A herpesvirus that is the causative agent of infectious mononucleosis. It is also associated with various types of human cancers.
[After Michael A. Epstein and and Y.M. Barr, 20th-century British virologists.]
Epstein-Barr virus
Dictionary:
Ep·stein-Barr virus (ĕp'stīn-bär')  |
n. (Abbr. EBV)
A herpesvirus that is the causative agent of infectious mononucleosis. It is also associated with various types of human cancers.
A herpesvirus that is the causative agent of infectious mononucleosis. It is also associated with various types of human cancers.
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Key Terms: Lymphocyte, Lymphoma, Malaria.
Definition
Epstein-Barr Virus, or EBV, is the name given to a member of the herpesvirus family that is associated with a variety of illnesses—from infectious mononucleosis (IM), to nasal-pharyngeal cancer, and Burkitt's lymphoma.
Description
Herpesviruses have long been known. The name actually comes from the Greek adjective herpestes, which means creeping. Many herpesvirus species appear to establish a life-long presence in the human body, remaining dormant for long periods and becoming active for some, often inexplicable, reason. EBV is only one of several members of the Herpesvirus family that have similar traits. Others include varicella zoster virus—the cause of both chickenpox and shingles—, and the herpes simplex virus responsible for both cold sores and genital herpes. EBV is usually transmitted through saliva but not blood, and is not normally an airborne infection.
EBV occurs in nearly all regions of the world, and is considered among the most common infectious viruses known to humankind. In the United States, the Center for Disease Control (CDC) estimates that 95% of adult Americans between the ages of 35 and 40 years have been infected, but it is less prevalent in children and teenagers. This pattern of infecting adults more than children persists throughout other prosperous western countries, but does not hold true in underdeveloped regions such as Africa and Asia. In Africa, most children have been infected by EBV by the age of three years
Individuals with EBV infections typically show some elevation in the white blood cell count and a noticeable increase in lymphocytes—white blood cells associated with the immune response of the body. IM is a time-limited infection that usually lasts from one to two months. Symptoms include fever, malaise, sore throat, swollen glands and (sometimes) swollen spleen and/or liver. EBV infections that lead to Burkitt's lymphoma in Africa typically affect the jaw and mouth area, while the (very rare) incidences of Burkitt's lymphoma found in developed countries are more apt to manifest tumors in the abdominal region. Nasopharyngeal cancer is uncommon in the West but more prevalent in the Far East. It affects more men than women, and usually occurs between the ages of 40 and 50 years.
Causes
EBV has been linked to IM in the Western world for decades. It has also become associated consistently with nasopharyngeal cancers in Asia (especially China) and Burkitt's lymphoma in Africa and Papua New Guinea. According to the CDC, EBV is not the sole cause of these two malignancies, but does play an important role in the development of both cancers. The mechanism that allows Epstein-Barr Virus to at least help in producing such diverse illnesses in diverse regions of the world has been the subject of increasing research and scrutiny.
It is known that, once it infects a person, EBV is one of the herpesviruses that remain in the human body for life. Under certain, still not-understood conditions, it alters white blood cells normally associated with the immune system, changing B lymphocytes (those normally associated with making antibodies), and causing them to reproduce rampantly. EBV can bind to these white blood cells to produce a solid mass made up of B lymphocytes—called Burkitt's lymphoma—or to the mucous membranes of the mouth and nose and cause nasopharyngeal cancer. Since Burkitt's lymphoma typically occurs in people living in moist, tropical climates, the same regions where people usually contract malaria, it has been speculated that the immune system is altered by its response to malaria. When EBV infection occurs, the altered immune system's reaction is the production of a tumor.
Special Concerns
Though studies about the hereditary tendency of abnormal cell development after EBV infection are incomplete, some studies have shown it to be a hereditary trait based upon the X chromosome.
Treatments
Because EBV infections are viral in origin, antibiotics are ineffective against them. Much research is geared toward the development of a vaccines effective against both the virus and cancer.
