- 同
- EBV
- 同
- EBV
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- EBV
WordNet
- a harmful or corrupting agency; "bigotry is a virus that must not be allowed to spread"; "the virus of jealousy is latent in everyone"
- (virology) ultramicroscopic infectious agent that replicates itself only within cells of living hosts; many are pathogenic; a piece of nucleic acid (DNA or RNA) wrapped in a thin coat of protein
- a software program capable of reproducing itself and usually capable of causing great harm to files or other programs on the same computer; "a true virus cannot spread to another computer without human assistance" (同)computer virus
- British sculptor (born in the United States) noted for busts and large controversial works (1880-1959) (同)Jacob Epstein, Sir Jacob Epstein
PrepTutorEJDIC
- ビールス,ろ過性病原体
- bariumの化学記号
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/12/17 10:52:13」(JST)
wiki en
| Epstein–Barr | |
|---|---|
| Two Epstein–Barr virions | |
| Virus classification | |
| Group: | Group I (dsDNA) |
| Order: | Herpesvirales |
| Family: | Herpesviridae |
| Subfamily: | Gammaherpesvirinae |
| Genus: | Lymphocryptovirus |
| Species: | Human herpesvirus 4 (HHV-4) |
| Synonyms | |
|
|
The Epstein–Barr virus (EBV), also called human herpesvirus 4 (HHV-4), is one of eight viruses in the herpes family, and is one of the most common viruses in humans.
It is best known as the cause of infectious mononucleosis (glandular fever). It is also associated with particular forms of cancer, such as Hodgkin's lymphoma, Burkitt's lymphoma, gastric cancer, nasopharyngeal carcinoma, and conditions associated with human immunodeficiency virus (HIV), such as hairy leukoplakia and central nervous system lymphomas.[1][2] There is evidence that infection with EBV is associated with a higher risk of certain autoimmune diseases,[3] especially dermatomyositis, systemic lupus erythematosus, rheumatoid arthritis, Sjögren's syndrome,[4][5] and multiple sclerosis.[6] Some 200,000 cancer cases per year are thought to be attributable to EBV.[7]
Infection with EBV occurs by the oral transfer of saliva[8] and genital secretions.
Most people become infected with EBV and gain adaptive immunity. In the United States, about half of all five-year-old children and about 90 percent of adults have evidence of previous infection.[9] 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 other developed countries, many people are not infected with EBV in their childhood years. When infection with EBV occurs during adolescence, it causes infectious mononucleosis 35 to 50 percent of the time.[10]
EBV infects B cells of the immune system and epithelial cells. Once EBV's initial lytic infection is brought under control, EBV latently persists in the individual's B cells for the rest of the individual's life.[8]
Contents
- 1 Virology
- 1.1 Structure and genome
- 1.2 Tropism
- 1.3 Replication cycle
- 1.3.1 Entry to the cell
- 1.3.2 Lytic replication
- 1.3.3 Latency
- 1.3.4 Reactivation
- 1.4 Transformation of B-lymphocytes
- 1.5 Latent antigens
- 1.6 Protein/genes
- 1.7 Subtypes of EBV
- 2 Role in disease
- 3 History
- 4 Research
- 5 See also
- 6 References
Virology
Simplified diagram of the structure of EBV
| This section may contain an excessive amount of intricate detail that may only interest a specific audience. Please help relocate any relevant information, and remove excessive detail that may be against Wikipedia's inclusion policy. (December 2015) |
Structure and genome
The virus is approximately 122 nm to 180 nm in diameter and is composed of a double helix of DNA of about 172,000 base pairs and containing about 85 genes.[8] The DNA is surrounded by a protein nucleocapsid. This nucleocapsid is surrounded by a tegument made of protein, which in turn is surrounded by an envelope containing both lipids[11] and surface projections of glycoproteins which are essential to infection of the host cell.[11]
Tropism
The term viral tropism refers to which cell types EBV infects. EBV can infect different cell types, including B cells and epithelial cells.[12]
The viral three-part glycoprotein complexes of gHgLgp42 mediate B cell membrane fusion; although the two-part complexes of gHgL mediate epithelial cell membrane fusion. EBV that are made in the B cells have low numbers of gHgLgp42 complexes, because these three-part complexes interact with Human-leukocyte-antigen class II molecules present in B cells in the endoplasmic reticulum and are degraded. In contrast, EBV from epithelial cells are rich in the three-part complexes because these cells do not normally contain HLA class II molecules. As a consequence, EBV made from B cells are more infectious to epithelial cells, and EBV made from epithelial cells are more infectious to B cells. Viruses lacking the gp42 portion are able to bind to human B cells but unable to infect.[13]
Replication cycle
The EBV replication cycle
Entry to the cell
EBV can infect both B cells and epithelial cells. The mechanisms for entering these two cells are different.
