Buisson M., Morand P., Genoulaz O., Bourgeat M. J., Micoud M., Seigneurin J. M. Changes in the dominant Epstein-Barr virus type during human immunodeficiency virus infection. It is known that IL-10 suppresses the CTL immune response mediated by IFN- and IL-2 production by the Th-1 subset of T-helper cells and that cells producing IL-10 can escape immune surveillance (155, 156). LMP-1 has been most directly linked to oncogenesis by virtue of its ability to recruit an array of cellular genes. Of the 100 viral proteins, only LMP-2 is expressed. Hennessy K., Heller M., van Santen V., Kieff E. Simple repeat array in Epstein-Barr virus DNA encodes part of the Epstein-Barr nuclear antigen. Bouvier G., Poirier S., Shao Y., Malaveille C., Ohshima H., Polack A., et al . Complementary strand transcripts (or Bam A rightward transcripts) are transcribed from a region mapping to the Bam H1A fragment of the viral genome (112). Latency II has been associated with Hodgkins disease, T-cell non-Hodgkins lymphoma, and nasopharyngeal carcinoma (129). Henle G., Henle W., Diehl V. Relation of Burkitts tumor-associated herpes-type virus to infectious mononucleosis. At the 3 end of the leader exon, virtually any exon may be spliced, creating a huge variety in the potential ends for EBNA-LP (reviewed in Ref. 38). EBV gene products induce an immune response; however, the immunocompromised state of the host allows for unrestricted gene expression without the consequences such expression would normally elicit in an immunocompetent host. Epstein-Barr Virus (EBV) Antibodies to Viral Capsid Antigen (VCA), IgG The type-specific epitopes of the Epstein-Barr virus nuclear antigen 2 are near the carboxy terminus of the protein. It also controls expression of numerous cytokines, including ones such as lymphotoxin, which is an autocrine growth factor for EBV-transformed cells (92). Iatrogenic immunosuppression leading to primary EBV infection or reactivation of latent EBV infection is followed by polyclonal expansion of B-cell populations with a selective growth advantage. It also inhibits apoptosis by elevating levels of Bcl-2 (85). The LMP-2 gene encodes two proteins: LMP-2A and LMP-2B. Regardless, whether EBV is present in breast cancer and its possible etiological role in oncogenesis remain to be clarified. Rowe D., Clarke J. BARF-1 produces a protein that shows some homology to the intracellular adhesion molecule 1, as well as the human colony-stimulating factor 1 receptor (125, 126). In 1958, Denis Burkitt (10) described a common cancer primarily affecting children in specific regions of Africa. EBNA-LP interacts with EBNA-2 to drive resting B lymphocytes into the G1 phase of the cell cycle (73) by binding and inactivating cellular p53 and retinoblastoma protein tumor suppressor gene products (74). In addition, tumor resistance may occur because of mutations in EBV epitopes recognized by CTLs or by other mechanisms (e.g., production of cytokines such as IL-10) exploited by the tumor to evade surveillance (299). Epstein-Barr virus and breast cancer: Serological study in a high EA-IgG, Zta-IgG, and Epstein-Barr virus (EBV) DNA load in non-invasive nasopharyngeal brushings (EBV-DNA brushings) have both high sensitivity and specificity, EBNA1-IgG and VCA-IgG have only high sensitivity, and EBNA1-IgA, VCA-IgA, Rta-IgG, Zta-IgA, HSP70, and serum sialic acid (SA) have only high specificity. Immunocompetent carriers control latent EBV infection via CTLs. Tsuchiyama J., Yoshino T., Mori M., Kondoh E., Oka T., Akagi T., et al Characterization of a novel human natural killer-cell line (NK-YS) established from natural killer cell lymphoma/leukemia associated with Epstein-Barr virus infection. International Agency for Research on Cancer. Nasal T/natural killer non-Hodgkins lymphoma cells exhibit several unique genotypic and phenotypic features. It is also an effective agent in the management of EBV-related lymphoproliferative disorders. This study investigated serum level of SA, Rta-IgG, EA-IgA and VCA-IgA in nasopharyngeal cancer patients and the diagnostic value of combined assay. Ott G., Kalla J., Ott M., Muller-Hermelink H. The Epstein-Barr virus in malignant non-Hodgkins lymphoma of the upper