Herpes simplex is a viral disease caused by the herpes simplex virus. Infection is categorized based on the infected part of the body. Oral herpes involves the face or mouth. This can cause small blisters in a group often called cold sores or blisters or fever may just cause a sore throat. Genital herpes, often only known as herpes, may have minimal symptoms or a blister form that breaks open and produces small ulcers. It usually heals more than two to four weeks. Tingling or shooting pain may occur before the blisters appear. Herpes cycle between periods of active disease followed by an asymptomatic period. The first episode is often more severe and may be associated with fever, muscle aches, swollen lymph nodes, and headaches. Over time, the episodes of active disease decrease in frequency and severity. Other disorders caused by herpes simplex include: herpetic whitlow when it involves the fingers, herpes eyes, herpes brain infection, and neonatal herpes when it affects the newborn, among others.
There are two types of herpes simplex virus, type 1 (HSV-1) and type 2 (HSV-2). HSV-1 more frequently causes infection around the mouth while HSV-2 more frequently causes genital infection. They are transmitted by direct contact with body fluids or lesions from infected individuals. Transmission may still occur when symptoms are not present. Genital herpes is classified as a sexually transmitted infection. It may spread to the baby during childbirth. Once infected, the virus is transported along the sensory nerve to the body of the nerve cells, where they live for life. The causes of recurrence may include: decreased immune function, stress, and sun exposure. Herpes of the mouth and genitalia are usually diagnosed based on the symptoms that appear. The diagnosis can be confirmed by viral culture or detecting herpes DNA in fluid from abrasions. Testing blood for antibodies against the virus can confirm previous infections but will be negative on new infections.
The most effective method to avoid genital infection is to avoid vaginal, oral, and anal sex. Condom use reduces the risk slightly. Daily antiviral drugs taken by someone who has the infection can also reduce the spread. There is no vaccine available and once infected, there is no cure. Paracetamol (acetaminophen) and topical lidocaine can be used to help with symptoms. Treatment with antiviral drugs such as aciclovir or valaciclovir may reduce the severity of symptomatic episodes.
Worldwide rates of either HSV-1 or HSV-2 are between 60% and 95% in adults. HSV-1 is usually obtained during childhood. Both rates increase with age. HSV-1 levels are between 70% and 80% in populations with low socioeconomic status and 40% to 60% in the socioeconomic status population better. An estimated 536 million people worldwide (16% of the population) were infected with HSV-2 in 2003 with higher rates among women and those in developing countries. Most people with HSV-2 are unaware that they are infected. His name is from Greek: ????? herp? which means "creep" or "latent".
Video Herpes simplex
Classification
Herpes simplex is divided into two types; HSV-1 primarily causes infections of the mouth, throat, face, eyes, and central nervous system, whereas HSV-2 primarily causes anogenital infections. However, each can cause infection in all areas.
Maps Herpes simplex
Signs and symptoms
HSV infection causes several different medical disorders. Common infections of the skin or mucosa may affect the face and mouth (orofacial herpes), genitalia (genital herpes), or the hand (herpetic whitlow). More serious disorders occur when the virus infects and damages the eyes (herpes keratitis), or attacks the central nervous system, damaging the brain (herpes encephalitis). People with immature or suppressing immune systems, such as newborns, transplant recipients, or people with AIDS, are prone to severe complications of HSV infection. HSV infection is also associated with a cognitive deficit of bipolar disorder, and Alzheimer's disease, although this often depends on the genetics of an infected person.
In all cases, HSV is never excluded from the body by the immune system. After primary infection, the virus enters the nerve at the site of primary infection, migrates to the neuron body cells, and becomes latent in the ganglion. As a result of primary infection, the body produces antibodies to certain types of HSV involved, preventing subsequent infections of that type in different places. In individuals infected with HSV-1, seroconversion after oral infection prevents additional HSV-1 infections such as whitlow, genital herpes, and eye herpes. Seroconversion HSV-1 previously seems to reduce the symptoms of HSV-2 infection, although HSV-2 can still be contracted.