To enter B cells, viral glycoprotein gp350 binds to cellular receptor CD21 (also known as CR2).[14] Then, viral glycoprotein gp42 interacts with cellular MHC class II molecules. This triggers fusion of the viral envelope with the cell membrane, allowing EBV to enter the B cell.[11] Human CD35, also known as complement receptor 1 (CR1), is an additional attachment factor for gp350/220, and can provide a route for entry of EBV into CD21-negative cells, including immature B-cells. EBV infection downregulates expression of CD35.[15]
To enter epithelial cells, viral protein BMRF-2 interacts with cellular β1 integrins. Then, viral protein gH/gL interacts with cellular αvβ6/αvβ8 integrins. This triggers fusion of the viral envelope with the epithelial cell membrane, allowing EBV to enter the epithelial cell.[11] Unlike B cell entry, epithelial cell entry is actually impeded by viral glycoprotein gp42.[14]
Once EBV enters the cell, the viral capsid dissolves and the viral genome is transported to the cell nucleus.
Lytic replication
The lytic cycle, or productive infection, results in the production of infectious virions. EBV can undergo lytic replication in both B cells and epithelial cells. In B cells, lytic replication normally only takes place after reactivation from latency. In epithelial cells, lytic replication often directly follows viral entry.[11]
For lytic replication to occur, the viral genome must be linear. The latent EBV genome is circular, so it must linearize in the process of lytic reactivation. During lytic replication, viral DNA polymerase is responsible for copying the viral genome. This contrasts with latency, in which host cell DNA polymerase copies the viral genome.[11]
Lytic gene products are produced in three consecutive stages: immediate-early, early, and late.[11] Immediate-early lytic gene products act as transactivators, enhancing the expression of later lytic genes. Immediate-early lytic gene products include BZLF1 (also known as Zta, EB1, associated with its product gene ZEBRA) and BRLF1 (associated with its product gene Rta).[11] Early lytic gene products have many more functions, such as replication, metabolism, and blockade of antigen processing. Early lytic gene products include BNLF2.[11] Finally, late lytic gene products tend to be proteins with structural roles, like VCA, which forms the viral capsid. Other late lytic gene products, such as BCRF1, help EBV evade the immune system.[11]
EGCG, a polyphenol in green tea, has shown in a study to inhibit EBV spontaneous lytic infection at the DNA, gene transcription and protein levels in a time and dose-dependent manner; the expression of EBV lytic genes Zta, Rta, and early antigen complex EA-D (induced by Rta), however the highly stable EBNA-1 gene found across all stages of EBV infection is unaffected.[16] Specific inhibitors (to the pathways) suggest that Ras/MEK/MAPK pathway contributes to EBV lytic infection though BZLF1 and PI3-K pathway through BRLF1, the latter completely abrogating the ability of a BRLF1 adenovirus vector to induce the lytic form of EBV infection.[16] Additionally, the activation of some genes but not others is being studied to determine just how to induce immune destruction of latently infected B-cells by use of either TPA or sodium butyrate.[16]
Unlike lytic replication for many other viruses, EBV lytic replication does not inevitably lead to lysis of the host cell because EBV virions are produced by budding from the infected cell. Lytic proteins include gp350 and gp110.[11][17]
Latency
Unlike lytic replication, latency does not result in production of virions.[11] Instead, the EBV genome circular DNA, resides in the cell nucleus as an episome, and is copied by cellular DNA polymerase.[11] In latency, only a portion of EBV's genes are expressed.[8] Latent EBV expresses its genes in one of three patterns, known as latency programs. EBV can latently persist within B cells and epithelial cells, but different latency programs are possible in the two types of cell.