aerodigestive tract. Cheung R., Dosch H. The tyrosine kinase lck is critically involved in the growth transformation of human B lymphocytes. The Epstein-Barr virus (EBV) small RNA EBER 1 binds and relocalizes ribosomal protein L22 in EBV-infected human B lymphocytes. Epstein-Barr virus is a virus that typically causes a mild to moderate illness. Essential for EBV immortalization of cell, overcomes retinoblastoma protein (pRB) checkpoint in cell cycle, interacts with CBF1, increases production of LMP1. What does a high ebv viral capsid antibody igg mean? Mimics CD40 ligand binding signal, elevates levels of. Elevated antinuclear antibodies and altered anti-Epstein-Barr virus Whether there is a direct causal relationship between EBV and the development of the translocation is not known. Kwong Y., Chan A., Liang R., Chiang A. K., Chim C. S., Chan T. K., et al CD56+ NK lymphomas: clinicopathological features and prognosis. This is followed by an increase in mRNA synthesis, blast transformation, homotypic cell adhesion, surface CD23 expression (a characteristic surface marker for activated B cells), and interleukin (IL)-6 production (32, 33, 34). Although any mechanism relating EBV to tumorigenesis in gastric malignancies remains highly speculative, it has been demonstrated that there is a delay in apoptosis in EBV-positive gastric carcinomas (associated with up-regulation of BCL-2 and p53) and a decrease in cellular differentiation (associated with decreased E-cadherin expression; Refs. In biopsy tissues, molecular detection of EBER transcripts by in situ hybridization remains the gold standard for proving that a histopathological lesion is EBV related. There is also data that suggests that the incidence of EBV-positive Hodgkins disease is age-related, with the virus being preferentially associated with tumors from pediatric and older patients (166, 167, 168, 169, 170). Interestingly, although LMP-1 and LMP-2 are both expressed, there seems to be no mounted CTL response to the Hodgkins-Reed Sternberg cells (151, 152, 153). Moss D., Schmidt C., Elliot S., Suhrbier A., Burrows S., Khanna R. Strategies involved in developing an effective vaccine for EBV-associated diseases. The limited repertoire of gene products also prevents frequent viral replication. Keywords: Adenoid hypertrophy; EBV; Otitis media with effusion. A putative origin of replication of plasmids derived from Epstein-Barr virus is composed of two. Strockbine L. D., Cohen J. I., Farrah T., Lyman S. D., Wagener F., DuBose R. F., et al The Epstein-Barr virus BARF1 gene encodes a novel, soluble colony-stimulating factor-1 receptor. Leiomyosarcomas are smooth muscle tumors. Persistently High Epstein-Barr Virus (EBV) Loads in Peripheral Blood Henkel T., Ling P., Hayward S., Peterson M. G. Mediation of Epstein-Barr virus EBNA2 transactivation by recombination signal-binding protein J . Hsieh J., Henkel T., Salmon P., Robey E., Peterson M. G., Hayward S. D. Truncated mammalian Notch1 activates CBF1/RBPJk-repressed genes by a mechanism resembling that of Epstein-Barr virus EBNA2. 296). In more developed areas, primary infection can be delayed until late adolescence or adulthood and results in infectious mononucleosis in some cases (9). Howie D., Sayos J., Terhorst C., Morra M. The gene defective in X-linked lymphoproliferative disease controls T-cell dependent immune surveillance against Epstein-Barr virus. Seemayer T., Gross T., Egeler R., Pirruccello S. J., Davis J. R., Kelly C. M., et al X-Linked lymphoproliferative disease: twenty-five years after the discovery. Sung N., Kenney S., Gutsch D., Pagano J. S. EBNA-2 transactivates a lymphoid-specific enhancer in the Bam HI C promoter of Epstein-Barr virus. The other three types of latency characterize a heterogenous group of malignancies. The role of IL-10 in the immortalization process and immune evasion remains a matter of debate (154). Chapman A., Rickinson A. Epstein-Barr virus in Hodgkins disease. Rousset F., Garcia E., Defrance T., Peronne C., Vezzio N., Hsu D. H., et al Interleukin-10 is a potent growth and differentiation factor for activated B lymphocytes. Lenoir G., Philip T., Sohier R. Burkitt-tupe lymphoma: EBV association and cytogenetic markers in