Many people infected with HSV-2 have no physical symptoms - asymptomatic individuals are described as asymptomatic or have subclinical herpes.
More
Herpes simplex neonatal is an HSV infection in infants. This is a rare but serious condition, usually caused by vertical transmission of HSV-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 erosion on the folds of the skin, with the appearance of a cut blade. Herpetic sycosis is a recurrent or early herpes simplex infection that primarily attacks hair follicles. Herpeticum eczema is an infection with herpes virus in patients with chronic atopic dermatitis may cause the spread of herpes simples throughout the eczematous area.
Herpes keratoconjunctivitis, a primary infection, usually appears as a swelling of the conjunctiva and eyelid (blepharoconjunctivitis), accompanied by a small white itchy lesion on the surface of the cornea.
Herpetic sycosis is a recurrent or early herpes simplex infection that primarily attacks hair follicles. Bells palsy
Although the exact cause of Bell's palsy - a kind of facial paralysis - is unknown, it may be associated with reactivation of HSV-1. This theory has been disputed, however, because HSV is detected in a large number of individuals who have never experienced facial paralysis, and higher levels of antibodies to HSV are not found in HSV-infected individuals with Bell's palsy compared with those who do not. Antiviral can improve the condition slightly when used in conjunction with corticosteroids in those with severe disease.
Alzheimer's Disease
HSV-1 has been proposed as a possible cause of Alzheimer's disease. In the presence of certain gene variations (APOE-epsilon4 allele carrier), HSV-1 appears to be very damaging to the nervous system and increases a person's risk of developing Alzheimer's disease. The virus interacts with the components and lipoprotein receptors, which can cause its development.
Pathophysiology
Herpes is contracted by direct contact with an active lesion or body fluid from an infected person. Herpes transmission occurs between the discordant partners; a person with a history of infection (HSV seropositive) may transmit the virus to HSV seronegative people. The herpes simplex virus 2 is usually contracted through skin-to-skin direct contact with an infected individual, but can also be contracted by exposure to infected saliva, semen, vaginal fluid, or fluid from herpes blisters. To infect new individuals, HSV runs through tiny cracks in the skin or mucous membranes in the mouth or genital area. Even microscopic blisters on the mucous membrane are sufficient to allow entry of the virus.
Asymptomatic wetting of HSV occurs at some time in most individuals infected with herpes. This can occur more than a week before or after symptom relapse in 50% of cases. Viruses enter cells susceptible to entry receptors such as nectin-1, HVEM and 3-O heparan sulfate sulfate. Infected people who show no visible symptoms may still shed and pass the virus through their skin; asymptomatic shedding may represent the most common form of HSV-2 transmission. Asymptomatic shedding is more frequent in the first 12 months after obtaining HSV. Infection with HIV increases the frequency and duration of asymptomatic shedding. Some individuals may have lower shedding patterns, but the supporting evidence is not fully verified; no significant differences were seen in asymptomatic shedding frequencies when comparing people with one to 12 annual recurrences in those without recurrence.
Antibodies that develop after initial infection with HSV type prevent re-infection with the same type of virus - a person with a history of orofacial infection caused by HSV-1 can not have herpes whitlow or genital infection caused by HSV-1. In monogamous couples, seronegative women have a 30% annual risk of contracting HSV infection from seropositive male partners. If HSV-1 infection is first contracted, seroconversion will occur after 6 weeks to provide protective antibodies against future genital HSV-1 infection. Herpes simplex is a double stranded DNA virus.
Diagnosis
Primary orofacial herpes are readily identified by clinical examination in people who have no previous history of lesions and contact with individuals with known HSV-1 infection. The appearance and distribution of injuries to these individuals usually presents as multiple oral, round, superficial ulcers, accompanied by acute gingivitis. Adults with atypical presentations are more difficult to diagnose. The prodromal symptoms that occur prior to the appearance of herpetic lesions help differentiate HSV symptoms from other similar symptoms of disorders, such as allergic stomatitis. When the lesion does not appear in the mouth, primary orofacial herpes is sometimes mistakenly thought to be impetigo, a bacterial infection. Common mouth ulcers (aphthous ulcers) also resemble intraoral herpes, but do not show vesicular stages.
