| Dictionary: herpes simplex |
[New Latin herpēs simplex : Latin herpēs, herpes + Latin simplex, simple.]
| 5min Related Video: herpes simplex |
| Oncology Encyclopedia: Herpes Simplex |
Description
Herpes simples virus (HSV, or herpesvirus) is a virus that causes infection of skin and mucous membrane and rarely infects other parts of the body. However, in the immunosuppressed patient, HSV may cause pneumonia and other more severe infections. When the infection occurs in the mouth it is commonly referred to as cold sores. An outbreak of HSV infection can be very painful. There are two distinct types of HSV: type 1 and type 2. It was believed that HSV-1 mostly caused oral herpes (herpes labialis), while HSV-2 generally caused genital herpes that typically affects the penis, vulva, and rectum. This is not completely true. Both type 1 and type 2 can cause herpes lesions on the lips or genitals. The first symptoms occur within 2-20 days after contact with an infected person.
Symptoms of the primary infection are usually more severe than those of recurrent infections. The primary infection can cause symptoms like those experienced in other viral infections, including lack of energy, headache, fever, and swollen lymph nodes in the neck. The first sign of infection is formation of fluid-filled blisters that may last up to two weeks. However, the pain in the area may last much longer. Once HSV enters the body it spreads to nearby mucosal areas through nerve cells. Once it infects the body the virus remains latent for the life of that individual. During the period of latency there are no symptoms. At times the infected person may shed the virus, even in the absence of visible symptoms, and infect others. Individuals infected with the virus can have recurrent infections; however, normally, recurrent infections are milder and shorter. However, cancer patients can have severe recurrences.
Typically, 50–80% of persons with oral herpes experience a prodrome (symptoms of oncoming disease) of pain, burning, itching, or tingling at the site where blisters will form. This prodrome stage may last anywhere from a few hours to one to two days. The herpes infection prodrome occurs in both the primary infection and recurrent infections.
Causes
Everyone with cancer has a higher risk of catching viral infections of any type. This is because the cancer itself, and the methods used to treat it, affect the immune defense mechanisms that fight infection. Normally the mucous membrane is one of the first lines of defense against infectious organisms. However, chemotherapy and radiation can damage this very important barrier. The barrier that skin provides is also compromised because of needles used for drawing blood or injecting drugs. Radiation and chemotherapy also suppress the immune system. Certain cancers like Hodgkin's disease, lymphoma, and T-cell leukemia cause defects in cellular immunity, which is a primary defense mechanism against viral infections. Thus cancer patients, especially those who are undergoing chemotherapy or radiation treatments, are at greater risk of primary and secondary herpes infections.
Oral herpes simplex infections are more common in children than adults following chemotherapy. Patients who have the virus latent in the system have a higher chance of recurrent infection. Primary infection generally causes gingivitis (inflammation of the gums, vesicles on the mucosa (blisters on the lining of the mouth), and a coated tongue (white covering on tongue). Women with genital herpes can have severe recurrence following chemotherapy because of immunosuppression.
Treatment
There is no cure for HSV infection although there are antiviral drugs available that have some effect in lessening the symptoms and decreasing the length of herpes outbreaks. There is evidence that some of these drugs may also prevent future outbreaks. For the best results drug treatment should begin during the prodrome stage before blisters are visible. Depending upon the length of the outbreak, drug treatment could continue up to 10 days.
Acyclovir (Zovirax) is the drug of choice for herpes infection and can be given intravenously or taken by mouth. It can be applied directly to sores as an ointment but is not very useful in this form. A liquid form for children is also available. Acyclovir is effective in treating both the primary infection and recurrent outbreaks. When taken by mouth to prevent an outbreak, acyclovir reduces the frequency of herpes outbreaks.