cases from various geographic locations Magrath I. Oconnor G. Ramor B. eds. - Anti-VCA IgG appears in the acute phase of EBV infection, peaks at two to four weeks after onset, declines slightly then persists for the rest of a person's life. 105, Takeda N., Ohigashi H., Hirai N., Koshimizu K., Suzuki M., Tatematsu A., et al Mass spectrometric identification of a phorbol diester 12-. Lanyi A., Li B., Li S., Talmadge C. B., Brichacek B., Davis J. R., et al A yeast artificial chromosome (YAC) contig encompassing the critical region of the X-linked lymphoproliferative disease (XLP) locus. Pagano J. Epstein-Barr virus: the first human tumor virus and its role in cancer. During acute infection, EBV primarily infects and replicates in the stratified squamous epithelium of the oropharynx (3, 4). All three EBNA-3s interact with Cp binding factor 1. Dalla-Favera R., Bregni M., Erickson J., Patterson D., Gallo R. C., Croce C. M. Human c-myc oncogene is located on the region of chromosome 8 that is translocated in Burkitt lymphoma cells. In addition, the small polyadenylated viral RNAs designated as EBERs 1 and 2 are also discerned. IFN-inducible dsRNA-dependent protein kinase is known to mediate protein synthesis control by dsRNA and has also been reported to phosphorylate the inhibitory subunit inhibitor of nuclear factor-B of the nuclear factor-B transcription factor. On the basis of sequence alignment, homology between the BDLF2 protein and human cyclin B1 has been suggested (115). Strickler J., Meneses M., Habermann T., Ilstrup D. M., Earle J. D., McDonald T. J., et al Polymorphic reticulosis: a reappraisal. EBNA-1 is a sequence-specific DNA binding phosphoprotein that is required for the replication and maintenance of the EBV genome (49). In healthy individuals, the virus persists episomally in resting memory B cells. EBNA-1 IgG antibody frequency ( p = 0.00005) and EBNA-1 and VCA IgG antibody levels ( p <0.0001 for both) were higher in patients than in controls. Indeed, in Taiwan, nasopharyngeal carcinoma is the most common cancer in men and the third most common in women (201, 202). EBNA-3C may overcome the retinoblastoma (retinoblastoma tumor suppressor gene checkpoint in the G1 phase of the cell cycle (81). A. Witherspoon R., Fisher L., Schoch G., Martin P., Sullivan K. M., Sanders J., et al Secondary cancers after bone marrow transplantation for leukemia or aplastic anemia. Davi F., Delecluse H., Guiet P., Gabarre J., Fayon A., Gentilhomme O., et al Burkitt-like lymphomas in AIDS patients: characterization within a series of 103 human immunodeficiency virus-associated non-Hodgkins lymphomas. Epstein-Barr virus antibodies in serum and DNA load in saliva are not EBV is known primarily for its ability to infect B cells, but it can also infect other cells. Schlager S., Speck S., Woisetschlager M. Transcription of the Epstein-Barr virus nuclear antigen 1 gene occurs before induction of the BCR2 (Cp) EBNA gene promoter during the initial stages of infection in B cells. Tomkinson B., Robertson E., Kieff E. Epstein-Barr virus nuclear proteins EBNA-3A and EBNA-3C are essential for B-lymphocyte growth transformation. Risk factors for Epstein Barr virus-associated cancers: a systematic However, harvesting autologous CTLs may often be impractical or impossible. Although an EBV-compatible receptor on epithelial cells has not been found, a surface protein that is antigenically related to the B cell. EBV infection of B lymphocytes is thought to occur in the oropharyngeal lymphoid organs, and in normal carriers, the virus persists in circulating memory B cells (5, 6, 7). Virus particles in cultured lymphoblasts from Burkitts lymphoma. The viral genome consists of a series of 0.5-kb terminal direct repeats at either end and internal repeat sequences that serve to divide the genome into short and long unique sequence domains that have most of the coding capacity (13). Meanwhile, the Janus kinase/signal transducers and activators of transcription cascade integrates with the activator protein-1 transcription factor pathway. The breaks in chromosome 8 generally occur outside the c-myc locus. Generation of EBV-specific CTLs from seropositive healthy donors generally takes 812 weeks. EBER