Herpes
Herpes | |
---|---|
Other names | Herpes simplex |
Infectious disease | |
Symptoms | Blisters that break open and form small ulcers, fever, swollen lymph nodes[1] |
Duration | 2–4 weeks[1] |
Causes | Herpes simplex virus spread by direct contact[1] |
Risk factors | Decreased immune function, stress, sunlight[2][3] |
Diagnostic method | Based on symptoms, PCR, viral culture[1][2] |
Medication | Aciclovir, valaciclovir, paracetamol (acetaminophen), topical lidocaine[1][2] |
Frequency | 60–95% (adults)[4] |
Herpes simplex, often known simply as herpes, is a
Oral herpes involves the face or mouth. It may result in small
Herpes cycles between periods of active disease followed by periods without symptoms.[1] The first episode is often more severe and may be associated with fever, muscle pains, swollen lymph nodes and headaches.[1] Over time, episodes of active disease decrease in frequency and severity.[1]
There are two types of herpes simplex virus, type 1 (HSV-1) and type 2 (HSV-2).
The most effective method of avoiding genital infections is by avoiding vaginal, oral, manual, and anal sex.[1][11] Condom use decreases the risk.[1] Daily antiviral medication taken by someone who has the infection can also reduce spread.[1] There is no available vaccine[1] and once infected, there is no cure.[1] Paracetamol (acetaminophen) and topical lidocaine may be used to help with the symptoms.[2] Treatments with antiviral medication such as aciclovir or valaciclovir can lessen the severity of symptomatic episodes.[1][2]
Worldwide rates of either HSV-1 or HSV-2 are between 60% and 95% in adults.[4] HSV-1 is usually acquired during childhood.[1] Since there is no cure for either HSV-1 or HSV-2, rates of both inherently increase as people age.[4] Rates of HSV-1 are between 70% and 80% in populations of low socioeconomic status and 40% to 60% in populations of improved socioeconomic status.[4] An estimated 536 million people worldwide (16% of the population) were infected with HSV-2 as of 2003 with greater rates among women and those in the developing world.[12] Most people with HSV-2 do not realize that they are infected.[1]
Etymology
The name is from Greek: ἕρπης herpēs, which is related to the meaning "to creep", referring to spreading blisters.[13] The name does not refer to latency.[14]
Signs and symptoms
HSV infection causes several distinct medical
In all cases, HSV is never removed from the body by the
Many people infected with HSV-2 display no physical symptoms—individuals with no symptoms are described as asymptomatic or as having subclinical herpes.[17] However, infection with herpes can be fatal.[18]
Types of 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 presentation. | |
Herpes labialis
|
Commonly referred to as cold sores or fever blisters, herpes labialis is the most common presentation of recurrent HSV-1 infection following the re-emergence of the virus from the trigeminal nerve. | |
Herpes genitalis | When symptomatic, the typical manifestation of a primary HSV-1 or HSV-2 genital infection is clusters of inflamed 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 the nail cuticle. Individuals who participate in contact sports such as wrestling, rugby, and football (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 meningitis
|
Herpes simplex encephalitis (HSE) is a rare life-threatening condition that is thought to be caused by the transmission of HSV-1 either from the nasal cavity to the brain's temporal lobe or from a peripheral site on the face, along the trigeminal nerve axon, to the brainstem.[19][20][21][22] Despite its low incidence, HSE is the most common sporadic fatal encephalitis worldwide. HSV-2 is the most common cause of Mollaret's meningitis, a type of recurrent viral meningitis. | |
Herpes esophagitis | Symptoms may include painful swallowing ( organ transplants ).