Alternative and Complementary Therapies
A number of steps can relieve the symptoms of herpes infections. It is important to keep the blisters or sores clean and dry with an agent like cornstarch. One should avoid touching the sores, and wash hands frequently. Local application of ice may relieve the pain. Over-thecounter medication for fever, pain, and inflammation—such as aspirin, acetaminophen, or ibuprofen—may help. Children should never be given aspirin. Sexual intercourse should be avoided during both the active stage and the prodrome stages. During an outbreak of cold sores salty foods, citrus foods (oranges etc.), and other foods that irritate the sores should be avoided. Over-thecounter lip products that contain the chemical "phenol" (such as Blistex Medicated Lip Ointment) and numbing ointments (such as Anbesol) help to relieve the pain of cold sores. A bandage may be placed over the sores to protect them and prevent spreading the virus to other sites on the lips or face.
A diet rich in the amino acid lysine may help prevent recurrences of cold sores. Foods that contain high levels of lysine include most vegetables, legumes, fish, turkey, and chicken. Oral lysine supplements in the amount of 1000 mg per day may help sores heal faster. There is a belief that foods with high lysine-to-arginine ratio will help prevent outbreaks of herpes simplex. That has not been proven, and it is important to include foods that have a low lysine-to-arginine ratio also, such as nuts, onion, garlic, and green vegetables. It is also suggested that the amount of arginine in the diet be limited as there is a belief that arginine is needed for herpesvirus growth. This amino acid is found in peanuts, beer, chocolate, gelatin, and raisins.
Resources
Periodicals
Whitley, Richard J., and Bernard Roizman. "Herpes Simplex Virus Infections." The Lancet 357 (May 12, 2001): 1513.
Organizations
American Herpes Foundation. (201) 342-4441.
—Belinda M. Rowland, Ph.D.; Malini Vashishtha, Ph.D.
| Dental Dictionary: herpes simplex |
An infection caused by the herpes simplex virus. Primary infection, occurring most often in children between 2 and 5 years of age, may result in apparent clinical disease or such manifestations as acute herpetic gingivostomatitis, keratoconjunctivitis, vulvovaginitis, or encephalitis. Recurrent manifestations may include herpes labialis (fever blisters or cold sores), dendritic corneal ulcers, or genital herpes simplex.
Herpes simplex. (Neville/Damm/Allen/Bouquot, 2002)
| Children's Health Encyclopedia: Herpes Simplex |
Definition
Herpes is an infection caused by a herpes simplex virus 1 or 2, and it primarily affects the mouth or genital area.
Description
There are two strains of herpes simplex viruses. Herpes simplex virus type 1 (HSV-1) is usually associated with infections of the lips, mouth, and face. It is the most common herpes simplex virus among the general population and is usually acquired in childhood. Herpes simplex virus 2 (HSV-2) is sexually transmitted and is usually associated with genital ulcers or sores. Individuals may harbor HSV-1 and or HSV-2 and not have developed any symptoms.
Transmission
HSV-1 causes lesions inside the mouth that are often referred to as cold sores or fever blisters, and it is transmitted by contact with infected saliva. By adulthood, up to 90 percent of the population has antibodies to HSV-1. HSV-2 is sexually transmitted and not everyone develops symptoms when they have it. Up to 30 percent of adults in the United States have antibodies against HSV-2. Cross infection of type 1 and 2 viruses may occur from oral-genital contact. Herpes viruses can be transmitted to a newborn during vaginal delivery in mothers infected with herpes viruses, especially if the infection is primary (first occurrence) and is active at the time of delivery. The virus can lead to complications such as meningoencephalitis, which is an infection of the lining of the brain and the brain itself. It can also cause eye infections, in particular, of the conjunctiva and cornea.