hybridization and EBV-LMP-1 immunostains are used routinely to detect latent EBV in tissues affected by PTLD. Anti-VCA IgM appears when you're first infected with EBV and usually disappears in 4 to 6 . VCA IgM antibodies occur at the beginning of the disease but decrease or even disappear within a few months.. All three types of latency express BARF-0s. Finally, there are AIDS-related lymphoproliferative disorders. The EBNA-1 coding sequence lies in the BKRF1 open reading frame (50, 51, 52, 53). There exist several distinct classes of EBV-associated lymphoproliferative disorders in immunocompromised individuals. It is known that the Y1 and Y2 genes are very important in the immortalization process. 1). In addition, intensity of immunosuppression, receiving T-cell-depleted marrow and concurrent cytomegalovirus may be important. The initial treatment of PTLD is reduction of immunosuppression. This pathway is important in cell fate determination in the fruit fly and may play a role in development of T-cell lymphoma in humans. Eliopoulos A. G., Gallagher N. J., Blake S. M. A., Dawson C. W., Young L. S. Activation of the p38 mitogen activated protein kinase pathway by Epstein-Barr virus-encoded latent membrane protein 1 coregulates interleukin-6 and interleukin-8 production. If the VCA-IgM is negative but VCA-IgG and an EBNA antibody are positive, then it is likely that the person tested had a previous EBV infection. A synthesis of the data supports a role for LMP-2 in modifying normal B-cell development to favor maintenance of EBV latency in the bone marrow (3). Oddly, cases involving Alaskan Inuits are almost always EBV-2 related but contain polymorphisms characteristic of Asian EBV-1 (217). Okano M. Epstein-Barr virus infection and its role in the expanding spectrum of human diseases. Miller W., Mosialos G., Kieff E., Raab-Traub N. Epstein-Barr virus LMP1 induction of the epidermal growth factor receptor is mediated through a TRAF signaling pathway distinct from NF-B activation. To circumvent this problem, arginine butyrate, which can selectively activate EBV thymidine kinase genes in lymphoma cells, has been administered together with gancyclovir; this combination has demonstrated some efficacy in patients with EBV-associated lymphoproliferations after solid organ transplantation (286). CAEBV is a severe illness with unusual EBV activation that may be fatal with multiple organ failure, and it is associated with malignant lymphoma without prior immunosuppression [ 2 , 3 ]. Optimal Result: 0 - 0.001 Units. Zutter M., Martin P., Sale G., Shulman H. M., Fisher L., Thomas E. D., et al Epstein-Barr virus lymphoproliferation after bone marrow transplantation. . Complementary strand transcripts encoded at high levels in nasopharyngeal carcinomas. In a primary EBV infection, three antibodies (-IgG, -IgM, and -IgA) are produced against EBV viral capsid antigen, two antibodies (-IgG and -IgA) are produced in response to early antigen D, and one antibody (-IgG) is produced in response to early antigen R (25). These cells are susceptible to genetic changes and BCL-6 may be one of the first such genes altered (268, 274). Get Started. Moorthy R., Thorley-Lawson D. Biochemical, genetic, and functional analyses of the phosphorylation sites on the Epstein-Barr virus encoded oncogenic latent membrane protein LMP-1. The. Undifferentiated nasopharyngeal cancer affects mostly individuals in their mid-40s and is more common in men (194). Circularization and W promoter expression launch an ordered cascade of events that leads to the expression of all of the EBNA proteins and the two latent membrane proteins (LMPs; Ref. In particular, defects in this gene may lead to a decreased ability to control immune responses to viruses, including EBV (259). More details on the infection? EBV was first identified in 1964 when Anthony Epsteins group discerned virus-like particles by electron microscopy in a cell line that had been established from a Burkitts lymphoma biopsy (11). Upon infection, the individual remains a lifelong carrier of the virus (2). Abdel-Hamid M., Chen J., Constantine N., Massoud M., Raab-Traub N. EBV strain variation: geographical distribution in relation to disease