herpes

ヘルペス 　 　 　

WordNet

1. viral diseases causing eruptions of the skin or mucous membrane
2. any of the animal viruses that cause painful blisters on the skin (同)herpes_virus

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1. 疱疹(ほうしん)

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/08/19 05:55:11」(JST)

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"Herpes" redirects here. For the virus that causes herpes simplex, see Herpes simplex virus. For all types of herpes viruses, see Herpesviridae.

Herpes simplex
Classification and external resources
Herpes labialis of the lower lip. Note the blisters in a group marked by an arrow.
ICD-10	A60, B00, G05.1, P35.2
ICD-9	054.0, 054.1, 054.2, 054.3, 771.2
DiseasesDB	5841 33021
eMedicine	med/1006
MeSH	D006561

Herpes simplex (Greek: ἕρπης herpēs, "creeping" or "latent") is a viral disease from the herpesviridae family caused by both Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2). Infection with the herpes virus is categorized into one of several distinct disorders based on the site of infection. Oral herpes, the visible symptoms of which are colloquially called cold sores or fever blisters, is an infection of the face or mouth. Oral herpes is the most common form of infection. Genital herpes, known simply as herpes, is the second most common form of herpes. Other disorders such as herpetic whitlow, herpes gladiatorum, ocular herpes, cerebral herpes infection encephalitis, Mollaret's meningitis, neonatal herpes, and possibly Bell's palsy are all caused by herpes simplex viruses.

Herpes viruses cycle between periods of active disease—presenting as blisters containing infectious virus particles—that last 2–21 days, followed by a remission period. Genital herpes, however, is often asymptomatic, though viral shedding may still occur. After initial infection, the viruses are transported along sensory nerves to the sensory nerve cell bodies, where they become latent and reside lifelong. Causes of recurrence are uncertain, though some potential triggers have been identified, including immunosuppressant drugs. The previously latent virus then multiplies new virus particles in the nerve cell and these are transported along the axon of each neuron to the nerve terminals in the skin, where they are released. Over time, episodes of active disease reduce in frequency and severity.

Herpes simplex is most easily transmitted by direct contact with a lesion or the body fluid of an infected individual. Transmission may also occur through skin-to-skin contact during periods of asymptomatic shedding. Barrier protection methods are the most reliable method of preventing transmission of herpes, but they merely reduce rather than eliminate risk. Oral herpes is easily diagnosed if the patient presents with visible sores or ulcers. Early stages of orofacial herpes and genital herpes are harder to diagnose; laboratory testing is usually required.

A cure for herpes has not yet been developed. Once infected, the virus remains in the body for life. Recurrent infections (outbreaks) may occur from time to time, especially in times of immune impairment such as HIV and cancer-related immune suppression. However, after several years, outbreaks become less severe and more sporadic, and some people will become perpetually asymptomatic and will no longer experience outbreaks, though they may still be contagious to others. Treatments with antivirals can reduce viral shedding and alleviate the severity of symptomatic episodes. It should not be confused with conditions caused by other viruses in the herpesviridae family such as herpes zoster, which is caused by varicella zoster virus. The differential diagnosis includes hand, foot and mouth disease due to similar lesions on the skin.

Classification

Herpes simplex is divided into two types: HSV type 1 and HSV type 2. HSV1 causes primarily mouth, throat, face, eye, and central nervous system infections, whereas HSV2 causes primarily anogenital infections. However, each may cause infections in all areas.

Signs and symptoms

HSV infection causes several distinct medical disorders. Common infection of the skin or mucosa may affect the face and mouth (orofacial herpes), genitalia (genital herpes), or hands (herpetic whitlow). More serious disorders occur when the virus infects and damages the eye (herpes keratitis), or invades the central nervous system, damaging the brain (herpes encephalitis). People with immature or suppressed immune systems, such as newborns, transplant recipients, or people with AIDS are prone to severe complications from HSV infections. HSV infection has also been associated with cognitive deficits of bipolar disorder, and Alzheimer's disease, although this is often dependent on the genetics of the infected person.

In all cases HSV is never removed from the body by the immune system. Following a primary infection, the virus enters the nerves at the site of primary infection, migrates to the cell body of the neuron, and becomes latent in the ganglion. As a result of primary infection, the body produces antibodies to the particular type of HSV involved, preventing a subsequent infection of that type at a different site. In HSV-1 infected individuals, seroconversion after an oral infection will prevent additional HSV-1 infections such as whitlow, genital herpes, and herpes of the eye. Prior HSV-1 seroconversion seems to reduce the symptoms of a later HSV-2 infection, although HSV-2 can still be contracted.

