TY - JOUR. T1 - Synthetic peptides deduced from the amino acid sequence of Epstein‐Barr virus nuclear antigen 6 (EBNA 6). T2 - Antigenic properties, production of monoreactive reagents, and analysis of antibody responses in man. AU - Falk, K.. AU - Linde, A.. AU - Johnson, D.. AU - Lennette, E.. AU - Ernberg, I.. AU - Lundkvist, A.. PY - 1995/8. Y1 - 1995/8. N2 - Studies on the antibody responses to various Epstein‐Barr virus (EBV) antigens have been instrumental in the understanding of the seroepidemiology and diagnosis of this viral infection and the subsequent carrier state. While antibodies to the viral capsid antigen (VCA), early antigen (EA), and nuclear antigens 1 and 2 (EBNA 1 and 2) have been well characterized, the antibody response to the other nuclear antigens is not well understood. EBNA 6 is expressed by lymphoblasts during acute EBV infection and may be an important antigen for diagnosis and evaluation of the immune response. In order to analyze the antibody response to EBNA ...

pathogen (EBV) latent membrane proteins 2A (LMP2A) is certainly widely portrayed in EBV-infected cells inside the contaminated individual host and EBV-associated malignancies suggesting that LMP2A is essential for EBV latency persistence and EBV-associated tumorigenesis. B lymphocytes contaminated in vitro with EBV become immortalized building lymphoblastoid cell lines DMH-1 (LCLs). This technique constitutes an in vitro model for the contribution of EBV to B lymphoid disease. EBV gene appearance in LCLs is fixed to six nuclear antigens (EBNA1 -2 -3 -3 -3 and -LP) three essential membrane protein (latent membrane proteins 1 DMH-1 [LMP-1] -2 and -2B) two nonpolyadenylated RNAs. ...

An eight year old English boy presented with an abdominal undifferentiated Burkitt-like lymphoma. Lymphoma cells from ascitic fluid were cultured on a human embryo fibroblast feeder layer and, after a short lag period, a cell line (DH-BL) was established which, like the original tumour, was both negative for the Epstein-Barr nuclear antigen (EBNA) and expressed a monoclonal pattern of surface immunoglobulin (alpha lambda). DH-BL also possessed the Burkitt-related 8:14 chromosome translocation in all metaphases analysed; no other chromosomal abnormalities were present. The cell surface phenotype of the original biopsy cells and the cultured tumour cells in early passage were investigated using a panel of monoclonal antibodies to B lineage-associated antigens. These antibodies had recently been used to characterise African endemic Burkitts lymphoma (BL) biopsy cells and their derived cell lines. The cell surface phenotype of this English EBNA negative Burkitt-like lymphoma biopsy was ...

We have previously proposed (Zhang and Coffino, 2004), and here test, the following simple model: Two elements of the 19S regulatory particle are postulated to function coordinately. The first is a site impelling translocation, the ATPase ring, which binds the substrate and advances it stepwise toward the 20S core particle. The second is a site of constriction within the regulatory particle, possibly the entrance to a translocation channel through the ATPase ring. This postulated constriction impairs transit of a folded domain. The ATPase ring produces energy that performs work on the substrate, some of which is used to unravel the folded domain. The mode of energy transmission may be as simple as a lever arm motion that applies a friction drive to the polypeptide chain (Hinnerwisch et al, 2005). In the normal case, energy supply continuously exceeds need, and the substrate polypeptide continuously advances. If this balance transiently swings in the other direction, with energy need exceeding ...