state. B., Shishodia S., Estrov Z., Kurzrock R. Autocrine lymphotoxin production in Epstein-Barr Virus (EBV)-immortalized B-cells: induction via NF-B activation mediated by EBV-derived latent membrane protein 1. This site uses cookies. Henle G., Henle W. Seroepidemiology of the virus Epstein M. A. Achong B. G. eds. Undifferentiated nasopharyngeal carcinoma is associated with EBV, whereas the association with the other two subtypes of nasopharyngeal cancer is controversial at best (193, 194). Choi P., Suen M., Huang D., Lo K. W., Lee J. C. Nasopharyngeal carcinoma: genetic changes, Epstein-Barr virus infection, or both. Several types of non-B-cell, non-Hodgkins lymphoma are associated with EBV (171, 172). Conclusion: Markedly increased serum anti-EBV VCA IgG antibodies in children who developed upper respiratory tract complications such as severe AH and COME may show the significant role of enhanced immune system reaction in the pathogenesis of these complications due to EBV infection. The titers of anti-EBV antibodies were as follows: VCA-IgG 5120, EADR-IgG 10 240 and EBNA 20. . Early antigen (EA) Anti-EA IgG appears in the acute phase of illness and generally falls to undetectable levels after three to six months. The disorder occurs commonly in combined liver-kidney transplants, followed by cardiac, liver, lung, and then kidney transplants. p38/mitogen-activated protein kinase is also a central signaling pathway and activates the ATF2 transcription factor. The EBNA-LP gene is characterized by a great deal of RNA splicing. Interpret your laboratory results instantly with us. Gross T., Patton D., Davis J. X-Linked lymphoproliferative disease manifested without apparent EBV infection. Vieira P., De Waal-Malefyt R., Dang M. N., Johnson K. E., Kastelein R., Fiorentino D. F., et al Isolation and expression of human cytokine synthesis inhibitory factor cDNA clones: homology to Epstein-Barr virus open reading frame BCRF1. EBV positivity for these lymphomas ranges from 30 to >90% (129, 278, 279, 280, 281, 282, 283). examined infection and clinical factors for GC, specifically anti-EBV antibody load prior to cancer being diagnosed (IgG and IgA anti-VCA, IgG anti-EA and IgG anti-EBNA) . Baumforth K. R. N., Young L. S., Flavell K. J., Constandinou C., Murray P. G. The Epstein-Barr virus and its association with human cancers. Tokunaga M., Land C., Uemura Y., Tokudome T., Tanaka S., Sato E. Epstein-Barr virus in gastric carcinoma. Murray P. G., Young L. S. Virus-targeted therapy for EBV-associated malignancies. Epstein-Barr Virus (EBV) Antibody Tests - Testing.com Drives EBV into latency. EBV binding to CD21 immediately activates tyrosine kinase lck and mobilizes calcium (30, 31). Farrell P. J. Epstein-Barr virus immortalizing genes. Bone marrow is less frequently involved in endemic disease, and patients are more sensitive to chemotherapy (145, 146). Only EBNA-1 is expressed in these cells. B. . Epstein-Barr virus reactivation may be the cause of long COVID symptoms Hennessy K., Kieff E. A second nuclear protein is encoded by Epstein-Barr virus in latent infection. EBNA-1 binding sites are also located at +10 and +34 nucleotides downstream of promoter Qp (64). Although most humans coexist with the virus without serious sequelae, a small proportion will develop tumors. Identification of Epstein-Barr virus sequences that encode a nuclear antigen expressed in latently infected lymphocytes. The EBV life cycle. These two serological types correspond to EBV-1 and EBV-2 (35, 67, 68). IARC Sci Publ. EBV-encoded viral IL-10 is increased in nasopharyngeal carcinoma and has been associated with increased production of IL-1 and IL-1 by epithelial cells and by CD4+ T cells, which may, in turn, contribute to the growth of the tumor and to immune evasion (227). Nasopharyngeal carcinoma cells possess normal antigen processing and are effectively recognized by EBV-specific CTLs, yet they are not destroyed (226). Epstein-Barr virus activators, mutagens, and volatile nitrosamines in preserved food samples from high risk areas for nasopharyngeal carcinoma. Wang F., Gregory C., Sample C., Rowe M., Liebowitz D., Murray R., et al Epstein-Barr virus latent infection membrane and nuclear proteins 