Many people infected with HSV-2 display no physical symptoms—individuals with no symptoms are described as asymptomatic or as having subclinical herpes.

Condition	Description	Illustration
Herpetic gingivostomatitis	Herpetic gingivostomatitis is often the initial presentation during the first herpes infection. It is of greater severity than herpes labialis, which is often the subsequent presentations.
Herpes labialis	Infection occurs when the virus comes into contact with oral mucosa or abraded skin.
Herpes genitalis	When symptomatic, the typical manifestation of a primary HSV-1 or HSV-2 genital infection is clusters of inflamed papules and vesicles on the outer surface of the genitals resembling cold sores.
Herpetic whitlow and Herpes gladiatorum	Herpes whitlow is a painful infection that typically affects the fingers or thumbs. On occasion, infection occurs on the toes or on the nail cuticle. Individuals that participate in contact sports such as wrestling, rugby, and soccer sometimes acquire a condition caused by HSV-1 known as herpes gladiatorum, scrumpox, wrestler’s herpes, or mat herpes, which presents as skin ulceration on the face, ears, and neck. Symptoms include fever, headache, sore throat and swollen glands. It occasionally affects the eyes or eyelids.
Herpesviral encephalitis and herpesviral meningitis	A herpetic infection of the brain that is thought to be caused by the retrograde transmission of virus from a peripheral site on the face following HSV-1 reactivation, along the trigeminal nerve axon, to the brain. HSV is the most common cause of viral encephalitis. When infecting the brain, the virus shows a preference for the temporal lobe. HSV-2 is the most common cause of Mollaret's meningitis, a type of recurrent viral meningitis.
Herpes esophagitis	Symptoms may include painful swallowing (odynophagia) and difficulty swallowing (dysphagia). It is often associated with impaired immune function (e.g. HIV/AIDS, immunosuppression in solid organ transplants).

Other

Neonatal herpes simplex is a HSV infection in an infant. It is a rare but serious condition, usually caused by vertical transmission of HSV (type 1 or 2) from mother to newborn. During immunodeficiency herpes simplex can cause unusual lesions in the skin. One of the most striking is the appearance of clean linear erosions in skin creases, with the appearance of a knife cut. Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicle. Eczema herpeticum is an infection with herpesvirus in patients with chronic atopic dermatitis may result in spread of herpes simples throughout the eczematous areas. Herpetic keratoconjunctivitis

is a primary infection typically presents as swelling of the conjunctiva and eyelids (blepharoconjunctivitis), accompanied by small white itchy lesions on the surface of the cornea.

Bell's palsy

Although the exact cause of Bell's palsy, a type of facial paralysis, is unknown it may be related to reactivation of herpes simplex virus type 1. This theory has been contested, however, since HSV is detected in large numbers of individuals having never experienced facial paralysis, and higher levels of antibodies for HSV are not found in HSV-infected individuals with Bell's palsy compared to those without. Regardless antivirals have been found to not improve outcomes.

Alzheimer's disease

HSV-1 has been proposed as a possible cause of Alzheimer's disease. In the presence of a certain gene variation (APOE-epsilon4 allele carriers), HSV-1 appears to be particularly damaging to the nervous system and increases one’s risk of developing Alzheimer’s disease. The virus interacts with the components and receptors of lipoproteins, which may lead to the development of Alzheimer's disease.

Pathophysiology

Herpes Shedding

HSV-2 genital	15–25% of days
HSV-1 oral	6–33% of days
HSV-1 genital	5% of days
HSV-2 oral	1% of days

Herpes is contracted through direct contact with an active lesion or body fluid of an infected person. Herpes transmission occurs between discordant partners; a person with a history of infection (HSV seropositive) can pass the virus to an HSV seronegative person. Herpes simplex virus 2 is typically contracted through direct skin-to-skin contact with an infected individual but can also be contacted via exposure to infected saliva, semen, vaginal fluid or the fluid from herpetic blisters. To infect a new individual, HSV travels through tiny breaks in the skin or mucous membranes in the mouth or genital areas. Even microscopic abrasions on mucous membranes are sufficient to allow viral entry.

HSV asymptomatic shedding occurs at some time in most individuals infected with herpes. It can occur more than a week before or after a symptomatic recurrence in 50% of cases. Virus enters into susceptible cells via entry receptors such as nectin-1, HVEM and 3-O sulfated heparan sulfate. Infected people that show no visible symptoms may still shed and transmit virus through their skin; asymptomatic shedding may represent the most common form of HSV-2 transmission. Asymptomatic shedding is more frequent within the first 12 months of acquiring HSV. Concurrent infection with HIV increases the frequency and duration of asymptomatic shedding. There are indications that some individuals may have much lower patterns of shedding, but evidence supporting this is not fully verified; no significant differences are seen in the frequency of asymptomatic shedding when comparing persons with one to twelve annual recurrences to those with no recurrences.