Genital herpes can be more difficult to diagnose than oral herpes, as most people infected with HSV-2 have no classic symptoms. Further diagnosis is confusing, some other conditions resemble genital herpes, including fungal infections, lichen planus, atopic dermatitis, and urethritis. Laboratory tests are often used to confirm the diagnosis of genital herpes. Laboratory tests include virus culture, fluorescent antibody (DFA) directly to detect viruses, skin biopsies, and polymerase chain reactions to test for the presence of viral DNA. Although this procedure produces highly sensitive and specific diagnoses, high costs and time constraints hamper their routine use in clinical practice.
Until 1980 serological tests for antibodies to HSV were seldom useful for diagnosis and were not routinely used in clinical practice. Older IgM serology tests can not distinguish between the antibodies produced in response to HSV-1 or HSV-2 infection. However, the HSV G-specific glycoprotein (IgG) test introduced in 1980 was more than 98% specific in HSV-1 differentiation from HSV-2.
It should not be confused with conditions caused by other viruses in the herpesviridae family such as herpes zoster, caused by varicella zoster virus. The differential diagnosis includes hand, foot and mouth disease because of similar lesions of the skin.
Prevention
Like almost all sexually transmitted infections, women are more prone to acquiring HSV-2 genital than men. Every year, without the use of antivirals or condoms, the risk of HSV-2 transmission from infected men to women is about 8-11%. This is believed to be due to exposure of the increased mucosal tissue to potential infection sites. The risk of transmission from infected women to men is about 4-5% per year. A suppressive antiviral therapy reduces this risk by 50%. Antivirals also help prevent the development of HSV symptoms in an infection scenario, which means the infected partner will be seropositive but symptom-free by about 50%. Condom use also reduces the risk of transmission significantly. Condom use is far more effective in preventing male-to-female transmission than otherwise . Previous HSV-1 infection may reduce the risk of acquiring HSV-2 infection among women by a factor of three, although one study stated it has a small sample size of 14 transmissions of 214 pairs.
However, asymptomatic carriers of the HSV-2 virus are still contagious. In many infections, the first symptoms of people will have their own infection is a horizontal transmission to a sexual partner or vertical transmission of neonatal herpes to a newborn. Because most asymptomatic individuals are unaware of their infection, they are considered at high risk for spreading HSV.
In October 2011, tenofovir anti-HIV drugs, when used topically in microbicidal vaginal gel, reportedly reduced the transmission of the herpes sexual virus by 51%.
Barrier method
Condoms offer moderate protection against HSV-2 in men and women, with consistent condom users having a 30% lower risk of acquiring HSV-2 compared with those who never used condoms. Female condoms can provide greater protection than male condoms, because male condoms cover the labia. Viruses can not pass through synthetic condoms, but the effectiveness of male condoms is limited because herpes ulcers can appear in areas not covered by it. Both types of condoms prevent contact with the scrotum, anus, buttocks, or upper thighs, areas that may be in contact with ulcers or genital secretions during sexual activity. The protection of herpes simplex depends on the location of the ulcer; Therefore, if ulcers appear in areas not covered by condoms, not performing sexual activity until ulcers are fully healed is one way to limit the risk of transmission. However, the risk is not eliminated, as the release of a virus capable of transmitting infection may still occur when an infected partner is asymptomatic. The use of condoms or dental dam also limits transmission of herpes from one partner's genitals to the other (or otherwise ) during oral sex. When one partner has herpes simplex infection and the other does not, the use of antiviral drugs, such as valacyclovir, along with condoms, further reduces the likelihood of transmission to an uninfected partner. Topical microbicides containing chemicals that directly disable viruses and block the entry of viruses are under investigation.
Antiviral can reduce asymptomatic shedding; without genital symptoms HSV-2 viral shedding is believed to occur in 20% of days per year in patients not on antiviral medication, versus 10% of the days of antiviral therapy.