Demographics
The prevalence of herpes simplex in the United States is as follows:
Causes and Symptoms
A primary infection of HSV-1 typically occurs between six months and five years of age and is systemic (affecting the whole body). Transmission is generally via respiratory droplets (HSV-1) or direct contact (HSV-1 and HSV-2). The virus enters the body through mucosal surfaces, replicates in the cell nucleus, and then kills the host cell. The initial infection is self-limiting, but the immune system does not destroy the virus. The virus migrates along nerves to an area of regional ganglia (nerve centers) and then typically enters into a latent (sleeping) phase. Reactivation of the virus occurs in 50 percent of patients within five years, and it can be triggered by various factors:
The symptoms of a herpes infection can vary tremendously. Many infected individuals have few, if any, noticeable symptoms. Those who do have symptoms usually notice them from two to 20 days after being exposed to someone with HSV infection. Symptoms can last for several weeks, but the first episode of herpes is usually worse than subsequent outbreaks. The predominant symptom of herpes is the outbreak of painful, itching blisters filled with fluid on and around the external sexual organs or, for oral herpes, on or very near the lip. Females may have a vaginal discharge and experience flu-like symptoms with HSV2 outbreaks, including fever, headache, muscle aches, and fatigue. There may be painful urination, and swollen and tender lymph glands in the groin. More often than not the blisters disappear without treatment in two to 10 days, but the virus remains in the body, lying dormant among clusters of nerve cells until another outbreak is triggered.
Many people are able to anticipate an outbreak when they notice a warning sign (a tingling sensation, called a prodrome) of the approaching illness. It is when they feel signs that an outbreak is about to start that they are particularly contagious, even though the skin still appears normal. Most people with genital herpes have five to eight outbreaks per year, but not everyone has recurrent symptoms. In time, the number of outbreaks usually decreases. Oral herpes can recur as often as monthly or only one or two times each year. Sores typically come back near the site of the first infection, but there are fewer sores with recurrences that heal faster and are less painful.
When to Call the Doctor
Anyone who has a history of herpes infection and current lesions should notify the physician if the lesions do not resolve after seven to ten days or if a condition exists that weakens the immune system. Children with a herpes infection most commonly have sores in the mouth usually caused by HSV-1. This infection causes fever, irritability, pain, decreased appetite, and ulcers in the mouth. The most common complication is dehydration secondary to a refusal to drink fluids because of mouth pain and difficulty swallowing. Treatment is usually not required, and symptoms generally improve in three to five days. If, however, the child does not improve, develops a fever, and becomes lethargic, the pediatrician should be called immediately.
Herpes infections that spread throughout the body in a newborn are usually more serious, but fortunately less common than the other types of neonatal infections. They typically occur in the first week of life, with symptoms including fever, difficulty breathing, seizures, lethargy, and irritability. Since many infants in the first month of life can have a herpes infection and not have skin lesions, it takes a great deal of time and effort to diagnose and treat these infections early. Herpes should be considered in any acutely ill newborn, especially if bacterial cultures are negative and the baby is not improving after two to three days. Parents should be informed to watch the baby closely if either one of them has a history of herpes infections.
Diagnosis
Testing for neonatal herpes infections may include special smears and/or viral cultures, blood antibody levels, and polymerase chain reaction (PCR) testing of spinal fluid. Cultures are usually obtained from skin vesicles, eyes, mouth, rectum, urine, stool, and blood. For older children and adults, if there is a question as to the cause of a sore, a tissue sample or culture can be taken to determine what type of virus or other microorganism is responsible. For herpes, it is preferable to have this test done within the first 48 hours after symptoms first show up for a more accurate result.
Treatment
There are three drugs proven to treat genital herpes symptoms: acyclovir, sold under the brand name Zovirax, Famvir, and Valtrex. These are all taken in pill form. Formulas applied to the surface of the skin provide little benefit, and they are not recommended. Drug therapy is not a cure, but it can make living with the condition easier. For an initial outbreak with symptoms such as sores, a doctor should begin a brief course of antiviral therapy to relieve the symptoms or prevent them from getting worse. Seven to ten days of treatment is recommended but if the lesions do not heal, a longer period of time may be required. Following the initial outbreak there are two options to consider for further outbreaks. One is intermittent treatment, which involves the physician prescribing an antiviral drug to keep on hand in case an individual has a flare-up. The pills can be taken for three to five days as soon as sores are noticed or when an outbreak tingling sensation occurs. Sores heal and disappear on their own, but taking the drugs helps to alleviate the symptoms. For individuals who have frequent outbreaks, a suppressive treatment may work better. This treatment involves taking an antiviral drug every day. For example, someone who typically has more than six outbreaks a year, suppressive therapy reduces the number of outbreaks by 70 to 80 percent. Moreover, many who take the antiviral drugs daily have no outbreaks at all.