Antibodies that develop following an initial infection with a type of HSV prevents reinfection with the same virus type—a person with a history of orofacial infection caused by HSV-1 cannot contract herpes whitlow or a genital infection caused by HSV-1.^{[citation needed]} In a monogamous couple, a seronegative female runs a greater than 30% per year risk of contracting an HSV infection from a seropositive male partner. If an oral HSV-1 infection is contracted first, seroconversion will have occurred after 6 weeks to provide protective antibodies against a future genital HSV-1 infection. Herpes simplex is a double stranded DNA virus.

Diagnosis

Primary orofacial herpes is readily identified by clinical examination of persons with no previous history of lesions and contact with an individual with known HSV-1 infection. The appearance and distribution of sores in these individuals typically presents as multiple, round, superficial oral ulcers, accompanied by acute gingivitis. Adults with non-typical presentation are more difficult to diagnose. Prodromal symptoms that occur before the appearance of herpetic lesions help differentiate HSV symptoms from the similar symptoms of other disorders, such as allergic stomatitis. When lesions do not appear inside the mouth, primary orofacial herpes is sometimes mistaken for impetigo, a bacterial infection. Common mouth ulcers (aphthous ulcer) also resemble intraoral herpes, but do not present a vesicular stage.

Genital herpes can be more difficult to diagnose than oral herpes, since most HSV-2-infected persons have no classical symptoms. Further confusing diagnosis, several other conditions resemble genital herpes, including fungal infection, lichen planus, atopic dermatitis, and urethritis. Laboratory testing is often used to confirm a diagnosis of genital herpes. Laboratory tests include: culture of the virus, direct fluorescent antibody (DFA) studies to detect virus, skin biopsy, and polymerase chain reaction (PCR) to test for presence of viral DNA. Although these procedures produce highly sensitive and specific diagnoses, their high costs and time constraints discourage their regular use in clinical practice.

Until recently, serological tests for antibodies to HSV were rarely useful to diagnosis and not routinely used in clinical practice. The older IgM serologic assay could not differentiate between antibodies generated in response to HSV-1 or HSV-2 infection. However, the new Immunodot glycoprotein G-specific (IgG) HSV test is more than 98% specific at discriminating HSV-1 from HSV-2. It is the opinion of some modern medical professionals that the new IgG test should always be clinically preferred to the old IgM test, however not all doctors appear to be informed of the availability of the newer, reliable IgG tests.

Prevention

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

As with almost all sexually transmitted infections, women are more susceptible to acquiring genital HSV-2 than men. On an annual basis, without the use of antivirals or condoms, the transmission risk of HSV-2 from infected male to female is approximately 8–11%. 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—meaning the infected partner will be seropositive but symptom free—by about 50%. Condom use also reduces the transmission risk significantly. Condom use is much more effective at preventing male to female transmission than vice-versa. The effects of combining antiviral and condom use is roughly additive, thus resulting in approximately a 75% combined reduction in annual transmission risk.^{[citation needed]} These figures reflect experiences with subjects having frequently recurring genital herpes (>6 recurrences per year). Subjects with low recurrence rates and those with no clinical manifestations were excluded from these studies.^{[citation needed]} Previous HSV-1 infection appears to reduce the risk for acquisition of HSV-2 infection among women by a factor of 3.

However, asymptomatic carriers of the HSV-2 virus are still contagious. In many infections, the first symptom a person will have of their own infection is the horizontal transmission to a sexual partner or the vertical transmission of neonatal herpes to a newborn at term. Since most asymptomatic individuals are unaware of their infection, they are considered at high risk for spreading HSV.^{[citation needed]}

In October 2011, it was reported that the anti-HIV drug tenofovir, when used topically in a microbicidal vaginal gel, reduced herpes virus sexual transmission by 51%.