Pregnancy
The risk of mother-to-child transmission is highest if the mother becomes infected around the time of delivery (30% to 60%), because insufficient time will occur for generations and transfer of protective mother's antibodies before the child's birth. Conversely, the risk drops to 3% if the infection recurs, and 1-3% if the woman is seropositive for both HSV-1 and HSV-2, and less than 1% if no visible lesions are present. Seropositive women for only one type of HSV are only half as likely to transmit HSV as a seronegative infected mother. To prevent neonatal infection, seronegative women are advised to avoid unprotected oral-genital contact with HSV-1-seropositive and conventional sex couples with a partner who has genital infection during the last trimester of pregnancy. Mothers infected with HSV are advised to avoid procedures that will cause trauma to infants during birth (for example, fetal scalp electrodes, forceps, and vacuum extractors) and, there should be lesions, to choose a caesarean section to reduce the child's exposure to infected infections. on the birth canal. The use of antiviral medications, such as acyclovir, is given from 36 weeks of pregnancy, limiting HSV recurrence and shedding during labor, thereby reducing the need for a cesarean section.
Aciclovir is the recommended antiviral therapy for herpes suppression during the last months of pregnancy. The use of valaciclovir and famciclovir, while potentially enhancing adherence, has less defined safety in pregnancy.
Management
There is no method of eradicating the herpes virus from the body, but antiviral drugs can reduce the frequency, duration, and severity of the outbreak. 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.
Some antiviral drugs are effective for treating herpes, including acyclovir, valacyclovir (valacyclovir), famiclovir, and penciclovir. Acyclovir is the first to be found and is now available generically. Valacyclovir is also available as a generic and slightly more effective than acyclovir to reduce healing time of lesions.
Evidence supports the use of acyclovir and valacyclovir in the treatment of herpes labialis as well as herpes infection in people with cancer. Evidence to support the use of acyclovir in primary herpes gingivostomatitis is weaker.
Topic
A number of topical antivirals are effective for herpes labialis, including acyclovir, penciclovir, and docosanol.
Alternative medicine
The evidence is not sufficient to support the use of many of these compounds, including echinacea, eleuthero, L-lysine, zinc, monolaurin bee products, and aloe vera. While a small number of studies have demonstrated the possible benefits of monolaurin, L-lysine, aspirin, lemon balm, topical zinc, or licorice root cream in treatment, this preliminary study has not been confirmed by high-quality randomized controlled studies.
Prognosis
After active infection, the herpes virus forms latent infection in the sensory and autonomic ganglia of the nervous system. Double-stranded DNA from viruses is incorporated into cell physiology by the infection of the nucleus of the nerve cell body. HSV latency is static; no virus produced; and is controlled by a number of viral genes, including latency-related transcripts.
Many people infected with HSV experience a relapse within the first year of infection. Prodrom precedes the development of the lesion. Prodromal symptoms include tingling (paresthesia), itching, and pain where the lumbosacral nerves supply the skin. Prodrom may occur for several days or as short as several hours before the lesion develops. Starting antiviral treatment when prodrom is experienced can reduce the appearance and duration of lesions in some individuals. During recurrence, fewer lesions are likely to develop and less painfully and quickly heal (within 5-10 days without antiviral treatment) than those occurring during primary infection. Subsequent events tend to be periodic or episodic, occurring on average four or five times a year when not using antiviral therapy.
The cause of reactivation is uncertain, but some potential triggers have been documented. A 2009 study showed that VP16 protein plays a key role in the reactivation of inactive viruses. Immune system changes during menstruation can play a role in HSV-1 reactivation. Concurrent infections, such as upper respiratory tract infections or other febrile illness, can cause an outbreak. Reactivation due to other infections is a possible source of the historic term 'cold sore' and 'blister fever'.
Other identified triggers include localized injuries to the face, lips, eyes, or mouth; trauma; operation; radiotherapy; and exposure to wind, ultraviolet light, or sunlight.