The Epstein-Barr virus (EBV) episome is known to interact with the three-dimensional structure of the human genome in infected cells. However, the exact locations of these interactions and their potential functional consequences remain unclear. Recently, high-resolution chromatin conformation capture (Hi-C) assays in lymphoblastoid cells have become available, enabling us to precisely map the contacts between the EBV episome(s) and the human host genome. Using available Hi-C data at a 10-kb resolution, we have identified 15,000 reproducible contacts between EBV episome(s) and the human genome. These contacts are highly enriched in chromatin regions denoted by typical or super enhancers and active markers, including histone H3K27ac and H3K4me1. Additionally, these contacts are highly enriched at loci bound by host transcription factors that regulate B cell growth (e.g., IKZF1 and RUNX3), factors that enhance cell proliferation (e.g., HDGF), or factors that promote viral replication (e.g., NBS1 ...

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1. GalluzziL. BrennerC. MorselliE. TouatZ. KroemerG. 2008 Viral control of mitochondrial apoptosis. PLoS Pathog 4 e1000018. 2. CuconatiA. WhiteE. 2002 Viral homologs of BCL-2: role of apoptosis in the regulation of virus infection. Genes and Development 16 2465 2478. 3. CuconatiA. DegenhardtK. SundararajanR. AnschelA. WhiteE. 2002 Bak and Bax function to limit adenovirus replication through apoptosis induction. J Virol 76 4547 4558. 4. MarchiniA. TomkinsonB. CohenJI. KieffE. 1991 BHRF1, the Epstein-Barr virus gene with homology to Bc12, is dispensable for B-lymphocyte transformation and virus replication. J Virol 65 5991 6000. 5. HendersonS. HuenD. RoweM. DawsonC. JohnsonG. 1993 Epstein-Barr virus-coded BHRF1 protein, a viral homologue of Bcl-2, protects human B cells from programmed cell death. Proc Natl Acad Sci U S A 90 8479 8483. 6. Thorley-LawsonDA. GrossA. 2004 Persistence of the Epstein-Barr virus and the origins of associated lymphomas. N Engl J Med 350 1328 1337. 7. ...

We describe a method for generating transformed B cell lines using Epstein-Barr virus. We also illustrate a novel assay that can...

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In this paper we have verified a key tenet of the GC model of EBV persistence by showing for the first time that EBV-infected cells expressing the default latency transcription program are physically located in GCs and express functional markers, homing receptors, and the phenotypic markers of GC cells. These experiments further demonstrate that EBV can reside latently within GC cells in vivo without imposing the growth latency transcription program and the lymphoblastoid form of latency. What distinguishes infected GC cells in vivo is expression of the viral default latency transcription program which, unlike the growth latency program, appears to be fully consistent with retention of GC function. Since direct infection of GC cells in vitro (43) or in vivo (26) produces the growth latency program and obliterates the GC phenotype, it follows that the latently infected GC cells we have described in vivo cannot arise through direct infection and must be derived by another mechanism, i.e., ...

The protein encoded by this gene is a uridine kinase. Uridine kinases catalyze the phosphorylation of uridine to uridine monophosphate. This protein has been shown to bind to Epstein-Barr nuclear antigen 3 as well as natural killer lytic-associated molecule. Ubiquitination of this protein is enhanced by the presence of natural killer lytic-associated molecule. In addition, protein levels decrease in the presence of natural killer lytic-associated molecule, suggesting that association with natural killer lytic-associated molecule results in ubiquitination and subsequent degradation of this protein. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Nov 2014] ...

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How is Word-Processing/Spread-Sheet abbreviated? WP/SS stands for Word-Processing/Spread-Sheet. WP/SS is defined as Word-Processing/Spread-Sheet very rarely.

Epstein-Barr virus (EBV) is the etiological agent of infectious mononucleosis and is associated with various diseases such as Burkitts lymphoma, nasopharyngeal carcinoma, and post-transplant lymphoproliferative disorder (PTLD). In all of these diseases, the expression of Epstein-Barr virus nuclear antigen 1 (EBNA-1) is common and therefore this viral protein represents a possible therapeutic target. Previous studies have intimated that EBNA-1 auto-inhibits its presentation to the immune system via the expression of a glycine-alanine rich domain that blocks proteasomal degradation. Thus to understand the expression of EBNA-1 and to evaluate the potential of targeting this viral antigen in the context of PTLD, we examined the role of glycine-alanine repeats (GAr) in EBNA-1 protein expression and further investigated the in vivo efficacy of an in-house produced α-EBNA-1 T cell receptor-like monoclonal antibody (α-EBNA-1 TCR-like mAb) using a mouse xenograft model of PTLD. With the aim of ...