Barrier methods

Condoms offer moderate protection against HSV-2 in both men and women, with consistent condom users having a 30% lower risk of HSV-2 acquisition compared with those that never use condoms. A female condom can provide greater protection than the male condom, as it covers the labia. The virus cannot pass through a synthetic condom, but a male condom's effectiveness is limited because herpes ulcers may appear on areas not covered by the male condom. Neither type of condom prevents contact with the scrotum, anus, buttocks, or upper thighs, areas that may come in contact with ulcers or genital secretions during sexual activity. Protection against herpes simplex depends on the site of the ulcer; therefore if ulcers appear on areas not covered by condoms, abstaining from sexual activity until the ulcers are fully healed is one way to limit risk of transmission. The risk is not eliminated, however, as viral shedding capable of transmitting infection may still occur while the infected partner is asymptomatic. The use of condoms or dental dams also limits the transmission of herpes from the genitals of one partner to the mouth of the other (or vice versa) during oral sex. When one partner has a herpes simplex infection and the other does not, the use of antiviral medication, such as valaciclovir, in conjunction with a condom further decreases the chances of transmission to the uninfected partner. Topical microbicides that contain chemicals that directly inactivate the virus and block viral entry are being investigated.

Antivirals

Antivirals may reduce asymptomatic shedding; it is believed asymptomatic genital HSV-2 viral shedding occurs on 20% of days per year in patients not undergoing antiviral treatment, versus 10% of days while on antiviral therapy.

Pregnancy

The risk of transmission from mother to baby is highest if the mother becomes infected at around the time of delivery (30% to 60%), since insufficient time will have occurred for the generation and transfer of protective maternal antibodies before the birth of the child. In contrast, the risk falls to 3% if it is a recurrent infection, and is 1–3% is the woman seropositive for both HSV-1 and HSV-2, and is less than 1% if there are no visible lesions. Women seropositive for only one type of HSV are only half as likely to transmit HSV as infected seronegative mothers. To prevent neonatal infections, seronegative women are recommended to avoid unprotected oral-genital contact with an HSV-1 seropositive partner and conventional sex with a partner having a genital infection during the last trimester of pregnancy. Mothers infected with HSV are advised to avoid procedures that would cause trauma to the infant during birth (e.g. fetal scalp electrodes, forceps, and vacuum extractors) and, should lesions be present, to elect caesarean section to reduce exposure of the child to infected secretions in the birth canal. The use of antiviral treatments, such as acyclovir, given from the 36th week of pregnancy, limits HSV recurrence and shedding during childbirth, thereby reducing the need for caesarean section.

Acyclovir is the recommended antiviral for herpes suppressive therapy during the last months of pregnancy. The use of valaciclovir and famciclovir, while potentially improving compliance have less well determined safety in pregnancy.

Treatment

There is no method to eradicate herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks. Analgesics such as ibuprofen and acetaminophen can reduce pain and fever. Topical anesthetic treatments such as prilocaine, lidocaine, benzocaine or tetracaine can also relieve itching and pain.

Antiviral

The antiviral medication acyclovir

There are several antivirals that are effective for treating herpes including: aciclovir (acyclovir), valaciclovir (valacyclovir), famciclovir, and penciclovir. Aciclovir was the first discovered and is now available in generic. Valacyclovir is also available as a generic.

Evidence supports the use of aciclovir and valaciclovir in the treatment of herpes labialis as well as herpes infections in people with cancer. The evidence to support the use of acyclovir in primary herpetic gingivostomatitis is less strong.

Topical

A number of topical antivirals are effective for herpes labialis including acyclovir, penciclovir, and docosanol.

Alternative medicine

Certain dietary supplements and alternative remedies are claimed to be beneficial in the treatment of herpes. There is however insufficient evidence to support use of many of these compounds including echinacea, eleuthero, L-lysine, zinc, monolaurin bee products and aloe vera. While there are a number of small studies showing possible benefit from monolaurin, L-lysine, aspirin, lemon balm, topical zinc or licorice root cream in treatment, these are preliminary studies that have not been confirmed by higher quality randomized controlled studies.

Prognosis

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

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

The causes of reactivation are uncertain, but several potential triggers have been documented. A recent study (2009) showed that the protein VP16 plays a key role in reactivation of the dormant virus. Changes in the immune system during menstruation may play a role in HSV-1 reactivation. Concurrent infections, such as viral upper respiratory tract infection or other febrile diseases, can cause outbreaks. Reactivation due to infection is the likely source of the historic terms cold sore and fever blister.

Other identified triggers include: local injury to the face, lips, eyes, or mouth, trauma, surgery, radiotherapy, and exposure to wind, ultraviolet light, or sunlight.

