1982 article in Time magazine called “Herpes: Today’s Scarlet Letter”; [53]
  • on television, a 1983 telefilm called “Intimate Agony”;[54]
  • in music, a 1993 Marilyn Manson song called “Herpes”;[55]
  • in the cinema, a 2005 film called “Merry Christmas… I Got You Herpes”;[56]
  • in literature, a 2006 novel called “Stigma”;[57]

More mainstream examples are often limited to brief mentions, such as in the 2006 film called “John Tucker Must Die”

Disclosure to new partners

People with genital herpes 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.[58] In addition, the perception of the likely reaction is sometimes taken into account before making a decision about whether to inform new partners. An event such as a couple moving in together was found to be the point when some people disclosed their status. Reactions by sexual partners may not always be negative, and individuals often use various strategies to mitigate the impact of disclosure such as keeping the issue "low key," choosing a relaxed environment and suggesting the couple being tested jointly for a range of sexually transmitted infections.

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.[59] There can be both criminal and civil possibilities. For example, in the criminal case of R. v. Sullivan heard in England and Wales, a man was prosecuted 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. Ultimately, the man was discharged due to an inability to prove prior knowledge. 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.

Myths

Some common misconceptions about herpes are:

  • that it is fatal. Fact: This is only true for newborns, which is rare, but it is fatal in 25% of all such cases. It can also possibly kill an adult if it infects the brain causing encephalitis, or infects the meninges causing meningitis. <I'm not sure this is true, but it's what was already stated, I'm just trying to make it easier to read>
  • that it only affects the genital areas. Fact: It can affect any part of the body. If you touch a genital herpes sore and then touch another part of your body, you can potentially spread the virus.
  • that condoms are completely effective in preventing the spread of this disease. Fact: They do greatly improve protection but are imperfect, only preventing transmission 50% of the time.
  • that it is only transmittable in the presence of symptoms. Fact: There is more viral shedding during an outbreak but it's possible to transmit any time.
  • that it can make you sterile Fact: Genital Herpes cannot make you sterile.
  • that Pap smears detect herpes Fact PAP smears are not designed to detect herpes simplex virus infections. Type-specific serology tests and viral cultures are used to diagnose genital herpes and are not normally conducted during a woman's annual gynecological examination.
  • that it can not be transmitted between the genitals and the mouth. Fact: Even the use of a condom will not prevent transmission between genital and oral regions.
  • that only promiscuous people get it. Fact: It is so common that anyone can contract it. The more sexual partners an individual has, however, the more likely they are to contract the disease.[60]

There is a basis in fact that herpes could be transmitted via an inanimate object such as a toilet seat or wet towel but the conditions required for this kind of transmission (high heat, high moisture, and a vulnerable exposure site) make it extremely unlikely. Although there are no confirmed cases of this type of transmission, sharing a towel with somebody with active lesions should be avoided. Likewise, sharing lip or mouth products (toothbrushes, lipstick, lip balm, or similar) with somebody with active lesions should also be avoided.