The frequency and severity of recurrent outbreaks vary greatly between people. Outbreaks of some individuals can be very debilitating, with large, painful lesions persisting for several weeks, while others experience only slight itching or burning for several days. Some evidence suggests genetics play a role in the frequency of cold sore outbreaks. The human chromosomal area 21 which includes six genes has been associated with frequent oral herpes. An immunity to viruses builds over time. Most people who are infected experience fewer outbreaks and the symptoms of outbreaks often become less severe. After a few years, some people become continuously asymptomatic and no longer have epidemics, although they may still be transmitted to others. Immunocompromised individuals may experience episodes that are longer, more frequent, and more severe. Antiviral drugs have been shown to shorten the frequency and duration of outbreaks. Epidemics may occur in the original site of infection or close to the reaching nerve endings of the infected ganglia. In case of genital infection, the wound can appear in the original place of infection or near the base of the spine, buttocks, or thighs. Individuals infected with HSV-2 are at higher risk for contracting HIV while having unprotected sex with HIV-positive people, especially during outbreaks with active lesions.
Epidemiology
HSV-1 and/or HSV-2 levels worldwide are between 60 and 95% in adults. HSV-1 is more common than HSV-2, with both rates increasing with age. HSV-1 levels are between 70% and 80% in populations with low socioeconomic status and 40% to 60% in populations with better socioeconomic status. An estimated 536 million people or 16% of the population worldwide are infected with HSV-2 in 2003 with higher rates among women and in developing countries. The rate of infection is determined by the presence of antibodies against the virus species.
In the US, 58% of the population is infected with HSV-1 and 16% are infected with HSV-2. Among those HSV-2-seropositive, only 19% are aware that they are infected. During 2005-2008, the prevalence of HSV-2 was 39% in blacks and 21% in women.
The annual incidence in Canadian genital herpes due to HSV-1 and HSV-2 infection is unknown (for HSV-1/HSV-2 prevalence review and incident studies worldwide, see Smith and Robinson 2002). As many as one in seven Canadians aged 14 to 59 may be infected with type 2 herpes simplex virus and more than 90 percent of them may be unaware of their status, a new study suggests. In the United States, it is estimated that around 1.64 million HSV-2 seroconversions occur each year (730,000 men and 910,000 women, or 8.4 per 1,000 people).
In British Columbia in 1999, serum seroprevalence of HSV-2 in serum remnants sent for antenatal testing revealed a prevalence of 17%, ranging from 7% in women 15-19 years to 28% in those aged 40-44 years.
In Norway, a study published in 2000 found that up to 70-90% of genital early infections are caused by HSV-1.
In Nova Scotia, 58% of 1,790 HSV isolates from cultured female genital lesions were HSV-1; in men, 37% of the 468 isolates were HSV-1.
History
Herpes has been known for at least 2,000 years. Emperor Tiberius is said to have been banned from kissing in Rome for a while because so many people suffered cold sores. In the 16th century Romeo and Juliet , blisters "o'er ladies' lips" were mentioned. In the 18th century, it was very common among prostitutes called "women's vocational disease". The term 'herpes simplex' appeared in Richard Boulton's Rational System and Chirurgery Practice in 1713, in which the terms 'herpes miliaris' and 'herpes exedens' also emerged. Herpes was not found to be a virus until the 1940s.
Herpes antiviral therapy began in the early 1960s with the use of experimental drugs that interfere with viral replication called deoxyribonucleic acid (DNA) inhibitors. The original use is against usually fatal or debilitating diseases such as adult encephalitis, keratitis, in immunocompromised patients (transplant), or disseminated herpes zoster. The original compounds used were 5-iodo-2'-deoxyuridine, AKA idoxuridine, IUdR, or (IDU) and 1 -? - D-arabinofuranosylcytosine or ara-C, then marketed under the name of cytosar or cytarabine. The use is expanded to include topical treatment of herpes simplex, zoster, and varicella. Some experiments combine different antivirus with different results. Introduction 9 -? - D-arabinofuranosyladenine, (fig-A or vidarabine), much less toxic than fig-C, in the mid-1970s, heralded the way for the beginning of ordinary neonatal antiviral treatment. Vidarabine is the first systemically administered antiviral drug against HSV activity whose therapeutic efficacy exceeds toxicity for the management of life-threatening HSV disease. Intravenous VIBABABINE was licensed for use by the US Food and Drug Administration in 1977. Other experimental antivirals in 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 increased antiviral treatment of other positions and led to trials of vidarabine vs acyclovir in the late 1980s. The low toxicity and ease of administration of vidarabine has led to acyclovir being the drug of choice for herpes treatment after being licensed by the FDA in 1998. Other advantages in the treatment of neonatal herpes include a greater reduction in mortality and morbidity with increased doses, which is not the case when compared with the increase dose of vidarabine. However, acyclovir appears to inhibit the antibody response, and newborns on acyclovir antiviral treatment have increased the antibody titer more slowly than in vidarabine.