2 and 3C are effectors of phenotypic changes in B lymgphocytes: EBNA2 and LMP cooperatively induce CD23. Nemerow G., Wolfert R., McNaughton M., Cooper N. Identification and characterization of the Epstein-Barr virus receptor on human B lymphocytes and its relationship to the C3d complement receptor (CR2). For the most part, EBV-associated lymphomas in the immunocompromised host are aggressive and difficult to treat. Yates J., Camiolo S. Dissection of DNA replication and enhancer activation function of Epstein-Barr virus nuclear antigen 1. It has been detected in oral hairy leukoplakia but not in other diseases characterized by latent infections. EBV undergoes latency II expression in undifferentiated nasopharyngeal carcinoma (216, 218, 219, 220, 221, 222, 223). The EBV nuclear antigen leader protein (EBNA-LP) and EBNA-2 proteins are the first proteins to be detected upon EBV infection (36, 37). Labreque L., Barnes D., Fentiman I., Griffin B. Epstein-Barr virus in epithelial cell tumors: a breast cancer study. The central nervous system lymphomas include immunoblastic and large noncleaved lymphomas. In American men of Japanese ancestry, Levine et al. Geographic variations of EBV positivity have also been studied. Simons M., Wee G., Day N., Morris P. J., Shanmugaratnam K. Immunogenetic aspects of nasopharyngeal carcinomas: I. Epstein-Barr Virus Laboratory Testing | CDC Oral excretion of Epstein-Barr viruses by healthy subjects and patients with infectious mononucleosis. However, EBV-2 is nearly as prevalent as EBV-1 in New Guinea, as well as in equatorial Africa (20, 21). Yoo L., Mooney M., Puglielli M., Speck S. H. B-Cell lines immortalized with an EBV mutant lacking the Cp EBNA2 enhancer are biased toward utilization of the oriP-proximal EBNA gene promoter Wp1. Methods PROSPERO registration number . EBV Ab VCA, IgG. IgG anti-VCA was specifically found to be associated with EBV-positive GC vs non-cancer controls. Breast Cancer. Jones C., Hayward S., Rawlins D. Interaction of the lymphocyte-derived Epstein-Barr virus nuclear antigen EBNA-1 with its DNA-binding sites. Autologous and haploidentical EBV-specific CTLs have also been administered. Komano J., Sugiura M., Takada K. Epstein-Barr virus contributes to the malignant phenotype and to apoptosis resistance in Burkitts lymphoma cell line Akata. EBV BCRF1 protein shows 84% sequence homology to human IL-10 (116). Lin C. T., Lin C. R., Tan G. K., Chen W., Dee A. N., Chan W. Y. TRAFs and tumor necrosis factor receptor-associated death domain interaction are mediated by separate regions of the LMP-1 COOH-terminal domain, known as transformation effector sites (92, 93). Itoigawa M., Ito C., Ju-ichi M., Nobukuni T., Ichiishi E., Tokuda H., et al Cancer chemopreventive activity of flavanones on Epstein-Barr virus activation and two-stage mouse skin carcinogenesis. Shibata D., Weiss L., Hernandez A., Nathwani B. N., Bernstein L., Levine A. M. Epstein-Barr virus-associated non-Hodgkins lymphoma in patients infected with the human immunodeficiency virus. Abdulkarim B., Bourhis J. Antiviral approaches for cancers related to Epstein-Barr virus and human papillomavirus. The drawback to antivirals is that they have no influence on the underlying immunosuppression that favors EBV-driven tumorigenesis. However, in some individuals, the virus is implicated in the development of malignancy. Dhar V., Schildkraut C. Role of EBNA-1 in arresting replication forks at the Epstein-Barr virus oriP family of tandem repeats. Epstein-Barr virus and Kaposis sarcoma herpesvirus/human herpesvirus 8. Why is EBV reported in some studies and not in others? However, recent studies suggest that selected antiviral compounds, as well as therapeutic strategies such as use of adoptive immunotherapy with EBV-specific CTLs or administration of targeted monoclonal antibodies, hold considerable promise for the treatment of EBV-related malignancies. Potential protein products may modify, Hodgkins disease Nasopharyngeal carcinoma Peripheral T/NK lymphoma, AIDS-associated lymphomas Posttransplant lymphoproliferative disorders, Nasal T/NK Angioimmunoblastic Lymphadenopathy, Controversial novel LMP-1 negative Latency III, Posttransplant lymphoproliferative