Anticancer drugs, such as cyclophosphamide, or radiation therapy have been shown to be effective against Burkitt's lymphoma in four out of five cases.
Alternative and Complementary Therapies
The goal of alternative treatment is to lower the white blood cell count to normal levels. Treatment often includes nutritional supplements such as flaxseed oil or shark cartilage, vitamins—including vitamins C and K, and mineral supplements containing magnesium and potassium. Well-conducted randomized clinical trials have not yet been conducted to prove efficacy of these therapies.
Resources
Organizations
Center for Disease Control, National Center for Infectious Diseases Epstein-Barr Virus and Infectious Mononucleosis. [cited March 26, 2001].
Queensland Institute of Medical Research. [cited December 7, 1999].
Questions to Ask the Doctor
- What tests can be done if Epstein-Barr Virus infection is suspected?
- Have any vaccines against Epstein-Barr Virus been developed?
—Joan Schonbeck, R.N.
| Sci-Tech Encyclopedia: Epstein-Barr virus |
An antigenically distinct member of the herpesvirus group of viruses, whose genome is DNA. EB virus is the cause of one benign disease (infectious mononucleosis), and is associated with certain types of cancer; however, the great majority of EB virus infections are clinically inapparent. The virus was detected initially by electron microscopy in a small proportion of cells in continuous lymphoblastoid cell lines derived from Burkitt's lymphoma (but particles have not been seen in cells of the tumor itself). The virus also has been detected in cell lines derived from nasopharyngeal carcinomas, a type of cancer found with high frequency in persons from southern China. The virus is found in peripheral blood leukocytes from normal individuals and from patients with infectious mononucleosis. See also Infectious mononucleosis; Lymphoma.
If EB virus is indeed confirmed as having a role in the development of human malignancies, then one major question to be resolved is how a virus so ubiquitous can be involved in so wide a variety of responses. However, it should be recalled that many virus infections (for example, polio virus, hepatitis viruses, certain of the arboviral encephalitides) have a wide spectrum of outcomes, ranging from inapparent infection to severe syndromes. See also Animal virus; Oncology.
| Dental Dictionary: Epstein-Barr virus |
n.pr
A herpesvirus associated with Burkitt’s lymphoma and reported in cases of infectious mononucleosis; more recently reported associated with acquired immune deficiency syndrome.
| Columbia Encyclopedia: Epstein-Barr virus |
Epstein-Barr virus (EBV), herpesvirus that is the major cause of infectious mononucleosis and is associated with a number of cancers, particularly lymphomas in immunosuppressed persons, including persons with AIDS. Epstein-Barr is a ubiquitous virus, so common that it has been difficult to determine whether it is the cause of certain diseases or whether it is simply there as an artifact. In Third World nations, most children are infected with EBV; in most industrialized nations, about 50% of the people are infected. Research has found that all of the lymphomas associated with AIDS and most lymphomas in other immunocompromised persons are connected with latent EBV infection. EBV has been found in biopsy tissue of patients with Hodgkin's disease, breast cancer, and some smooth muscle tumors. EBV also was formerly suspected as the cause of chronic fatigue syndrome (originally named chronic EBV syndrome).
| Veterinary Dictionary: EBV |
Estimated breeding value.
| Wikipedia: Epstein-Barr virus |
This article is about the virus itself. For the chronic fatigue syndrome, see Chronic Epstein-Barr virus.
| Epstein-Barr | |
|---|---|
 |
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| Two Epstein-Barr virions | |
| Virus classification | |
| Group: | Group I (dsDNA) |
| Family: | Herpesviridae |
| Subfamily: | Gammaherpesvirinae |
| Genus: | Lymphocryptovirus |
| Species: | Human herpesvirus 4 (HHV-4) |
The Epstein-Barr virus (EBV), also called human herpesvirus 4 (HHV-4), is a virus of the herpes family, which includes herpes simplex virus, and is one of the most common viruses in humans. Epstein-Barr virus occurs worldwide.