In the early 2000s herpes vaccines are being investigated, and an effective vaccine may be available in before 2010. Vaccines will only function to prevent the infection in new patients. Those who already have the simplex virus disease will probably not benefit.
Nutritional Concerns
Diet is a very important factor in keeping herpes in remission. It has been found that foods high in arginine may cause herpes outbreaks. Supplementation with free-form lysine has shown to be beneficial in controlling herpes along with a diet high in lysine and low in arginine. The amount of lysine required to control herpes varies from case to case, but a typical adult dose to maintain remission is 500 mg daily, and active herpes requires 1–6 g between meals to induce healing.
Prognosis
There is no cure for herpes simplex. Once it is contracted, it is always in a person's system. However, with treatment therapies, the problems previously encountered are lessened considerably.
Prevention
Whereas it is almost impossible to keep a baby or child from being exposed to herpes simplex due to its universal presence, there are conditions that can be used to prevent its transmission. Hand washing is one of the biggest factors in the transmission of all diseases, and it is especially true of herpes simplex since it is spread by respiratory droplets through mucosal membranes. In terms of genital herpes, education regarding the use of condoms is the best tool. Young adults should also be reminded that herpes simplex can be transferred from oral-genital contact. Since many teenagers do not consider oral or anal sex as sexual intercourse per se, it is imperative to spell out exactly what, when, and how these viruses can be spread.
Parental Concerns
It is important that the pediatrician discusses the possibility of herpes infections with new parents, particularly if they have a history of genital herpes. Signs and symptoms need to be gone over, i.e., lethargy, fever, as well as the fact that there may or may not be lesions present. A newborn's own immune system begins to function around the third month, and if a mother is breast-feeding, she is passing antibodies to her baby. The primary concern is that a herpes infection does not become systemic. Thus, if the child seems to be getting sicker instead of better, parents should call the doctor immediately.
Resources
Books
Ebel, Charles, and A. Wald. Managing Herpes: How to Live and Love with a Chronic STD. Durham, NC: American Social Health Association, 2002.
The Official Patient's Sourcebook on Genital Herpes. San Diego, CA: Icon Group International, 2002.
Spencer, Judith V., et al. Herpes. Langhorne, PA: Chelsea House Publishers, 2005.
Westheimer, Ruth K. Dr. Ruth's Guide to Talking about Herpes. New York: Grove/Atlantic Inc., 2004.
Organizations
American Social Health Association. PO Box 13827, Research Triangle Park, NC 27709. Web site: www.ashastd.org/hrc/.
[Article by: Linda K. Bennington, MSN, CNS]
| Britannica Concise Encyclopedia: herpes simplex |
For more information on herpes simplex, visit Britannica.com.
| Columbia Encyclopedia: herpes simplex |
Outbreaks of both types of herpes simplex alternate with periods when the virus lies dormant in the nerve cells. The reappearance of blisters may be triggered by such factors as fever, infectious diseases, exposure to sunlight, menstruation, or pregnancy. The blisters usually last from 10 to 14 days. Treatment for recurrent herpes includes elimination of the precipitating conditions, local antibiotic treatment to prevent bacterial infection, and treatment with antiviral drugs such as acyclovir, although some resistant strains (see drug resistance) have developed. There is no cure. The herpes simplex virus is also the cause of a form of viral encephalitis.
See also herpes zoster (shingles).
| Veterinary Dictionary: Herpesviridae |
A family of viruses, the members of which are about 150 nm in diameter, enveloped, with a nucleocapsid of about 100 nm in diameter, composed of 162 capsomers and contain a large, double-stranded DNA. The viruses replicate in the nucleus of the infected cell, where they induce the formation of a characteristic inclusion body; some also induce formation of a cytoplasmic inclusion body. The herpesviruses are classified into three subfamilies: (1) Alphaherpesvirinae, which are rapidly growing viruses that cause acute diseases, except Marek's disease which causes tumors in chickens; (2) Betaherpesvirinae, which are slow growing, highly cell-associated viruses, also called cytomegaloviruses, which produce subtle diseases with a prolonged clinical course; and (3) Gammaherpesvirinae, some of which produce low grade, prolonged clinical illness typified by infectious mononucleosus/glandular fever of humans, caused by Epstein–Barr virus, and probably a similar disease of horses caused by equine herpesvirus 2; the primate viruses are associated with tumors.