EBV can exhibit one of three latency programs: Latency I, Latency II, or Latency III. Each latency program leads to the production of a limited, distinct set of viral proteins and viral RNAs.[18][19]
| Gene Expressed | EBNA-1 | EBNA-2 | EBNA-3A | EBNA-3B | EBNA-3C | EBNA-LP | LMP-1 | LMP-2A | LMP-2B | EBER |
|---|---|---|---|---|---|---|---|---|---|---|
| Product | Protein | Protein | Protein | Protein | Protein | Protein | Protein | Protein | Protein | ncRNAs |
| Latency I | + | – | – | – | – | – | – | – | – | + |
| Latency II | + | – | – | – | – | + | + | + | + | + |
| Latency III | + | + | + | + | + | + | + | + | + | + |
It is also postulated that a program exists in which all viral protein expression is shut off (Latency 0).
Within B cells, all three latency programs are possible.[8] EBV latency within B cells usually progresses from Latency III to Latency II to Latency I. Each stage of latency uniquely influences B cell behavior.[8] Upon infecting a resting naive B cell, EBV enters Latency III. The set of proteins and RNAs produced in Latency III transforms the B cell into a proliferating blast (also known as B cell activation).[8][11] Later, the virus restricts its gene expression and enters Latency II. The more limited set of proteins and RNAs produced in Latency II induces the B cell to differentiate into a memory B cell.[8][11] Finally, EBV restricts gene expression even further and enters Latency I. Expression of EBNA-1 allows the EBV genome to replicate when the memory B cell divides.[8][11]
Within epithelial cells, only Latency II is possible.[citation needed]
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.[20]
Reactivation
Latent EBV in B cells can be reactivated to switch to lytic replication. This is known to happen in vivo, but what triggers it is not known precisely. In vitro, latent EBV in B cells can be reactivated by stimulating the B cell receptor, so reactivation in vivo probably takes place when latently infected B cells respond to unrelated infections.[11] In vitro, latent EBV in B cells can also be reactivated by treating the cells with sodium butyrate or TPA.[citation needed]
Transformation of B-lymphocytes
When EBV infects B cells 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, whereas EBNA-LP and the EBERs are not.[21]
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.[22]
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, which bind to certain nucleoprotein particles, enabling binding to PKR (dsRNA dependent serin/threonin protein kinase) thus inhibiting its function. EBER-particles also induce the production of IL-10, which enhances growth and inhibits cytotoxic T-cells. |
| v-snoRNA1 | latent | Epstein–Barr virus snoRNA1 is a box CD-snoRNA generated by the virus during latency. V-snoRNA1 may act as a miRNA-like precursor that is processed into 24 nucleotide sized RNA fragments that target the 3'UTR of viral DNA polymerase mRNA.[23] |
| ebv-sisRNA | latent | Ebv-sisRNA-1 is a stable intronic sequence RNA generated during latency program III. After the EBERs it is the third most abundant small RNA produced by the virus during this program.[24] |
| 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, whereas 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[25][26] |
Subtypes of EBV
EBV can be divided into two major types, EBV type 1 and EBV type 2. These two subtypes have different EBNA-3 genes. As a result, the two subtypes differ in their transforming capabilities and reactivation ability. Type 1 is dominant throughout most of the world, but the two types are equally prevalent in Africa. One can distinguish EBV type 1 from EBV type 2 by cutting the viral genome with a restriction enzyme and comparing the resulting digestion patterns by gel electrophoresis.[11]
Role in disease
EBV has been implicated in several diseases that include infectious mononucleosis,[27] Burkitt's lymphoma,[28] Hodgkin's lymphoma,[29] gastric cancer,[30] nasopharyngeal carcinoma, multiple sclerosis,[6] and lymphomatoid granulomatosis.[31]
The Epstein–Barr virus has been implicated also in disorders related to alpha-synuclein aggregation (e.g. Parkinson's disease, dementia with Lewy bodies and multiple system atrophy).[32]