|
Other
Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicle.[24]: 369 [25]
Bell's palsy
Although the exact cause of
Alzheimer's disease
HSV-1 has been proposed as a possible cause of
Pathophysiology
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.[34] 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 contracted by exposure to infected saliva, semen, vaginal fluid, or the fluid from herpetic blisters.[35] 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.[36] Virus enters into susceptible cells by entry receptors[37] such as nectin-1, HVEM and 3-O sulfated heparan sulfate.[38] Infected people who show no visible symptoms may still shed and transmit viruses through their skin; asymptomatic shedding may represent the most common form of HSV-2 transmission.[36] 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.[39] 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 12 annual recurrences to those with no recurrences.[36]
Antibodies that develop following an initial infection with a type of HSV can reduce the odds of reinfection with the same virus type.[40] 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.[41] 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.[40] Herpes simplex is a double-stranded DNA virus.[42]
Diagnosis
Classification
Herpes simplex virus is divided into two types.[4] However, each may cause infections in all areas.[4]
- HSV-1 causes primarily mouth, throat, face, eye, and central nervous system infections.[4]
- HSV-2 causes primarily anogenital infections.[4]
Examination
Primary orofacial herpes is readily identified by examination of persons with no previous history of lesions and contact with an individual with known HSV infection. The appearance and distribution of sores is typically presents as multiple, round, superficial oral ulcers, accompanied by acute
Genital herpes can be more difficult to diagnose than oral herpes, since most people have none of the classical symptoms.
Laboratory testing
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 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.[43]
Until the 1980s serological tests for antibodies to HSV were rarely useful to diagnosis and not routinely used in clinical practice.[43] The older IgM serologic assay could not differentiate between antibodies generated in response to HSV-1 or HSV-2 infection. However, a glycoprotein G-specific (IgG) HSV test introduced in the 1980s is more than 98% specific at discriminating HSV-1 from HSV-2.[44]
Differential diagnosis
It should not be confused with conditions caused by other viruses in the
Prevention
As with almost all sexually transmitted infections, women are more susceptible to acquiring genital HSV-2 than men.[45] On an annual basis, without the use of antivirals or condoms, the transmission risk of HSV-2 from infected male to female is about 8–11%.[41][46] 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 around 4–5% annually.[46] Suppressive antiviral therapy reduces these risks by 50%.[47] 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.[48][49] Condom use is much more effective at preventing male-to-female transmission than vice versa.[48] Previous HSV-1 infection may reduce the risk for acquisition of HSV-2 infection among women by a factor of three, although the one study that states this has a small sample size of 14 transmissions out of 214 couples.[50]
However, asymptomatic carriers of the HSV-2 virus are still contagious. In many infections, the first symptom people will have of their own infections 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.[51]
In October 2011, the anti-HIV drug
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 who never use condoms.
Antivirals
Antivirals may reduce asymptomatic shedding; asymptomatic genital HSV-2 viral shedding is believed to occur on 20% of days per year in patients not undergoing antiviral treatment, versus 10% of days while on antiviral therapy.[36]
Pregnancy
The risk of transmission from mother to baby is highest if the mother becomes infected around the time of delivery (30% to 60%),[58][59] 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 the infection is recurrent,[60] and is 1–3% if the woman is seropositive for both HSV-1 and HSV-2,[60][61] and is less than 1% if no lesions are visible.[60] 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.[16] The use of antiviral treatments, such as aciclovir, given from the 36th week of pregnancy, limits HSV recurrence and shedding during childbirth, thereby reducing the need for caesarean section.[16]
Aciclovir 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.
Management
No method eradicates herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks. Analgesics such as ibuprofen and paracetamol (acetaminophen) can reduce pain and fever. Topical anesthetic treatments such as prilocaine, lidocaine, benzocaine, or tetracaine can also relieve itching and pain.[62][63][64]
Antiviral
Several
Evidence supports the use of aciclovir and valaciclovir in the treatment of herpes labialis[68] as well as herpes infections in people with cancer.[69] The evidence to support the use of aciclovir in primary herpetic gingivostomatitis is weaker.[70]
Topical
A number of
Alternative medicine
Evidence is insufficient to support use of many of these compounds, including
Prognosis
Following active infection, herpes viruses establish a
Many HSV-infected people experience recurrence within the first year of infection.[16] 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 and are less painful and heal faster (within 5–10 days without antiviral treatment) than those occurring during the primary infection.[16] Subsequent outbreaks tend to be periodic or episodic, occurring on average four or five times a year when not using antiviral therapy.