The important diseases of animals caused by herpesviruses are dealt with under their individual headings: aujeszky's disease, infectious bovine rhinotracheitis, infectious pustular vulvovaginitis, equine viral abortion, equine viral rhinopneumonitis, equine coital exanthema, equine herpesvirus 2 infection, the Allerton form of lumpy-skin disease, the generalized infection of cattle with bovine herpesvirus 2, bovine herpes mammillitis, the African ‘wildebeest-associated’ malignant catarrhal fever, canine herpesvirus respiratory, genital and neonatal infections, feline viral rhinotracheitis. In birds there are infectious laryngotracheitis, pigeon herpesvirus, duck plague and marek's disease.
| Wikipedia: Herpesviridae |
| Herpesviridae | ||||||
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| Virus classification | ||||||
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| Genera | ||||||
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Subfamily Alphaherpesvirinae |
The Herpesviridae are a large family of DNA viruses that cause diseases in animals, including humans.[1][2][3] The members of this family are also known as herpesviruses. The family name is derived from the Greek word herpein ("to creep"), referring to the latent, recurring infections typical of this group of viruses. Herpesviridae can cause latent or lytic infections.
Contents |
Herpesviruses all share a common structure—all herpesviruses are composed of relatively large double-stranded, linear DNA genomes encoding 100-200 genes encased within an icosahedral protein cage called the capsid which is itself wrapped in protein layers called the tegument and a lipid bilayer membrane called the envelope. This whole particle is known as the virion.
All Herpesviruses are nuclear-replicating—the viral DNA is transcribed to RNA within the infected cell's nucleus.
Infection is initiated when a viral particle contacts a cell with specific types of receptor molecules on the cell surface. Following binding of viral envelope glycoproteins to cell membrane receptors, the virion is internalized and dismantled, allowing viral DNA to migrate to the cell nucleus. Within the nucleus, replication of viral DNA and transcription of viral genes occurs.
During symptomatic infection, infected cells transcribe lytic viral genes. In some host cells, a small number of viral genes termed latency associated transcript (LAT) accumulate instead. In this fashion the virus can persist in the cell (and thus the host) indefinitely. While primary infection is often accompanied by a self-limited period of clinical illness, long-term latency is symptom-free.
Reactivation of latent viruses has been implicated in a number of diseases (e.g. Shingles, Pityriasis Rosea). Following activation, transcription of viral genes transitions from latency-associated LAT to multiple lytic genes; these lead to enhanced replication and virus production. Often, lytic activation leads to cell death. Clinically, lytic activation is often accompanied by emergence of non-specific symptoms such as low grade fever, headache, sore throat, malaise, and rash as well as clinical signs such as swollen or tender lymph nodes and immunological findings such as reduced levels of natural killer cells.