History
The Epstein–Barr virus was named after Michael Anthony Epstein (born 18 May 1921), now a professor emeritus at the University of Bristol, and Yvonne Barr (born 1932), a 1966 Ph.D graduate from the University of London, who together both discovered[33] and, in 1964, published on the existence of the virus.[34] In 1961, Epstein, a pathologist and expert electron microscopist, attended a lecture on "The Commonest Children's Cancer in Tropical Africa—A Hitherto Unrecognised Syndrome." This lecture, by Denis Parsons Burkitt, a surgeon practicing in Uganda, was the description of the "endemic variant" (pediatric form) of the disease that bears his name. In 1963, a specimen was sent from Uganda to Middlesex Hospital to be cultured. Virus particles were identified in the cultured cells, and the results were published in The Lancet in 1964 by Epstein, Bert Achong, and Barr. Cell lines were sent to Werner and Gertrude Henle at the Children's Hospital of Philadelphia who developed serological markers. In 1967, a technician in their laboratory developed mononucleosis and they were able to compare a stored serum sample, showing that antibodies to the virus developed.[35][36][37] In 1968, they discovered that EBV can directly immortalize B cells after infection, mimicking some forms of EBV-related infections,[38] and confirmed the link between the virus and infectious mononucleosis.[39]
Research
As a relatively complex virus, EBV is not yet fully understood. Laboratories around the world continue to study the virus and develop new ways to treat the diseases it causes. One popular way of studying EBV in vitro is to use bacterial artificial chromosomes.[40] Epstein–Barr virus can be maintained and manipulated in the laboratory in continual latency (a property shared with Kaposi's sarcoma-associated herpesvirus, another of the eight human herpesviruses). Although many viruses are assumed to have this property during infection of their natural hosts, there is not an easily managed system for studying this part of the viral lifecycle. Genomic studies of EBV have been able to explore lytic reactivation and regulation of the latent viral episome.[41]
See also
| Medicine portal | |
| Viruses portal |
- Epstein–Barr virus vaccine
- Epstein–Barr virus infection
- James Corson Niederman, the physician who proved how the Epstein–Barr virus is transmitted in infectious mononucleosis
- Transcriptome and epigenome of EBV
References
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- ^ Toussirot E, Roudier J (October 2008). "Epstein–Barr virus in autoimmune diseases". Best Practice & Research. Clinical Rheumatology 22 (5): 883–96. doi:10.1016/j.berh.2008.09.007. PMID 19028369.
- ^ Dreyfus DH (December 2011). "Autoimmune disease: A role for new anti-viral therapies?". Autoimmunity Reviews 11 (2): 88–97. doi:10.1016/j.autrev.2011.08.005. PMID 21871974.
- ^ Pender MP (2012). "CD8+ T-Cell Deficiency, Epstein–Barr Virus Infection, Vitamin D Deficiency, and Steps to Autoimmunity: A Unifying Hypothesis". Autoimmune Diseases 2012: 189096. doi:10.1155/2012/189096. PMC 3270541. PMID 22312480.
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- ^ http://www.cancerresearchuk.org/about-us/cancer-news/press-release/2014-03-24-developing-a-vaccine-for-the-epstein-barr-virus-could-prevent-up-to-200000-cancers-globally-say
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- ^ About 90% of adults have antibodies that show that they have a current or past EBV infection. National Center for Infectious Diseases
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- ^ Hutzinger, R.; Feederle, R.; Mrazek, J.; Schiefermeier, N.; Balwierz, J.; Zavolan, M.; Polacek, N.; Delecluse, J.; Hüttenhofer, A. (Aug 2009). Cullen, Bryan R, ed. "Expression and processing of a small nucleolar RNA from the Epstein-Barr virus genome" (Free full text). PLoS Pathogens 5 (8): e1000547. doi:10.1371/journal.ppat.1000547. ISSN 1553-7366. PMC 2718842. PMID 19680535.
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- ^ 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:10.1016/j.jmb.2009.06.034. PMID 19538972.