The causes of reactivation are uncertain, but several potential triggers have been documented. A 2009 study showed the protein VP16 plays a key role in reactivation of the dormant virus.[75] Changes in the immune system during menstruation may play a role in HSV-1 reactivation.[76][77] Concurrent infections, such as viral upper respiratory tract infection or other febrile diseases, can cause outbreaks. Reactivation due to other infections 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;
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 experience only minor itching or burning for a few days. Some evidence indicates genetics play a role in the frequency of cold sore outbreaks. An area of human chromosome 21 that includes six genes has been linked to frequent oral herpes outbreaks. An immunity to the virus is built over time. Most infected individuals experience fewer outbreaks and outbreak symptoms often become less severe. After several years, some people become perpetually asymptomatic and no longer experience outbreaks, though they may still be contagious to others. Immunocompromised individuals may experience longer, more frequent, and more severe episodes. Antiviral medication has been proven to shorten the frequency and duration of outbreaks.[83] 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.[84]
Epidemiology
Worldwide rates of either HSV-1 and/or HSV-2 are between 60 and 95% in adults.
In the US, 58% of the population is infected with HSV-1[86] and 16% are infected with HSV-2. Among those HSV-2-seropositive, only 19% were aware they were infected.[87] During 2005–2008, the prevalence of HSV-2 was 39% in black people and 21% in women.[88]
The annual incidence in Canada of genital herpes due to HSV-1 and HSV-2 infection is not known (for a review of HSV-1/HSV-2 prevalence and incidence studies worldwide, see Smith and Robinson 2002). As many as one in seven Canadians aged 14 to 59 may be infected with herpes simplex type 2 virus[89] and more than 90 per cent of them may be unaware of their status, a new study suggests.[90] In the United States, it is estimated that about 1,640,000 HSV-2 seroconversions occur yearly (730,000 men and 910,000 women, or 8.4 per 1,000 persons).[91]
In British Columbia in 1999, the seroprevalence of HSV-2 antibody in leftover serum submitted for antenatal testing revealed a prevalence of 17%, ranging from 7% in women 15–19 years old to 28% in those 40–44 years.[92]
In Norway, a study published in 2000 found that up to 70–90% of genital initial infections were due to HSV-1.[93]
In Nova Scotia, 58% of 1,790 HSV isolates from genital lesion cultures in women were HSV-1; in men, 37% of 468 isolates were HSV-1.[94]
History
Herpes has been known for at least 2,000 years. Emperor Tiberius is said to have banned kissing in Rome for a time due to so many people having cold sores. In the 16th century Romeo and Juliet, blisters "o'er ladies' lips" are mentioned. In the 18th century, it was so common among prostitutes that it was called "a vocational disease of women".[95] 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.[95]
Herpes antiviral therapy began in the early 1960s with the experimental use of medications that interfered with viral replication called
Society and culture
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
In a 2007 study, 1,900 people (25% of which had herpes) ranked genital herpes second for social stigma, out of all sexually transmitted diseases (HIV took the top spot for STD stigma).[114][115][116]
Support groups
United States
A source of support is the National Herpes Resource Center which arose from the work of the American Sexual Health Association (ASHA).[117] The ASHA was created in 1914 in response to the increase in sexually transmitted diseases that had spread during World War I.[118] During the 1970s, there was an increase in sexually transmitted diseases. One of the diseases that increased dramatically was genital herpes. In response, ASHA created the National Herpes Resource Center in 1979. The Herpes Resource Center (HRC) was designed to meet the growing need for education and awareness about the virus. One of the projects of the HRC was to create a network of local support (HELP) groups. The goal of these HELP groups was to provide a safe, confidential environment where participants can get accurate information and share experiences, fears, and feelings with others who are concerned about herpes.[119][120]
UK
In the UK, the Herpes Association (now the Herpes Viruses Association) was started in 1982, becoming a registered charity with a Department of Health grant in 1985. The charity started as a string of local group meetings before acquiring an office and a national spread.[121]
Research
Research has gone into vaccines for both prevention and treatment of herpes infections.
As of October 2022, the U.S. FDA have not approved a vaccine for herpes.[122] However, there are herpes vaccines currently in clinical trials, such as Moderna mRNA-1608.[123] Unsuccessful clinical trials have been conducted for some glycoprotein subunit vaccines.[citation needed] As of 2017, the future pipeline includes several promising replication-incompetent vaccine proposals while two replication-competent (live-attenuated) HSV vaccine are undergoing human testing.[citation needed]
A
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External links
- Herpes at Curlie