Herpesviruses are known for their ability to establish lifelong infections. One way this is possible is through immune evasion. Herpesviruses have found many different ways to evade the immune system. One such way is by encoding a protein mimicking human interleukin 10 (hIL-10) and another is by downregulation of the Major Histocompatibility Complex II (MHC II) in infected cells. Research conducted on cytomegalovirus (CMV) indicates that the viral human IL-10 homolog, cmvIL-10, is important in inhibiting pro-inflammatory cytokine synthesis. The cmvIL-10 protein has 27% identity with hIL-10 and only one conserved residue out of the nine amino acids that make up the functional site for cytokine synthesis inhibition on hIL-10. There is, however, much similarity in the functions of hIL-10 and cmvIL-10. Both have been shown to down regulate IFN-γ, IL-1α, GM-CSF, IL-6 and TNF- α, which are all pro-inflammatory cytokines. They have also been shown to play a role in downregulating MHC I and MHC II and up regulating HLA-G (non-classical MHC I). These two events allow for immune evasion by suppressing the cell-mediated immune response and natural killer cell response, respectively. The similarities between hIL-10 and cmvIL-10 may be explained by the fact that hIL-10 and cmvIL-10 both use the same cell surface receptor, the hIL-10 receptor. One difference in the function of hIL-10 and cmvIL-10 is that hIL-10 causes human peripheral blood mononuclear cells (PBMC) to both increase and decrease in proliferation whereas cmvIL-10 only causes a decrease in proliferation of PBMCs. This indicates that cmvIL-10 may lack the stimulatory effects that hIL-10 has on these cells. [4]
It was found that cmvIL-10 functions through phosphorylation of the Stat3 protein. It was originally thought that this phosphorylation was a result of the JAK-STAT pathway. However, despite evidence that JAK does indeed phosphorylate Stat3, its inhibition has no significant influence on cytokine synthesis inhibition. Another protein, PI3K, was also found to phosphorylate Stat3. PI3K inhibition, unlike JAK inhibition, did have a significant impact on cytokine synthesis. The difference between PI3K and JAK in Stat3 phosphorylation is that PI3K phosphorylates Stat3 on the S727 residue whereas JAK phosphorylates Stat3 on the Y705 residue. This difference in phosphorylation positions seems to be the key factor in Stat3 activation leading to inhibition of pro-inflammatory cytokine synthesis. In fact, when a PI3K inhibitor is added to cells, the cytokine synthesis levels are significantly restored. The fact that cytokine levels are not completely restored indicates there is another pathway activated by cmvIL-10 that is inhibiting cytokine synthesis. The proposed mechanism is that cmvIL-10 activates PI3K which in turn activates PKB (Akt). PKB may then activate mTOR, which may target Stat3 for phosphorylation on the S727 residue.[5]
Another one of the many ways in which herpes viruses evade the immune system is by down regulation of MHC I and MHC II. This is observed in almost every human herpesvirus. Down regulation of MHC I and MHC II can come about by many different mechanisms, most causing the MHC to be absent from the cell surface. As discussed above, one way is by a viral chemokine homolog such as IL-10. Another mechanism to down regulate MHCs is to encode viral proteins that detain the newly formed MHC in the endoplasmic reticulum (ER). The MHC cannot reach the cell surface and therefore cannot activate the T cell response. The MHCs can also be targeted for destruction in the proteasome or lysosome. The ER protein TAP also plays a role in MHC down regulation. Viral proteins inhibit TAP preventing the MHC from picking up a viral antigen peptide. This prevents proper folding of the MHC and therefore the MHC does not reach the cell surface.[6]
It is important to note that HLA-G is often up regulated in addition to downregulation of MHC I and MHC II. This prevents the natural killer cell response.
There are eight distinct viruses in this family known to cause disease in humans.[7][8]
| Human Herpesvirus (HHV) classification[1][7] | ||||||
| Type | Synonym | Subfamily | Primary Target Cell | Pathophysiology | Site of Latency | Means of Spread |
|---|---|---|---|---|---|---|
| HHV-1 | Herpes simplex virus-1 (HSV-1) | α (Alpha) | Mucoepithelial | Oral and/or genital herpes (predominantly orofacial) | Neuron | Close contact |
| HHV-2 | Herpes simplex virus-2 (HSV-2) | α | Mucoepithelial | Oral and/or genital herpes (predominantly genital) | Neuron | Close contact (sexually transmitted disease) |
| HHV-3 | Varicella zoster virus (VZV) | α | Mucoepithelial | Chickenpox and shingles | Neuron | Respiratory and close contact |