Most people become infected with EBV sometime during their lives, and therefore gain adaptive immunity, preventing repeated sickness from re-infection through EBV antibodies.[1] In the United States, as many as 95% of adults between 35 and 40 years of age have been infected. Infants become susceptible to EBV as soon as maternal antibody protection disappears. Many children become infected with EBV, and these infections usually cause no symptoms or are indistinguishable from the other mild, brief illnesses of childhood. In the United States and in other developed countries, many persons are not infected with EBV in their childhood years. When infection with EBV occurs during adolescence or young adulthood, it causes infectious mononucleosis 35% to 69% of the time. In immunocompromised individuals, the Epstein-Barr virus can also present as an opportunistic infection known as hairy leukoplakia.
Contents |
History
EBV is named after Anthony Epstein and Yvonne Barr, who together with Bert Achong,[2] discovered the virus in 1964 in cells cultured from the tumor specimens sent to them from Mulago Hospital in Kampala, Uganda by Denis Burkitt.[3] Burkitt and Epstein had met three years earlier in London during a talk by Burkitt on his findings regarding children's cancers in tropical Africa. In the talk, Burkitt postulated that there may be an infectious component to what he referred to as "African Lymphoma". After the presentation, the two men met and Burkitt agreed to send Epstein frozen specimens for him to analyze.[4] Epstein, Barr and Achong were working as a team at the Middlesex Hospital at the time.
Virology
The virus can execute many distinct programs of gene expression which can be broadly categorized as being lytic cycle or latent cycle.
- The lytic cycle or productive infection results in staged expression of several viral proteins with the ultimate objective of producing infectious virions. Formally, this phase of infection does not inevitably lead to lysis of the host cell as EBV virions are produced by budding from the infected cell. Lytic proteins include gp350 and gp110.[5]
- The latent cycle (lysogenic) programs are those that do not result in production of virions. A very limited, distinct set of viral proteins are produced during latent cycle infection. These include Epstein-Barr nuclear
antigen (EBNA)-1, EBNA-2, EBNA-3A, EBNA-3B, EBNA-3C, EBNA-leader protein (EBNA-LP) and latent membrane proteins (LMP)-1, LMP-2A and LMP-2B and the Epstein-Barr encoded RNAs (EBERs). In addition, EBV codes for at least twenty microRNAs which are expressed in latently infected cells.[6]
Programs
From studies of EBV gene expression in cultured Burkitt's lymphoma cell lines, at least three programs exist:
- EBER1&2 LMP2A EBNA1 (Latency I)
- EBER1&2 LMP2A LMP2B EBNA1 LMP1 (Latency II)
- EBER1&2 LMP2A LMP2B EBNA1 LMP1 EBNA2,3,4,5,6 (Latency III)
It is also postulated that a program exists in which all viral protein expression is shut off(latency 0).
Latent cycle
Epstein-Barr virus and its sister virus KSHV can be maintained and manipulated in the laboratory in continual latency. While many viruses are assumed to have this property during infection of their natural host, they do not have an easily managed system for studying this part of the viral lifecycle. Further, Walter Henle and Gertrude Henle[1], together with Harald zur Hausen who later discovered the papillomaviruses[2] causing cervical cancer, discovered that EBV can directly immortalize B cells after infection, mimicking some forms of EBV-related neoplasia[3].
On infecting the B-lymphocyte, the linear genome circularizes and the virus subsequently persists within the cell as an episome.
In primary infection, EBV replicates in oro-pharyngeal epithelial cells and establishes Latency III, II, and I infections in B-lymphocytes. EBV latent infection of B-lymphocytes is necessary for virus persistence, subsequent replication in epithelial cells, and release of infectious virus into saliva. EBV Latency III and II infections of B-lymphocytes, Latency II infection of oral epithelial cells, and Latency II infection of NK- or T-cell can result in malignancies, marked by uniform EBV genome presence and gene expression.[7]
Transformation
When EBV infects B-lymphocytes in vitro, lymphoblastoid cell lines eventually emerge that are capable of indefinite growth. The growth transformation of these cell lines is the consequence of viral protein expression.