Society and culture
Genital herpes simplex is not always stigmatized. It was just a cold sore in an unusual place until the 1970's. By the end of 1975, a study of "psychological morbidity in the clinic for sexually transmitted diseases" did not mention herpes simplex because at the time, no significant morbidity problems (ie mental anxiety or illness) were associated with the virus.
Pedro Cuatrecasas states, "during R & D acyclovir (Zovirax), marketing [Burroughs Wellcome department] insists that there is 'no market' for this compound, most have hardly heard of genital herpes..." So, marketing medical conditions - separating the 'normal cold sore' from 'stigmatization' genital infection is the key to marketing the drug, a process now known as 'mongering disease'.
Since the creation of herpes hype, some people experience negative feelings associated with conditions after diagnosis, especially if they have acquired genital form of the disease. Feelings can include depression, fear of rejection, feelings of isolation, fear of being discovered, and self-destructive feelings. This feeling usually diminishes over time. Much of the hysteria and stigma surrounding herpes comes from a media campaign that began in the late 1970s and culminated in the early 1980s. Some articles are written in frightening and anxious terminology, such as the ubiquitous "attack", "plague", "victim", and "sufferer". At one point, the term "herpetic" even entered the popular lexicon. The articles are published by Reader's Digest , AS. News , and magazine Time , among others. A movie made for TV is named Intimate Agony. The peak is when the Time magazine has Herpes: The New Scarlet Letter 'on its cover in August 1982, forever stigmatizing the word in the public mind. Herpes support groups have been established in the United States and Britain, providing information about herpes and running message forums and dating sites for patients. People with herpes virus often hesitate to divulge to others, including friends and family, that they are infected. This is especially true for new or potential sexual partners that they consider normal.
In a 2007 study, 1900 people (25% of whom had herpes) ranked second genital herpes for social stigma, from all sexually transmitted diseases (HIV occupies the top position for STD stigma).
Support group
United States
An important source of support is the National Herpes Resource Center that emerged from the work of the American Social Health Association (ASHA). ASHA was created in 1914 in response to an increase in social diseases that had spread during World War 1. During the 1970s, there was an increase in sexually transmitted diseases. One of the most dramatically increasing diseases is genital herpes. In response, ASHA created the National Herpes Resource Center in 1979. HRC is designed to meet the growing need for education and awareness about viruses. One of The Herpes Resource Center (HRC) projects is to create a local support group network (HELP). The purpose of these HELP groups is to provide a safe and confidential environment where participants can obtain accurate information and share experiences, fears, and feelings with others who care about herpes.
English
In Britain, Herpes Association (now the Herpes Virus Association) began in 1982, becoming a registered charity with a grant from the Department of Health in 1985. The charity began as a series of local group meetings before it acquired national offices and deployments.
Research
Research has become a vaccine for the prevention and treatment of herpes infections. A failed clinical trial has been performed for several glycoprotein subunit vaccines. By 2017, the future pipe includes several incompetent and promising replication vaccine proposals, while two replicating (live-attenuated) HSV vaccines are undergoing human testing.
A genome study of the herpes simplex virus type 1 confirmed the theory of human migration patterns known as hypotheses outside Africa.
References
External links
- Herpes simplex in Curlie (based on DMOZ)
Source of the article : Wikipedia
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