The frequency and severity of recurrent outbreaks vary greatly between people. Some individuals' outbreaks can be quite debilitating with large, painful lesions persisting for several weeks, while others will experience only minor itching or burning for a few days. There is some evidence that genetics plays a role in the frequency of cold sore outbreaks. An area of human chromosome 21 that includes 6 genes has been linked to frequent oral herpes outbreaks. An immunity to the virus is built over time. Most infected individuals will experience fewer outbreaks and outbreak symptoms will often become less severe. After several years, some people will become perpetually asymptomatic and will no longer experience outbreaks, though they may still be contagious to others. Immuno-compromised individuals may experience episodes that are longer, more frequent, and more severe. Antiviral medication has been proven to shorten the frequency and duration of outbreaks. Outbreaks may occur at the original site of the infection or in proximity to nerve endings that reach out from the infected ganglia. In the case of a genital infection, sores can appear at the original site of infection or near the base of the spine, the buttocks, or the back of the thighs. HSV-2 infected individuals are at higher risk for acquiring HIV when practicing unprotected sex with HIV-positive persons, in particular during an outbreak with active lesions.

Epidemiology

Main article: Epidemiology of herpes simplex

Worldwide rates of either HSV-1 and/or HSV-2 are between 60-95% in adults. HSV1 is more common than HSV2 with rates of both increasing as people age. HSV-1 rates are between 70% to 80% in populations of low socio-economic status and 40% to 60% in populations of improved socio-economic status. Prevalence of HSV-2 is those between the ages of 15 and 50 is approximately 535 million as of 2003 or 16% of the population with greater rates among women and in those in the developing world. Rates of infection are determined by the presence of antibodies against either viral species.

An estimated 536 million people worldwide were infected with HSV-2 in 2003, with the highest rates in sub-Saharan Africa and the lowest rates in western Europe.

In the US, 57.7% of the population is infected with HSV-1 and 16.2% are infected with HSV-2. Among those HSV-2 seropositive, only 18.9% were aware that they were infected. During 2005–2008, the prevalence of HSV-2 was 39.2% in blacks and 20.9% in women.

History

Herpes has been known for at least 2,000 years. It is said that Emperor Tiberius banned kissing in Rome for a time due to so many people having cold sores. In the 16th century Romeo and Juliet, it is mentioned that there are blisters "o'er ladies' lips." In 18th century it was so common among prostitutes that it was called "a vocational disease of women." The term Herpes Simplex appeared in Richard Boulton's A System of Rational and Practical Chirurgery in 1713, where the terms Herpes miliaris and Herpes exedens also appeared. Herpes was not found to be a virus until the 1940s.

Herpes antiviral therapy began in the early 1960s with the experimental use of medication that interfered with viral replication called deoxyribonucleic acid (DNA) inhibitors. The original use was against normally fatal or debilitating illness such as adult encephalitis, keratitis, in immunocompromised (transplant) patients, or disseminated herpes zoster. The original compounds used were 5-iodo-2'-deoxyuridine, AKA idoxuridine, IUdR, or(IDU) and 1-β-D-arabinofuranosylcytosine or ara-C, later marketed under the name cytosar or cytorabine. The usage expanded to include topical treatment of herpes simplex, zoster, and varicella. Some trials combined different antivirals with differing results. The introduction of 9-β-D-arabinofuranosyladenine, AKA ara-A or vidarabine, considerably less toxic than Ara-C, in the mid-1970s, heralded the way for the beginning of regular neonatal antiviral treatment. Vidarabine was the first systemically administered antiviral medication with activity against HSV for which therapeutic efficacy outweighed toxicity for the management of life-threatening HSV disease. Intravenous vidarabine was licensed for use by the U.S. Food and Drug Administration (FDA) in 1977. Other experimental antivirals of that period included: Heparin, trifluorothymidine (TFT), Ribivarin, interferon, Virazole, and 5-methoxymethyl-2'-deoxyuridine (MMUdR). The introduction of 9-(2-hydroxyethoxymethyl)guanine, AKA acyclovir, in the late 1970s raised antiviral treatment another notch and led to vidarabine vs. acyclovir trials in the late 1980s. The lower toxicity and ease of administration over vidarabine has led to acyclovir becoming the drug of choice for herpes treatment after it was licensed by the FDA in 1998. Another advantage in the treatment of neonatal herpes included greater reductions in mortality and morbidity with increased dosages, something that did not occur when compared with increased dosages of vidarabine. On the other side of the equation, acyclovir seems to inhibit antibody response and newborns on acyclovir antiviral treatment experienced a slower rise in antibody titer than those on vidarabine.

Society and culture

Herpes simplex was not always stigmatised. It was merely a cold sore in an unusual place until the 1970s. As late as 1975, a study of "Psychological morbidity in a clinic for sexually transmitted disease” does not mention herpes simplex because at that time, there was no significant morbidity problem (i.e. mental anxiety or illness) associated with the virus.