disorders, Leiomyosarcomas in immunosuppressed individuals. Introduction Epstein-Barr Virus Epstein-Barr Virus (EBV) is a lymphotropic herpes virus and the causative agent of infectious mononucleosis (IM) ( 1 - 4 ). Ambinder R., Shah W., Rawlins D., Hayward G. S., Hayward S. D. Definition of the sequence requirements for binding of the EBNA-1 protein to its palindromic target sites in Epstein-Barr virus DNA. Kaiser C., Laux G., Eick D., Jochner N., Bornkamm G. W. The proto-oncogene. Because these lymphomas use IL-6 as a growth factor, anti-IL-6 monoclonal antibodies have also been tried. Nuclear factor-B is a key transcription factor involved in regulation of cell growth and apoptosis. Middleton T., Sugden B. For other (nontransplant) EBV-related malignancies, there is only limited clinic experience with EBV-specific CTLs. Karlin S., Blaisdell B., Schachtel G. Contrasts in codon usage of latent versus productive genes of Epstein-Barr virus: data and hypotheses. Because of this translocation, the oncogene c-myc (chromosome 8) is juxtaposed to the immunoglobulin heavy-chain (chromosome 14) or light-chain genes (chromosomes 2 or 22). Phone: (713) 794-1226; Fax: (713) 745-2374; E-mail: rkurzroc@mdanderson.org. Kume T., Oshima K., Shinohara T., Takeo H., Yamashita Y., Shirakusa T., et al Low rate of apoptosis and overexpression of bcl-2 in Epstein-Barr virus-associated gastric carcinoma. Given the morphological similarities between lymphoepithelioma-like gastric carcinoma and undifferentiated nasopharyngeal carcinomas, it has been proposed that in lymphoepithelioma-like gastric carcinoma, EBV spreads from the nasopharynx to the stomach (243, 244). dAmore F., Johansen P., Hournand A., Weisenburger D. D., Mortensen L. S. Epstein-Barr virus genome in non-Hodgkins lymphomas occurring in immunocompetent patients: highest prevalence in nonlymphoblastic T-cell lymphoma and correlation with a poor prognosis. The EBV genomes present in the epithelial cells of the nasopharynx are of clonal origin, and EBV is absent from surrounding tissues and invading T lymphocytes (147, 215). 299). These aggressive disorders include both central nervous system and systemic lymphomas. EBNA-3 family members are encoded by three genes that are adjacent on the viral genome (53). Luqmani Y., Shousha S. Presence of Epstein-Barr virus in breast carcinoma. Iezzoni J., Gaffey M., Weiss L. The role of Epstein-Barr virus in lymphoepithelioma-like carcinomas. On the other hand, EA-IgA is suitable for the diagnosis but not NPC screening. Allday M., Crawford D., Griffin B. Epstein-Barr virus latent gene expression during the initiation of B cell immortalization. If someone has positive VCA-IgG and EA-D IgG tests, then it is highly likely that the person has a current or recent EBV infection. In addition, transfection of the EBER genes into the EBV-negative Akata cell line restored the oncogenic potential that was originally present in the EBV-positive Akata cells but was lost in the EBV-negative subclones (113). Pathmanathan R., Prasad U., Sadler R., Flynn K., Raab-Traub N. Clonal proliferations of cells infected with Epstein-Barr virus in preinvasive lesions related to nasopharyngeal carcinoma. However, more remains to be understood on the function of EBNA-LP in transformation and during the viral life cycle. MC, mixed cellularity; IP-CNS, immunoblastic primary central nervous system lymphoma; LD, lymphocyte depleted; LP, lymphocyte predominant; NK, natural killer; NS, nodular sclerosing. Lyons S., Liebowitz D. The roles of human viruses in the pathogenesis of lymphoma. During a latent infection, EBNA-3A, EBNA-3B, and EBNA-3C all elicit specific CTL responses, which seem to be the dominant latency response to EBV proteins (26, 27, 28). It also has a central role in maintaining latent EBV infection. Borisch B., Hennig I., Laeng H., Waelti E. R., Kraft R., Laissue J. Woisetschlaeger M., Jin X., Yandava C., Furmanski L. A., Strominger J. L., Speck S. H. Role for the Epstein-Barr virus nuclear antigen 2 in viral promoter switching during initial stages of infection.
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high ebv ab vca igg and cancer
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