| HHV-4 | Epstein-Barr virus (EBV), lymphocryptovirus | γ (Gamma) | B cells and epithelial cells | Infectious mononucleosis, Burkitt's lymphoma, CNS lymphoma in AIDS patients, post-transplant lymphoproliferative syndrome (PTLD), nasopharyngeal carcinoma, HIV-associated hairy leukoplakia |
B cell | Close contact, transfusions, tissue transplant, and congenital |
| HHV-5 | Cytomegalovirus (CMV) | β (Beta) | Monocyte, lymphocyte, and epithelial cells | Infectious mononucleosis-like syndrome,[9] retinitis, etc. | Monocyte, lymphocyte, and ? | Saliva |
| HHV-6 | Roseolovirus, Herpes lymphotropic virus | β | T cells and ? | Sixth disease (roseola infantum or exanthem subitum) | T cells and ? | Respiratory and close contact? |
| HHV-7 | Roseolovirus | β | T cells and ? | Sixth disease (roseola infantum or exanthem subitum) | T cells and ? | ? |
| HHV-8 | Kaposi's sarcoma-associated herpesvirus (KSHV), a type of rhadinovirus |
γ | Lymphocyte and other cells | Kaposi's sarcoma, primary effusion lymphoma, some types of multicentric Castleman's disease | B cell | Close contact (sexual), saliva? |
In addition to the herpesviruses considered endemic in humans, some viruses associated primarily with animals may infect humans. These are zoonotic infections:
| Zoonotic Herpesviruses | ||||
| Species | Type | Synonym | Subfamily | Human Pathophysiology |
|---|---|---|---|---|
| Macaque monkey | CeHV-1 | Cercopithecine herpesvirus-1, (Monkey B virus) | α | Very unusual, with only approximately 25 human cases reported.[10] Untreated infection is often deadly; sixteen of the 25 cases resulted in fatal encephalomyelitis. At least four cases resulted in survival with severe neurologic impairment.[10][11] Symptom awareness and early treatment are important for laboratory workers facing exposure.[12] |
| Mouse | MHV-68 | Murine gammaherpesvirus-68 | γ | Zoonotic infection found in 4.5% of general population and more common in laboratory workers handling infected mice.[13] ELISA tests show factor-of-four (x4) false positive results, due to antibody cross-reaction with other Herpes viruses.[13] |
In animal virology the most important herpesviruses belong to the Alphaherpesvirinae. Research on pseudorabies virus (PrV), the causative agent of Aujeszky's disease in pigs, has pioneered animal disease control with genetically modified vaccines. PrV is now extensively studied as a model for basic processes during lytic herpesvirus infection, and for unravelling molecular mechanisms of herpesvirus neurotropism, whereas bovine herpesvirus 1, the causative agent of bovine infectious rhinotracheitis and pustular vulvovaginitis, is analyzed to elucidate molecular mechanisms of latency. The avian infectious laryngotracheitis virus is phylogenetically distant from these two viruses and serves to underline similarity and diversity within the Alphaherpesvirinae.[2][3]
The following genera are included in the family Herpesviridae:
Research is currently ongoing into a variety of side-effect or co-conditions related to the herpesviruses. These include:
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| Simplexvirus |
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 | Dictionary. The American Heritage® Dictionary of the English Language, Fourth Edition Copyright © 2007, 2000 by Houghton Mifflin Company. Updated in 2007. Published by Houghton Mifflin Company. All rights reserved. Read more |
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| Oncology Encyclopedia. Gale Encyclopedia of Cancer. Copyright © 2006 by The Gale Group, Inc. All rights reserved. Read more |
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| Dental Dictionary. Mosby's Dental Dictionary. Copyright © 2004 by Elsevier, Inc. All rights reserved. Read more |
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| Children's Health Encyclopedia. © 2006 through a partnership of Answers Corporation. All rights reserved. Read more |
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| Britannica Concise Encyclopedia. Britannica Concise Encyclopedia. © 2006 Encyclopædia Britannica, Inc. All rights reserved. Read more |
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| Columbia Encyclopedia. The Columbia Electronic Encyclopedia, Sixth Edition Copyright © 2003, Columbia University Press. Licensed from Columbia University Press. All rights reserved. www.cc.columbia.edu/cu/cup/ Read more |
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| Veterinary Dictionary. Saunders Comprehensive Veterinary Dictionary 3rd Edition. Copyright © 2007 by D.C. Blood, V.P. Studdert and C.C. Gay, Elsevier. All rights reserved. Read more |
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