Epstein-Barr virus (EBV) has been causally associated with at least five human malignancies. The exact contributions made by EBV to these cancers remain unknown. We demonstrate that one viral protein found in all EBV-associated malignancies, Epstein-Barr nuclear antigen 1 (EBNA-1), is required for survival of one of these cancers, EBV-positive Burkitts lymphoma. Inhibition of EBNA-1 decreases survival of these tumor cells by inducing apoptosis. Expression of EBNA-1 in uninfected cells also can inhibit apoptosis induced by expression of p53 in the absence of the EBV genome. Our findings demonstrate that EBNA-1 is critical for the continued survival of EBV-associated Burkitts lymphoma, and, by extension, for the other B cell tumors with which EBV is associated. Efficient inhibitors of EBNA-1s functions would likely prove useful in the therapy of EBV-associated malignancies.

Nasopharyngeal carcinoma (NPC) is an epithelial malignancy, which commonly occurs in Southern China, Taiwan, North Africa and Southeast Asia. Nasopharyngeal carcinoma is strongly associated with Epstein-Barr virus infection. The p53 tumour suppressor protein is rarely mutated in NPC suggesting that the inactivation of p53 pathway in NPC could be due to the presence of EBV proteins. The aim of this work was to determine the effects of EBV proteins namely LMP1 and LMP2A on the expression levels of p53 protein. In this work we found that LMP1, but not LMP2A, decreased p53 protein levels. Overexpression of LMP1 resulted in increased ubiquitination of p53 suggesting that the decreased p53 protein levels by LMP1 was due to increased degradation of the protein. The reduction of p53 protein levels was independent of the PI3K-Akt pathway. LMP1, but not LMP2A, reduced p53 protein levels through the increase in the polyubiquitination of p53 protein and was independent of the PI3K-Akt pathway.

Epstein-Barr virus (EBV) is a gamma-herpes virus that widely infects human populations predominantly at an early age but remains mostly asymptomatic. EBV has been linked to a wide spectrum of human malignancies, including nasopharyngeal carcinoma and other hematologic cancers, like Hodgkins lymphoma, Burkitts lymphoma (BL), B-cell immunoblastic lymphoma in HIV patients, and posttransplant-associated lymphoproliferative diseases. EBV has the unique ability to establish life-long latent infection in primary human B lymphocytes. During latent infection, EBV expresses a small subset of genes, including 6 nuclear antigens (EBNA-1, -2, -3A, -3B, -3C, and -LP), 3 latent membrane proteins (LMP-1, -2A, and -2B), 2 small noncoding RNAs (EBER-1 and 2). On the basis of these latent gene expression, three different latency patterns associated with the types of cancers are recognized ...

Description of the Results/Findings of the Project: This project led directly to the writing of the manuscript Mechanisms and timing of the activation of the EBI2 gene by Epstein-Barr Virus which is slated for submission to Journal of Virology before the end of 2014. Our work with EBV also lead to an invitation to author a book chapter, Epstein-Barr Virus in the upcoming scholarly book Viral Arthritis. The drafts for this book chapter are due by Nov 30th, 2014. The funding from the MEG also allowed for the publication of three other journal articles with student co- authors. These works were finishing up our previous work on IRF5 in lupus, and a review article dealing with how pathogens, such as Epstein-Barr virus, contribute to the spreading of immunity and autoimmune disease. We had several unexpected findings during this project. We found that EBI2 expression is transient after infection with EBV, and that long-term infected cells actually express this gene at very low levels. We ...