References

  1. ^ Center for Disease Control (CDC) - Herpes Fact Sheet Accessed February 7, 2007.
  2. ^ U.K Herpes Viruses Association - [1] Accessed March 15, 2007.
  3. ^ "Herpes Online: Exploring the "H" Community" (PDF). American Social Health Association. 1996. pp. 1–4. Retrieved 2007-03-29.
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  6. ^ Jones CA (2004). "Vaccines to prevent neonatal herpes simplex virus infection". Expert Rev. Vaccines. 3 (4): 363–364. PMID 15270635.
  7. ^ http://www.cdc.gov/std/Herpes/STDFact-Herpes.htm#signs
  8. ^ Kim H, Meier A, Huang M, Kuntz S, Selke S, Celum C, Corey L, Wald A (2006). "Oral herpes simplex virus type 2 reactivation in HIV-positive and -negative men". J Infect Dis. 194 (4): 420–7. PMID 16845624.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ Carla K. Johnson (Aug 23, 2006). "Percentage of people with herpes drops". Associated Press.
  10. ^ a b Wald A, Langenberg AG, Link K, Izu AE, Ashley R, Warren T, Tyring S, Douglas JM Jr, Corey L. (2001). "Effect of condoms on reducing the transmission of herpes simplex virus type 2 from men to women". JAMA. 285 (24): 3100–3106. PMID 11427138.{{cite journal}}: CS1 maint: multiple names: authors list (link) Cite error: The named reference "Wald" was defined multiple times with different content (see the help page).
  11. ^ Casper C, Wald A. (2002). "Condom use and the prevention of genital herpes acquisition". Herpes. 9 (1): 10–14. PMID 11916494.
  12. ^ de Visser RO, Smith AM, Rissel CE, Richters J, Grulich AE. (2003). "Sex in Australia: safer sex and condom use among a representative sample of adults". Aust. N. Z. J. Public Health. 27 (2): 223–229. PMID 14696715.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ^ Seppa, Nathan (2005-01-05). "One-Two Punch: Vaccine fights herpes with antibodies, T cells". Science News. p. 5. Retrieved 2007-03-29.
  14. ^ Betanzos-, G (2004-09-15). "Inactivation of HSV-2 by ascorbate-Cu(II) and its protecting evaluation in CF-1 mice against encephalitis". Journal of virological methods. 120 (2). Elsevier/North-Holland Biomedical Press: 161–165. doi:2004-09-15. 15288958. Retrieved 2007-03-29. {{cite journal}}: Check |doi= value (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  15. ^ Graham Worrall (1996). "Evidence for efficacy of topical acyclovir in recurrent herpes labialis is weak". BMJ. 313: 46. {{cite journal}}: Unknown parameter |month= ignored (help)- Letter
  16. ^ Graham Worrall (1996). "Acyclovir in recurrent herpes labialis". BMJ. 312: 6. {{cite journal}}: Unknown parameter |month= ignored (help) - Editorial
  17. ^ Leung DT, Sacks SL. (2003). "Current treatment options to prevent perinatal transmission of herpes simplex virus". Expert Opin. Pharmacother. 4 (10): 1809–1819. PMID 14521490.
  18. ^ Thackray AM, Field HJ. (1996). "Differential effects of famciclovir and valaciclovir on the pathogenesis of herpes simplex virus in a murine infection model including reactivation from latency". J. Infect. Dis. 173 (2): 291–299. PMID 8568288.
  19. ^ Kapinska-Mrowiecka M, Toruwski G (1996.). "Efficacy of cimetidine in treatment of herpes zoster in the first 5 days from the moment of disease manifestation". Pol Tyg Lek. 51 (23–26): 338–339. PMID 9273526. {{cite journal}}: Check date values in: |year= (help)CS1 maint: year (link)
  20. ^ Hayne ST, Mercer JB (1983). "Herpes zoster:treatment with cemetidine". Can Med Assoc J. 129 (12): 1284–1285. PMID 6652595.
  21. ^ Komlos L, Notmann J, Arieli J; et al. (1994). "In vitro cell-mediated immune reactions in herpes zoster patients treated with cimetidine". Asian Pac J Allelrgy Immunol. 12 (1): 51–58. PMID 7872992. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  22. ^ De Bony F, Tod M, Bidault R, On NT, Posner J, Rolan P. (2002). "Multiple interactions of cimetidine and probenecid with valaciclovir and its metabolite acyclovir". Antimicrob. Agents Chemother. 46 (2): 458–463. PMID 11796358.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  23. ^ Winstead ER. "Two new anti-herpes drugs tested". Genome News Network. Retrieved 2006-03-20. {{cite web}}: Unknown parameter |publishyear= ignored (help)
  24. ^ Kleymann G, Fischer R, Betz UA, Hendrix M, Bender W, Schneider U, Handke G, Eckenberg P, Hewlett G, Pevzner V, Baumeister J, Weber O, Henninger K, Keldenich J, Jensen A, Kolb J, Bach U, Popp A, Maben J, Frappa I, Haebich D, Lockhoff O, Rubsamen-Waigmann H. (2002). "New helicase-primase inhibitors as drug candidates for the treatment of herpes simplex disease". Nat. Med. 8 (4): 392–398. PMID 11927946.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  25. ^ Crute JJ, Grygon CA, Hargrave KD, Simoneau B, Faucher AM, Bolger G, Kibler P, Liuzzi M, Cordingley MG. (2002). "Herpes simplex virus helicase-primase inhibitors are active in animal models of human disease". Nat. Med. 8 (4): 386–391. PMID 11927945.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  26. ^ Liuzzi M, Kibler P, Bousquet C, Harji F, Bolger G, Garneau M, Lapeyre N, McCollum RS, Faucher AM, Simoneau B, Cordingley MG. (2004). "Isolation and characterization of herpes simplex virus type 1 resistant to aminothiazolylphenyl-based inhibitors of the viral helicase-primase". Antiviral Res. 64 (3): 161–170. PMID 15550269.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  27. ^ Schang LM, Coccaro E, Lacasse JJ. (2005). "Cdk inhibitory nucleoside analogs prevent transcription from viral genomes". Nucleosides Nucleotides Nucleic Acids. 24 (5–7): 829–837. PMID 16248044.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  28. ^ Diwan P, Lacasse JJ, Schang LM. (2004). "Roscovitine inhibits activation of promoters in herpes simplex virus type 1 genomes independently of promoter-specific factors". J. Virol. 78 (17): 9352–9365. PMID 15308730.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  29. ^ Schang LM. (2005). "Advances on cyclin-dependent kinases (CDKs) as novel targets for antiviral drugs". Curr. Drug Targets Infect. Disord. 5 (1): 29–37. PMID 15777196.