- ^ Buisson, M.; Géoui, T.; Flot, D.; Tarbouriech, N.; Ressing, M. E.; Wiertz, E. J.; Burmeister, W. P. (2009). "A Bridge Crosses the Active-Site Canyon of the Epstein–Barr Virus Nuclease with DNase and RNase Activities". Journal of Molecular Biology 391 (4): 717–728. doi:10.1016/j.jmb.2009.06.034. PMID 19538972.
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UpToDate Contents
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- 1. エプスタインバーウイルス（EBウイルス）感染の臨床的特徴および治療 clinical manifestations and treatment of epstein barr virus infection
- 2. エプスタインバーウイルス（EBウイルス）のウイルス学 virology of epstein barr virus
- 3. 成人および思春期の伝染性単核球症 infectious mononucleosis in adults and adolescents
- 4. ホジキンリンパ腫におけるエプスタイン・バール・ウイルス the role of epstein barr virus in hodgkin lymphoma
- 5. 非ホジキンリンパ腫の病理の概要 overview of the pathobiology of the non hodgkin lymphomas
English Journal
- Cordycepin enhances Epstein-Barr virus lytic infection and Epstein-Barr virus-positive tumor treatment efficacy by doxorubicin.
- Du Y1, Yu J2, Du L1, Tang J2, Feng WH3.
- Cancer letters.Cancer Lett.2016 Jul 1;376(2):240-8. doi: 10.1016/j.canlet.2016.04.001. Epub 2016 Apr 7.
- The consistent latent presence of Epstein-Barr virus (EBV) in tumor cells offers potential for virus-targeted therapies. The switch from the latent form of EBV to the lytic form in tumor cells can lead to tumor cell lysis. In this study, we report that a natural small molecule compound, cordycepin,
- PMID 27063964
- Epstein-Barr and cytomegalovirus DNA salivary shedding correlate with long-term plasma HIV RNA detection in HIV-infected men who have sex with men.
- Scaggiante R1, Andreis S2, Basso M2, Franchin E2, Franzetti M1, Del Vecchio C2, Torti C3, Mengoli C2, Cruciani M4, Sarmati L5, Palù G2, Parisi SG2.
- Journal of medical virology.J Med Virol.2016 Jul;88(7):1211-21. doi: 10.1002/jmv.24441. Epub 2015 Dec 15.
- The aim of the study was to evaluate cytomegalovirus (CMV) and Epstein-Barr virus (EBV) DNA salivary shedding in HIV-positive men who have sex with men (MSM) and to determine whether viro-immunological parameters and long-term (24 months) plasma HIV RNA (pHIV) detection may predict herpesviruses rep
- PMID 26636290
- Immunological methods for the detection of porcine lymphotropic herpesviruses (PLHV).
- Plotzki E1, Keller M2, Ehlers B3, Denner J4.
- Journal of virological methods.J Virol Methods.2016 Jul;233:72-7. doi: 10.1016/j.jviromet.2016.02.017. Epub 2016 Mar 29.
- Porcine lymphotropic herpesviruses (PLHV-1, -2, and -3) are widespread in pigs and closely related to the human pathogenic gammaherpesviruses Epstein-Barr virus (human herpesvirus 4, HHV-4) and Kaposi sarcoma herpesvirus (HHV-8). In minipigs, PLHV-1 causes a porcine post-transplantation lymphoprolif
- PMID 27036503
Japanese Journal
- 製薬会社とのライセンス経験から見た抗体医薬開発
- 高田 賢蔵
- 薬学雑誌 133(1), 61-66, 2013
- NAID 40019555347
- 鼻部に生じたメトトレキサート関連リンパ増殖性疾患の1例 (特集 白血病・リンフォーマ)
- 渡邊 友也,蒲原 毅,松倉 節子 [他]
- 皮膚科の臨床 54(13), 1835-1839, 2012-12
- NAID 40019515405
- 肺原発リンパ上皮腫様癌
- 井上 尚,稲葉 浩久,熱田 幸司 [他]
- 胸部外科 65(13), 1123-1126, 2012-12
- NAID 40019497421
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