TY - JOUR. T1 - Detection and quantification of Epstein-Barr virus EBER1 in EBV-infected cells by fluorescent in situ hybridization and flow cytometry. AU - Stowe, Raymond P.. AU - Cubbage, Michael L.. AU - Sams, Clarence F.. AU - Pierson, Duane L.. AU - Barrett, Alan D.T.. PY - 1998/11/1. Y1 - 1998/11/1. N2 - A rapid and highly sensitive fluorescent in situ hybridization (FISH) assay was developed to detect Epstein-Barr virus (EBV)-infected cells in peripheral blood. Multiple fluorescein-labeled antisense oligonucleotide probes were designed to hybridize to the EBER1 transcript, which is highly expressed in latently infected cells. After a rapid (30 min) hybridization, the cells were analyzed by flow cytometry. EBER1 was detected in several positive control cell lines that have variable numbers of EBV genome copies. No EBER1 was detected in two known EBV-negative cell lines. Northern blot analyses confirmed the presence and quantity of EBER1 transcripts in each cell line. This method was used ...

Epstein-Barr virus protein and DNA. Molecular model of the DNA-binding domain of a viral protein (pink-blue) bound to a lytic gene promoter element (viral strand of DNA, left). The viral protein is the Epstein-Barr virus (EBV) transcription factor ZEBRA (Zta, Z, EB1), also known as BZLF1 trans-activator protein. EBV is a herpesvirus (it is also called human herpesvirus 4 or HHV-4). It is the cause of glandular fever (also called infectious mononucleosis). The DNA strand is viral DNA that forms during the lytic phase of the virus life cycle, where the viral DNA exists within the host cell separately from the host cells DNA (deoxyribonucleic acid). - Stock Image C015/4303

How is Epstein-Barr Virus Insertion Site 1 abbreviated? EBVS1 stands for Epstein-Barr Virus Insertion Site 1. EBVS1 is defined as Epstein-Barr Virus Insertion Site 1 rarely.

In raising murine hybridoma antibodies against Epstein-Barr virus (EBV)-induced membrane antigens (MA), we found one antibody that blocked the release of infectious EBV from cultured P3HR-1 cells. This monoclonal antibody (mAb) recognized a 200 kD, phosphonoacetic acid-sensitive (late) MA, and did not directly neutralize virus without complement. When this mAb was added to 33 degrees C-cultured, spontaneously EBV-producing P3HR-1 cells, the intracellular expression of viral capsid antigen and infectious virus was not inhibited, but the appearance of infectious virus in the culture medium was significantly reduced. The duration of this suppression was dependent upon the concentration of the mAb, an effect being observed to a 1:4 X 10(5) titer of the ascites mAb preparation. A more acute effect of suppression of EBV release was observed in a second model of 12-o-tetradecanoyl phorbol-13-acetate and n-butyrate induction of EBV in 37 degrees C-cultured P3HR-1 cells. Again, intracellular infectious ...

The various antigen complexes of the Epstein-Barr virus (EBV) are broadly classified as the viral capsid antigen (VCA), diffuse early antigen (EA-D), restricted early antigen (EA-R), membrane antigen (MA) and the Epstein-Barr nuclear antigen (EBNA). The different EBV-related diseases may be differentiated according to the reactivity of these different classes of antibodies towards the various classes of antigen complexes. However, with the recent development of molecular biology, it is now known that the individual polypeptides of the different EBV antigen complexes can be used as serological markers for the detection of nasopharyngeal carcinoma (NPC). Among the useful serological markers which have been used in enzyme-linked immunosorbent assay (ELISA) for the detection of NPC are the gp125 from the VCA complex (IgA), pp58 from the EA-D complex (IgG), ribonucleotide reductase (IgG and IgA), DNase (IgA) and thymidine kinase (IgA) from the EA-R complex, gp 250/200 from the MA complex (IgA) and ...