EBNA-2, EBNA-3C and LMP-1 are essential for transformation while EBNA-LP and the EBERs are not. The EBNA-1 protein is essential for maintenance of the virus genome.[8]
It is postulated that following natural infection with EBV, the virus executes some or all of its repertoire of gene expression programs to establish a persistent infection. Given the initial absence of host immunity, the lytic cycle produces large amounts of virus to infect other (presumably) B-lymphocytes within the host.
The latent programs reprogram and subvert infected B-lymphocytes to proliferate and bring infected cells to the sites at which the virus presumably persists. Eventually, when host immunity develops, the virus persists by turning off most (or possibly all) of its genes, only occasionally reactivating to produce fresh virions. A balance is eventually struck between occasional viral reactivation and host immune surveillance removing cells that activate viral gene expression.
The site of persistence of EBV may be bone marrow. EBV-positive patients who have had their own bone marrow replaced with bone marrow from an EBV-negative donor are found to be EBV-negative after transplantation.[9]
Latent antigens
All EBV nuclear proteins are produced by alternative splicing of a transcript starting at either the Cp or Wp promoters at the left end of the genome (in the conventional nomenclature). The genes are ordered EBNA-LP/EBNA-2/EBNA-3A/EBNA-3B/EBNA-3C/EBNA-1 within the genome.
The initiation codon of the EBNA-LP coding region is created by an alternate splice of the nuclear protein transcript. In the absence of this initiation codon, EBNA-2/EBNA-3A/EBNA-3B/EBNA-3C/EBNA-1 will be expressed depending on which of these genes is alternatively spliced into the transcript.
Protein/genes
| Protein/gene/antigen | Stage | Description |
|---|---|---|
| EBNA-1 | latent+lytic | EBNA-1 protein binds to a replication origin (oriP) within the viral genome and mediates replication and partitioning of the episome during division of the host cell. It is the only viral protein expressed during group I latency. |
| EBNA-2 | latent+lytic | EBNA-2 is the main viral transactivator. |
| EBNA-3 | latent+lytic | These genes also bind the host RBP-Jκ protein. |
| LMP-1 | latent | LMP-1 is a six-span transmembrane protein that is also essential for EBV-mediated growth transformation. |
| LMP-2 | latent | LMP-2A/LMP-2B are transmembrane proteins that act to block tyrosine kinase signaling. |
| EBER | latent | EBER-1/EBER-2 are small nuclear RNAs of an unknown role. --> They bind to certain nucleoptrotein particles. Particles that contain EBER bind to PKR (dsRNA dependent serin/threonin protein kinase) and inhibit its function. EBER-particle also induce the production of IL-10 which enhances growth and inhibits cytotoxic T-cells. |
| miRNAs | latent | EBV microRNAs are encoded by two transcripts, one set in the BART gene and one set near the BHRF1 cluster. The three BHRF1 miRNAS are expressed during type III latency while the large cluster of BART miRNAs (up to 20 miRNAs) are expressed during type II latency. The functions of these miRNAs are currently unknown. |
| EBV-EA | lytic | early antigen |
| EBV-MA | lytic | membrane antigen |
| EBV-VCA | lytic | viral capsid antigen |
| EBV-AN | lytic | alkaline nuclease[10][4] |
Surface receptors
The Epstein-Barr Virus surface glycoprotein H (gH) is essential for penetration of B cells but also plays a role in attachment of virus to epithelial cells.[11]
In laboratory and animal trials in 2000, it was shown that both antagonism of RA-mediated growth inhibition and promotion of LCL proliferation were efficiently reversed by the glucocorticoid receptor (GR) antagonist RU486.[12]
References
- ^ "Mononucleosis". http://www.umm.edu/altmed/articles/mononucleosis-000109.htm. Retrieved 2009-10-27.
- ^ "NIHERST: Caribbean Icons in STI". http://caribbean-icons.org/science/bert-achong.htm. Retrieved 2008-10-05.