Pedro Cuatrecasas states, "during the R&D of acyclovir (Zovirax), marketing [department of Burroughs Wellcome] insisted that there were 'no markets’ for this compound. Most had hardly heard of genital herpes...” Thus marketing the medical condition – separating the 'normal cold sore’ from the 'stigmatized genital infection’ was to become the key to marketing the drug, a process now known as 'disease mongering’.

Since the creation of the herpes hype, some people experience negative feelings related to the condition following diagnosis, in particular if they have acquired the genital form of the disease. Feelings can include depression, fear of rejection, feelings of isolation, fear of being found out, and self-destructive feelings. These feelings usually lessen over time. Much of the hysteria and stigma surrounding herpes stems from a media campaign beginning in the late 1970s and peaking in the early 1980s. There were multiple articles worded in fear-mongering and anxiety-provoking terminology, such as the now ubiquitous "attacks," "outbreaks," "victims," and "sufferers." At one point the term "herpetic" even entered the popular lexicon. The articles were published by Reader's Digest, U.S. News, and Time magazine, among others. A made-for-TV movie was named Intimate Agony. The peak was when Time magazine had 'Herpes: The New Scarlet Letter' on the cover in August 1982, forever stigmatizing the word in the public mind. Herpes support groups have been formed in the United States and the UK, providing information about herpes and running message forums and dating websites for sufferers. People with the herpes virus are often hesitant to divulge to other people, including friends and family, that they are infected. This is especially true of new or potential sexual partners whom they consider casual.

Research

Main article: Herpes simplex research

Researchers at the University of Florida have made a Hammerhead ribozyme that targets and cleaves the mRNA of essential genes in HSV-1. The hammerhead, which targets the mRNA of the UL20 gene, greatly reduced the level of HSV-1 ocular infection in rabbits, and reduced the viral yield in vivo. The gene-targeting approach uses a specially designed RNA enzyme to inhibit strains of the herpes simplex virus. The enzyme disables a gene responsible for producing a protein involved in the maturation and release of viral particles in an infected cell. The technique appears to be effective in experiments with mice and rabbits, but further research is required before it can be attempted in people infected with herpes.

Another possibility to eradicate the HSV-1 variant is being pursued by a team at Duke University. By figuring out how to switch all copies of the virus in the host from latency to their active stage at the same time, rather than the way the virus copies normally stagger their activity stage, leaving some dormant somewhere at all times, it is thought that conventional anti-viral drugs can kill the entire virus population completely, since they can no longer hide in the nerve cells. One class of drugs called antagomir could serve this purpose. These are chemically engineered oligonucleotides or short segments of RNA, that can be made to mirror their target genetic material, namely herpes microRNAs. They could be engineered to attach and thus 'silence' the microRNA, thus rendering the virus incapable of remaining latent in its host. Professor Cullen believes a drug could be developed to block the microRNA whose job it is to suppress HSV-1 into latency.

References

External links

• Herpes simplex at the Open Directory Project

UpToDate Contents

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• 1. 性器単純ヘルペスウイルス感染の治療 treatment of genital herpes simplex virus infection
• 2. 性器単純ヘルペスウイルス感染の疫学、臨床症状、および診断 epidemiology clinical manifestations and diagnosis of genital herpes simplex virus infection
• 3. 性器単純ヘルペスウイルス感染と妊娠 genital herpes simplex virus infection and pregnancy
• 4. 性器ヘルペスウイルス感染の予防 prevention of genital herpes virus infections
• 5. HIV感染患者における薬剤抵抗性性器単純ヘルペスウイルス感染の治療 treatment of drug resistant genital herpes simplex virus infection in hiv infected patients

English Journal

• A potentiometric biosensor for rapid on-site disease diagnostics.

• Tarasov A1, Gray DW2, Tsai MY3, Shields N2, Montrose A4, Creedon N4, Lovera P4, O'Riordan A4, Mooney MH2, Vogel EM3.
• Biosensors & bioelectronics.Biosens Bioelectron.2016 May 15;79:669-78. doi: 10.1016/j.bios.2015.12.086. Epub 2015 Dec 24.
• Quantitative point-of-care (POC) devices are the next generation for serological disease diagnosis. Whilst pathogen serology is typically performed by centralized laboratories using Enzyme-Linked ImmunoSorbent Assay (ELISA), faster on-site diagnosis would infer improved disease management and treatm
• PMID 26765531

• Cytomegalovirus Pneumonia in Patients with Rheumatic Diseases After Immunosuppressive Therapy: A Single Center Study in China.