The demand of monospecific high affinity binding reagents, particularly monoclonal antibodies, has been steadily increasing over the last years. Enhanced throughput of antibody generation has been addressed by optimizing in vitro selection using phage display which moved the major bottleneck to the production and purification of recombinant antibodies in an end-user friendly format. Single chain (sc)Fv antibody fragments require additional tags for detection and are not as suitable as immunoglobulins (Ig)G in many immunoassays. In contrast, the bivalent scFv-Fc antibody format shares many properties with IgG and has a very high application compatibility. In this study transient expression of scFv-Fc antibodies in human embryonic kidney (HEK) 293 cells was optimized. Production levels of 10-20 mg/L scFv-Fc antibody were achieved in adherent HEK293T cells. Employment of HEK293-6E suspension cells expressing a truncated variant of the Epstein Barr virus (EBV) nuclear antigen (EBNA) 1 in combination with

The family of repeats (FR) is a major upstream enhancer of the Epstein-Barr virus (EBV) latent C promoter (Cp) that controls transcription of six different latent nuclear proteins following interaction with the EBV nuclear protein EBNA1. Here, it was shown that Cp could also be activated by octamer-binding factor (Oct) proteins. Physical binding to the FR by the cellular transcription factors Oct-1 and Oct-2 was demonstrated by using an electrophoretic mobility-shift assay. Furthermore, Oct-1 in combination with co-regulator Bob.1, or Oct-2 alone, could drive transcription of a heterologous thymidine kinase promoter linked to the FR in both B cells and epithelial cells. Cp controlled by the FR was also activated by binding of Oct-2 to the FR. This may have direct implications for B cell-specific regulation of Cp.

Mouse anti Epstein-Barr virus viral capsid antibody, clone 0231 recognizes the viral capsid antigen of Epstein-Barr Virus (EBV), also know

Definition of Epstein-Barr virus - a herpesvirus causing glandular fever and associated with certain cancers, for example Burkitts lymphoma.

The virus is spread by intimate oral contact among adolescents, but how preadolescents acquire the virus is not known. During the incubation period of approximately 6 weeks, viral replication first occurs in the oropharynx followed by viremia as early as 2 weeks before onset of illness. The acute illness is marked by high viral loads in both the oral cavity and blood accompanied by the production of immunoglobulin M antibodies against EBV viral capsid antigen and an extraordinary expansion of CD8+ T lymphocytes directed against EBV-infected B cells. ,diet plan,healthy eating,healthy food,pregnancy tips,glucose tolerance test,diabetes test. During convalescence, CD8+ T cells return to normal levels and antibodies develop against EBV nuclear antigen-1. A typical clinical picture in an adolescent or young adult with a positive heterophile test is usually sufficient to make the diagnosis of infectious mononucleosis, but heterophile antibodies are not specific and do not develop in some patients ...

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The initiation of cell-mediated immunity to Epstein-Barr virus (EBV) has been analyzed with cells from EBV-seronegative blood donors in culture. The addition of dendritic cells (DCs) is essential to prime naive T cells that recognize EBV-latent antigens in enzyme-linked immunospot assays for interferon γ secretion and eradicate transformed B cells in regression assays. In contrast, DCs are not required to control the outgrowth of EBV-transformed B lymphocytes from seropositive donors. Enriched CD4+ and CD8 + T cells mediate regression of EBV-transformed cells in seronegative and seropositive donors, but the kinetics of T-dependent regression occurs with much greater speed with seropositives. EBV infection of DCs cannot be detected by reverse transcription-polymerase chain reaction with primers specific for mRNA for the EBNA1 U and K exons. Instead, DCs capture B cell debris and generate T cells specific for EBV latency antigens. We suggest that the cross-presentation of EBV-latent antigens from