  30. ^ McCune MA, Perry HO, Muller SA, O'Fallon WM. (2005). "Treatment of recurrent herpes simplex infections with L-lysine monohydrochloride". Cutis. 34 (4): 366–373. PMID 6435961.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  31. ^ a b Griffith RS, Walsh DE, Myrmel KH, Thompson RW, Behforooz A. (1987). "Success of L-lysine therapy in frequently recurrent herpes simplex infection. Treatment and prophylaxis". Dermatologica. 175 (4): 183–190. PMID 3115841.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  32. ^ Griffith RS, Norins AL, Kagan C. (1978). "A multicentered study of lysine therapy in Herpes simplex infection". Dermatologica. 156 (5): 257–267. PMID 640102.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  33. ^ Lo JC, Chertow GM, Rennke H, Seifter JL. (1996). "Fanconi's syndrome and tubulointerstitial nephritis in association with L-lysine ingestion". Am. J. Kidney Dis. 28 (4): 614–617. PMID 8840955.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  34. ^ Zacharopoulos VR, Phillips DM. (1997). "Vaginal formulations of carrageenan protect mice from herpes simplex virus infection". Clin. Diagn. Lab. Immunol. 4 (4): 465–468. PMID 9220165.
  35. ^ Carlucci MJ, Scolaro LA, Damonte EB. (1999). "Inhibitory action of natural carrageenans on Herpes simplex virus infection of mouse astrocytes". Chemotherapy. 45 (6): 429–436. PMID 10567773.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  36. ^ Andersen JH, Jenssen H, Gutteberg TJ. (2003). "Lactoferrin and lactoferricin inhibit Herpes simplex 1 and 2 infection and exhibit synergy when combined with acyclovir". Antiviral Res. 58 (3): 209–215. PMID 12767468.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  37. ^ Docherty JJ, Fu MM, Stiffler BS, Limperos RJ, Pokabla CM, DeLucia AL. (1999). "Resveratrol inhibition of herpes simplex virus replication". Antiviral Res. 43 (3): 145–155. PMID 10551373.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  38. ^ Docherty JJ, Smith JS, Fu MM, Stoner T, Booth T. (2004). "Effect of topically applied resveratrol on cutaneous herpes simplex virus infections in hairless mice". Antiviral Res. 61 (1): 19–26. PMID 14670590.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  39. ^ Karadi I, Karpati S, Romics L. (1998). "Aspirin in the management of recurrent herpes simplex virus infection". Ann. Intern. Med. 128 (8): 696–697. PMID 9537952.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  40. ^ Gebhardt BM, Varnell ED, Kaufman HE. (2004). "Acetylsalicylic acid reduces viral shedding induced by thermal stress". Curr. Eye Res. 29 (2–3): 119–125. PMID 15512958.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  41. ^ Unknown (2005). "Herpes simplex virus oral". In Klasco RK (ed.) (ed.). AltMedDex System. Greenwood Village, CO: Thomson Micromedex. {{cite book}}: |editor= has generic name (help); Cite has empty unknown parameter: |chapterurl= (help)
  42. ^ Snipes W, Person S, Keith A, Cupp J. "Butylated hydroxytoluene inactivates lipid-containing viruses" Science. 1975;188(4183):64-6
  43. ^ Richards JT, Katz ME, Kern ER. "Topical butylated hydroxytoluene treatment of genital herpes simplex virus infections of guinea pigs" Antiviral Res 1985;5(5):281-90
  44. ^ Poon AP, Liang Y, Roizman B. (2003). "Herpes simplex virus 1 gene expression is accelerated by inhibitors of histone deacetylases in rabbit skin cells infected with a mutant carrying a cDNA copy of the infected-cell protein no. 0". J. Virol. 77 (23): 12671–12678. PMID 14610189.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  45. ^ Brocklehurst P, Kinghorn GA; et al. "randomised placebo controlled trial of suppressive acyclovir in late pregnancy in women with recurrent genital herpes infection". 105 (3): 275–80. {{cite journal}}: Cite journal requires |journal= (help); Explicit use of et al. in: |author= (help); Unknown parameter |Journal= ignored (|journal= suggested) (help); Unknown parameter |Year= ignored (|year= suggested) (help)
  46. ^ "Recurring viral meningitis & herpes II". Med Help International. Retrieved 2006-11-21.
  47. ^ Vezina C, Steben M. (2001). "Genital Herpes: Psychosexual Impacts and Counselling". The Canadian Journal of CME (June): 125–134.
  48. ^ Herpes Support Groups & Clinics
  49. ^ Herpes message forum with over 4000 members
  50. ^ H-Date, a dating site for persons with either or both of HSV-1 or HSV-2
  51. ^ MPwH - Meeting People with Herpes, a dating site with over 65000 members
  52. ^ Webpage on social aspects of genital herpes
  53. ^ Time Magazine archives
  54. ^ Film Database description of Intimate Agony
  55. ^ Wikipedia article including reference to the song Herpes
  56. ^ Film Database description of Merry Christmas...
  57. ^ Description of novel Stigma
  58. ^ 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)
  59. ^ Webpage on social aspects of genital herpes
  60. ^ "Myths and Facts about Genital Herpes". Famciclovir. 2007. Retrieved 2007-01-31.
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