• Xue Y, Jiang L, Wan WG, Chen YM, Zhang J, Zhang ZC1.
• Chinese medical journal.Chin Med J (Engl).2016 5th Feb;129(3):267-273. doi: 10.4103/0366-6999.174490.
• BACKGROUND: Rheumatic diseases involve multiple organs that are affected by immunological mechanisms. Treatment with corticosteroids and immunosuppressive agents may also increase the frequency of infection. Cytomegalovirus (CMV) is a widespread herpes virus and a well-recognized pathogen, which cau
• PMID 26831226

• Corrigendum: Clinical Efficacy of Oral Ganciclovir for Prophylaxis and Treatment of Recurrent Herpes Simplex Keratitis.

• [No authors listed]
• Chinese medical journal.Chin Med J (Engl).2016 5th Jan;129(1):115. doi: 10.4103/0366-6999.172610.
• [This corrects the article DOI: 10.4103/0366-6999.147808.].
• PMID 26712448

• In the Cradle of Death: A Rare Case of Intrauterine Herpes Simplex Virus Infection.

• Co MA1, Koneru M1, Santiago J1, Beeram MR1, Uddin MN2.
• Clinical pediatrics.Clin Pediatr (Phila).2016 Mar;55(3):301-3. doi: 10.1177/0009922815596071. Epub 2015 Jul 15.
• PMID 26183325

Japanese Journal

• 運動障害が疼痛に先行した帯状疱疹痛の1症例

• 武川 仁子
• 麻酔 61(7), 752-754, 2012-07
• NAID 40019379231

• 悪性中皮腫の遺伝子治療 : 腫瘍溶解性ウイルスによる次世代のがん遺伝子治療

• 高橋 克仁,山村 倫子
• 呼吸器内科 21(6), 518-523, 2012-06
• NAID 40019361316

• Herpes simplex virus US3 protein kinase regulates host responses and determines neurovirulence

• Mori Isamu
• Microbiology and immunology 56(6), 351-355, 2012-06
• NAID 40019311478

Related Links

• Herpes simplex - Wikipedia, the free encyclopedia

Herpes simplex (Greek: ἕρπης herpēs, "creeping" or "latent") is a viral disease from the herpesviridae family caused by both Herpes simplex virus type 1 (HSV-1 ) and type 2 (HSV-2). Infection with the herpes virus is categorized into one of ...

• STD Facts - Genital Herpes

19 Sep 2012 ... Genital Herpes Fact Sheet from CDC. What is Herpes? How common is Herpes? How do people get Herpes? And more...

• Herpes Information Resource - Genital Herpes (HSV 2) and Oral ...

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★リンクテーブル★

リンク元	「100Cases 16」「疱疹」「ヘルペス」
拡張検索	「Kaposi sarcoma herpesvirus」「Kaposi's sarcoma-associated herpes virus」「Kaposi's sarcoma-associated herpesvirus」「alphaherpesvirus」「herpes simplex genitalis」

「100Cases 16」

　　[★]

☆case16　膝の痛み

■glossary

indigestion 消化障害、消化不良

■症例

80歳　男性

主訴：左膝の痛みと腫脹

現病歴：左膝の痛みを2日前から認めた。膝は発熱・腫脹しており、動かすと疼痛を生じる。時々胸焼けと消化不良が見られる。6ヶ月前のhealth checkで、高血圧(172/102mmHg)と血中クレアチニンが高い(正常高値)こと以外は正常といわれた。その4週間数回血圧を測定したが、高値が継続したため、2.5mg bendrofluamethizide(UK)/ベンドロフルメチアジドbendroflumethiazide(US)で治療を開始した。最近の血圧は138/84 mmHgであった。

喫煙歴：なし。

飲酒歴：一週間に平均4unit。

既往歴：股関節に中程度(mild)の変形性関節症

家族歴：特記なし

服薬歴：アセトアミノフェン(股関節の疼痛に対して)

身体所見 examination

　血圧 142/86mmHg。体温37.5℃。脈拍88/分。grade 2 hypertensive retinopathy(高血圧症性網膜症)。心血管系、呼吸器系に検査場異常なし。手にDIPにヘバーデン結節なし。

　左膝が発熱し腫脹している。関節内に液、patellar tap陽性。90℃以上膝関節を屈曲させると痛みを生じる。右の膝関節は正常に見える。

検査　investigation

　生化学：白血球増多、ESR上昇、尿素高値、グルコース高値

　単純X線：関節間隙やや狭小。それ以外に異常は認めない。

■problem list

　#1 左膝の痛み

　#2 胸焼け

　#3 消化不良

　#4 高血圧

　#5 クレアチニン正常高値

　#6 股関節の変形性リウマチ

　#7 高血圧性網膜症

■考え方

　・関節痛の鑑別診断を考える。

　・VINDICATEで考えてみてもよいでしょう。

　・関節痛の頻度としては　外傷＞慢性疾患(OAなど)＞膠原病＞脊椎疾患＞悪性腫瘍

■関節痛の鑑別疾患

DIF 282

V Vascular 血友病 hemophilia, 壊血病 scurvy, 無菌性骨壊死 aseptic bone necrosis (Osgood-Schlatter diseaseとか)