The CD8+ T cell response to Epstein-Barr virus (EBV) is well characterized. Much less is known about the evolution of the CD4+ T cell response. Here we show that EBV stimulates a primary burst of effector CD4+ T cells and this is followed by a period of down-regulation. A small population of EBV-specific effector CD4+ T cells survives during the lifelong persistent phase of infection. The EBV-specific effector CD4+ T cells accumulate within a CD27+ CD28+ differentiation compartment during primary infection and remain enriched within this compartment throughout the persistent phase of infection. Analysis of CD4+ T cell responses to individual epitopes from EBV latent and lytic cycle proteins confirms the observation that the majority of the effector cells express both CD27 and CD28, although CD4+ T cells specific for lytic cycle antigens have a greater tendency to express CD45RA than those specific for the latent antigens. In clear contrast, effector CD4+ T cells specific for cytomegalovirus (CMV)

Introns from the Epstein-Barr virus (EBV) BART RNAs produce up to 20 micro RNAs (miRNAs) but the spliced exons of the BART RNAs have also been investigated as possible mRNAs, with the potential to express the RPMS1 and A73 proteins. Recombinant RPMS1 and A73 proteins were expressed in Escherichia coli and used to make new monoclonal antibodies that reacted specifically with artificially expressed RPMS1 and A73. These antibodies did not detect endogenous expression of A73 and RPMS1 proteins in a panel of EBV-infected cell lines representing the different known types of EBV infection. BART RNA could not be detected on Northern blots of cytoplasmic poly(A)+ RNA from the C666.1 NPC cell line and BART RNA was found to be mainly in the nucleus of C666.1 cells, arguing against an mRNA role for BART RNAs. In contrast, some early lytic cycle EBV mRNAs were found to be expressed in C666.1 cells. Artificially expressed A73 protein was known to be able to bind to the cellular RACK1 protein and has now also been

No Significant Association of Epstein-Barr Virus Infection with Invasive Breast Carcinoma: We studied 48 cases of invasive breast carcinoma for evidence of Epst

This topic contains 47 study abstracts on Epstein-Barr Virus Infections indicating that the following substances may be helpful: Curcumin, Licorice, and Turmeric

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In this study we analyzed the effect of CD40 stimulation on the activity and nuclear appearance of Rel/nuclear factor kappaB (NF-kappaB) factors in primary murine B lymphocytes. We show that triggering of CD40 signaling pathway(s) by CD40 ligands expressed on L cells led to strong activation of an NF-kappaB-controlled beta-globin reporter gene in primary B lymphocytes from transgenic mice. Analyses of nuclear translocation of individual members of Rel proteins after CD40 induction of primary B cells showed a strong and long-lasting accumulation of RelB and, less pronounced, of c-Rel. LPS stimulation did not give rise to a persistent nuclear accumulation of RelB and c-Rel, whereas nuclear c-Rel, but not RelB, accumulated after B cell receptor stimulation. CD40 induced not only nuclear translocation but also de novo synthesis of RelB RNA and protein. S107 plasmacytoma cells, which express CD40 but are defective for the nuclear appearance of p50/p65-NF-kappaB, do not express RelB after CD40 stimulation. In

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The Epstein-Barr virus (EBV) is a well-known example of a human virus which interacts most intimately with the immune system. EBV is a polyclonal B lymphocyte activator, can immortalize B cells and,...

People react differently when they are diagnosed with a disease of chronic Epstein-Barr virus. Some depressed people, while others remain positive and hopeful. In fact, some people find that EBV disease using grow emotionally, making them stronger and more tolerant, more understanding.. Here are some methods that can help you better cope with the disease of chronic Epstein-Barr virus.. First, it is important that the expression of emotions. Be honest and admit your health, instead of pretending not to exist. People who communicate their feelings tend to need less treatment, and offers fewer symptoms and keep more independence and physical performance.. The next thing to do is to control. And more people to actively manage chronic Epstein-Barr virus themselves, the better they do. Set goals, such as what you eat, and how they stay fit, and how it will be easier to manage your stress, what supplements to take and what is much better than the passive acceptance of what the treatment is given for ...