- ^ Epstein MA, Achong BG, Barr YM (March 1964). "Virus particles in cultured lymphoblasts from Burkitt's lymphoma". Lancet 1 (7335): 702–3. doi:. PMID 14107961.
- ^ Coakley D (2006). "Denis Burkitt and his contribution to haematology/oncology". Br J Haematol 135 (1): 17–25. doi:. PMID 16939495.
- ^ Lockey TD, Zhan X, Surman S, Sample CE, Hurwitz JL (2008). "Epstein-Barr virus vaccine development: a lytic and latent protein cocktail". Front. Biosci. 13: 5916–27. doi:. PMID 18508632. http://www.bioscience.org/2008/v13/af/3126/fulltext.htm.
- ^ The nomenclature used here is that of the Kieff lab. Other laboratories use different nomenclatures.
- ^ Robertson, ES (editor) (2010). Epstein-Barr Virus: Latency and Transformation. Caister Academic Press. ISBN 978-1-904455-62-2.
- ^ Yates JL, Warren N, Sugden B (1985). "Stable replication of plasmids derived from Epstein-Barr virus in various mammalian cells". Nature 313 (6005): 812–5. doi:. PMID 2983224.
- ^ Gratama JW, Oosterveer MA, Zwaan FE, Lepoutre J, Klein G, Ernberg I (1988). "Eradication of Epstein-Barr virus by allogeneic bone marrow transplantation: implications for sites of viral latency". Proc. Natl. Acad. Sci. U.S.A. 85 (22): 8693–6. doi:. PMID 2847171.
- ^ Buisson M, Géoui T, Flot D, Tarbouriech N, Ressing ME, Wiertz EJ, Burmeister WP (2009). "A bridge crosses the active-site canyon of the Epstein-Barr virus nuclease with DNase and RNase activities". J Mol. Biol. 319 (4): 717–28. doi:. PMID 19538972.
- ^ Molesworth SJ, Lake CM, Borza CM, Turk SM, Hutt-Fletcher LM (July 2000). "Epstein-Barr virus gH is essential for penetration of B cells but also plays a role in attachment of virus to epithelial cells". Journal of virology 74 (14): 6324–32. doi:. PMID 10864642. PMC 112138. http://jvi.asm.org/cgi/pmidlookup?view=long&pmid=10864642.
- ^ Quaia M, Zancai P, Cariati R, Rizzo S, Boiocchi M, Dolcetti R (July 2000). "Glucocorticoids promote the proliferation and antagonize the retinoic acid-mediated growth suppression of Epstein-Barr virus-immortalized B lymphocytes". Blood 96 (2): 711–8. PMID 10887139. http://www.bloodjournal.org/cgi/pmidlookup?view=long&pmid=10887139.
External links
- Epstein-Barr Virus: Implicated in Cancer Etiology in China, Impetus for a Vaccine Article in The Scientist 13(6):1, Mar. 15, 1999 (registration required)
- National (USA) Center for Infectious Diseases website on EBV
- Epstein Barr Virus Editor: Erle S. Robertson Department of Microbiology and the Abramson Comprehensive Cancer Center, University of Pennsylvania Medical School, Philadelphia, Pennsylvania 19104, USA
- International Association for Research on EBV Body that organizes the two-yearly EBV research meeting.
- Caribbean Icons, org Burt Achong
- http://www.webmd.com/multiple-sclerosis/news/20090504/epstein-barr-virus-linked-to-ms
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Mentioned in
- lymphocryptovirus
- EBV (abbreviation)
- Mononucleosis (in medicine)
- Hairy leukoplakia of the tongue (in medicine)
- Herpesviruses (in medicine)
- Infectious mononucleosis (in medicine)
- Infectious disease (in medicine)
- herpesvirus (disease, virus)
- Epstein-Barr Virus Test: Purpose
- Burkitt's lymphoma (malignant lymphoma)
- Gammaherpesvirinae
- viral hepatitis
- oral hairy leukoplakia
- Cytomegalovirus Antibody Screening Test: Purpose