I Inflammatory 淋疾 gonorrhea, ライム病 lyme disease, 黄色ブドウ球菌 Staphylococcus, 連鎖球菌 Streptococcus, 結核 tuberculosis, 梅毒 syphilis, 風疹 rubella, 単純ヘルペス herpes simplex, HIV human immunodeficiency virus, サイトメガロウイルス cytomegalovirus

N Neoplastic disorders 骨原性肉腫 osteogenic sarcoma, 巨細胞腫 giant cell tumors

D Degenerative disorders degenerative joint disease or 変形性関節症 osteoarthritis

I Intoxication 痛風 gout (uric acid), 偽痛風 pseudogout (calcium pyrophosphate), ループス症候群 lupus syndrome of hydralazine (Apresoline) and procainamide, gout syndrome of diuretics

C Congenital and acquired malformations bring to mind the joint deformities of tabes dorsalis and syringomyelia and congenital dislocation of the hip. Alkaptonuria is also considered here.

A Autoimmune indicates (多い)関節リウマチ RA (可能性)血清病 serum sickness, 全身性エリテマトーデス lupus erythematosus, リウマチ熱 rheumatic fever, ライター症候群 Reiter syndrome, 潰瘍性大腸炎 ulcerative colitis, クローン病=限局性回腸炎 regional ileitis, 乾癬性関節炎 psoriatic arthritis (老人であり得る)リウマチ性多発筋痛症 polymyalgia rheumatica

T Trauma 外傷性滑膜炎 traumatic synovitis, tear or rupture of the collateral or cruciate ligaments, 亜脱臼 subluxation or laceration of the meniscus (semilunar cartilage), 脱臼 dislocation of the joint or patella, a 捻挫　sprain of the joint, and fracture of the bones of the joint.

E Endcrine 先端肥大症 acromegaly, 閉経 menopause, 糖尿病 diabetes mellitus

■答え

　骨格筋系-関節炎-単関節炎-急性単関節炎

　痛風　尿酸　→　発熱、ESR↑、白血球↑

　偽痛風　ピロリン酸カルシウム

　高齢女性でチアジド系利尿薬の使用により痛風が誘発されやすい。特に腎機能低下、糖尿病の人はこのリスクが高まる。

■(BSTからの知識「)循環器領域での利尿薬

・心不全の治療において、循環血漿量を減らし、心臓の前負荷を軽減する。

・利尿薬は高尿酸血症を起こす。(けど、心不全の治療において高尿酸血症になったからといって痛風を発症している患者はみたことない)

・電解質異常を起こしやすいので、血液生化学の検査でモニタして注意する。たとえば低Kで不整脈のリスクが高まる。

・チアジド系の利尿薬は血糖を上げるし、尿酸を上げる

・長期の使用で腎機能を低下させる

■initial plan

　Dx 1. 関節液の吸引：関節液の一般検査、生化学検査、培養検査、

　　　　・白血球が増加していれば急性炎症性であることを示す。

　　　　・偏光顕微鏡で関節液を検鏡する。

　　　　　・尿酸の結晶：針状結晶。negatively birefringent

　　　　　・ピロリン酸カルシウムの結晶：positively birefringent

　Tx 1. 関節液の吸引：炎症が軽度改善

　　 2. NSAIDによる疼痛管理

　　 3. PPI：NSAID潰瘍を予防するため

　　 4. ACE inhibitorの導入

「疱疹」

　　[★]

英

blister、herpes

関

水疱、ヘルペス

「ヘルペス」

　　[★]

英

herpes

関

疱疹

「Kaposi sarcoma herpesvirus」

　　[★] カポジ肉腫関連ヘルペスウイルス, KSHV

「Kaposi's sarcoma-associated herpes virus」

　　[★] カポジ肉腫関連ヘルペスウイルス

「Kaposi's sarcoma-associated herpesvirus」

　　[★] カポジ肉腫関連ヘルペスウイルス

「alphaherpesvirus」

　　[★]

• アルファヘルペスウイルス

「herpes simplex genitalis」

　　[★]

外陰部単純ヘルペス