EBV infection is primarily controlled by a delicate balance of B and T cells. Outgrowth of EBV-infected B cells is a direct consequence of inadequate EBV-specific cytotoxic T lymphocytes, hence the higher incidence of EBV-associated malignancy in immunocompromised hosts (12). While no vaccine is currently available for the disease, adoptive transfer of EBV-specific T lymphocytes that recognize EBV antigens have emerged as a promising therapeutic option. These ex vivo-manufactured donor T cells and patient-derived EBV-specific T cells have eradicated disease in patients with refractory EBV+ polymorphic and monomorphic PTLD (13-15). Thus, the role of T cells in controlling EBV in immunocompetent hosts and in eradicating EBV in immunocompromised hosts following ex vivo antigen-specific priming is clear and encourages the development and design of EBV vaccines. The quest for an EBV-directed vaccine has proven quite challenging, in large part because of the lack of preclinical models for vaccine ...

New research investigating possible interactions between Epstein-Barr virus and neurological diseases has successfully infected neuronal-like cells in vitro.

BioAssay record AID 288762 submitted by ChEMBL: Inhibition of TPA-induced Epstein-Barr virus early antigen activation assessed as EBV-EA induction in Raji cells at 3.2 nM after 48 hrs relative to TPA.

BURKITT-LYMPHOM (PATHOLOGIE); ZELLLINIEN + ZELLLINIENISOLIERUNG (CYTOLOGISCHE METHODEN); EPSTEIN-BARR-VIRUS (VIROLOGIE); TRANSKRIPTION (MOLEKULARE GENETIK); DNA-MIKROARRAY TECHNOLOGIE; BURKITT LYMPHOMA (PATHOLOGY); CELL LINES + CELL LINE ISOLATION (CYTOLOGICAL METHODS); EPSTEIN-BARR-VIRUS (VIROLOGY); TRANSCRIPTION (MOLECULAR GENETICS); DNA ...

Which method should be used?Some investigators found EIA to be more sensitive than IFA, particularly the anticomplement immunofluorescence technique (22); others found the EIA technology to be as sensitive as IFA or even more sensitive than EIA (23, 27). Already in the mid-1980s the results of assays performed with the first generations of EIAs correlated nicely with those of IFA with purified VCA and EBNA proteins as antigens (9). EIA performance characteristics strongly depend on the nature of the antigens and the preparation and the selection of antigens used (14). As a consequence, the differences in performance characteristics observed between IFA and EIA (i.e., relative sensitivity, relative specificity, and predictive values) are due to the use of various different forms and different selections of antigens with the EIA and to the different IFA substrates used (i.e., different prototype-derived EBV-transformed cell lines [e.g., Raji cells instead of P3HR-1 cells] for detection of ...

The Epstein-Barr Virus (Paperback, Softcover reprint of the original 1st ed. 1979) / Editor: M.A. Epstein / Editor: B. G. Achong ; 9783642672385 ; General issues, Medicine, Books

Epstein-Barr virus early antigen: synthesized before or in the absence of viral-progeny DNA replication & present only in infected cells

The ubiquitous Epstein-Barr virus (EBV) is associated with several human tumors, which include lymphoid and epithelial malignancies. It is known that EBV persistently infects the memory B cell pool of healthy individuals by activating growth and surv

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Did you know, you probably have virus lurking in the shadows? Its called the Epstein-Barr virus (EBV) and an estimated 90 percent of us have it. Fortunately, for most of us it lies dormant, like a sleeping giant. Only when something triggers a reactivation of EBV does this virus rear its ugly head.

EBV or Epstein-Barr virus is an extremely common virus that 95% of adults have without knowing it. Once you have EBV, it results in a lifelong infection that has little to no symptoms.

Studies involving miRNAs have opened discussions about their broad participation in viral infections. Regarding the Human gammaherpesvirus 4or Epstein-Barr virus (EBV), miRNAs are important...

Initial results from clinical trials show new drug therapies are effective against lymphomas and other cancers connected to the Epstein-Barr virus.

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Epstein-Barr disease (EBV) continues to be associated with various kinds human cancers. discusses and elements how EBV lytic an infection plays a part in individual malignancies. and are initial transcribed to encode the transactivators Zta and Rta respectively accompanied by appearance of the first genes necessary for EBV genome replication. After EBV DNA replication AV-951 past due genes are portrayed that encode generally viral structural protein including capsid antigens and membrane protein accompanied by viral genome encapsidation as well as the creation of mature virions. Although all EBV-associated malignancies involve the latent routine of EBV the viral lytic routine also plays a part in the advancement and maintenance of malignancies through the induction of development elements and oncogenic cytokine creation 3-5. Within this review we describe latest advances about the systems root EBV reactivation concentrating on the control of the web host as well as the trojan itself and discuss ...

For nearly two decades now, various studies have reported detecting the Epstein-Barr virus (EBV) in breast cancer (BC) cases. Yet the results are unconvincing, and their interpretation has remained a matter of debate. We have now presented prospective data on the effect of EBV infection combined with survival in patients enrolled in a prospective study. We assessed 85 BC patients over an 87-month follow-up period to determine whether EBV infection, evaluated by qPCR in both peripheral blood mononuclear cells (PBMCs) and tumor biopsies, interacted with host cell components that modulate the evolution parameters of BC. We also examined the EBV replicating form by the titration of serum anti-ZEBRA antibodies. Immunological studies were performed on a series of 35 patients randomly selected from the second half of the survey, involving IFN-γ and TNF-α intracellular immunostaining tests performed via flow cytometry analysis in peripheral NK and T cells, in parallel with EBV signature. The effect of the EBV

Accessory files for RNA-seq based EBV transcriptome analysis:. OGrady, T, Wang, X, Honer Zu Bentrup, K, Baddoo, M, Concha, M, Flemington, EK. Global transcript structure resolution of high gene density genomes through multi-platform data integration. Nucleic Acids Res. 2016 Jul 12. Pii:gkw629. PMCID:. OGrady, T, Cao, S, Strong, MJ, Concha, M, Wang, X, Splinter BonDurant, S, Adams, M, Baddoo, M, Srivastav, SK, Lin, Z, Fewell, C, Yin, Q, and Flemington, EK. Global bidirectional transcription of the Epstein-Barr virus genome during reactivation. J Virol. 2014 88: 1604-1616. PMCID: PMC3911580. Lin, Z, Wang, X, Strong, MJ, Concha, M, Baddoo, M, Xu, G, Baribault, C, Fewell, C, Hulme, W, Hedges, D, Taylor, CM, Flemington, EK. Whole genome sequencing of the Akata and Mutu Epstein-Barr virus strains. J Virol. 2012: 87:1172-82. (PMID: 23152513).. Concha, M, Wang, X, Cao, S, Baddoo, M, Fewell, C, Lin, Z, Hulme, W, Hedges, D, McBride, J, Flemington, EK. Identification of new viral genes and transcript ...

Van Besien K, Bachier-Rodriguez L, Satlin M, Brown MA, Gergis U, Guarneri D, Hsu J, Phillips AA, Mayer SA, Singh AD, Soave R, Rossi A, Small CB, Walsh TJ, Rennert H, Shore TB. Prophylactic rituximab prevents EBV PTLD in haplo-cord transplant recipients at high risk. Leuk Lymphoma. 2019 07; 60(7):1693-1696 ...

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Principal Investigator：FUJIWARA Shigeyoshi, Project Period (FY)：1996 - 1997, Research Category：Grant-in-Aid for Scientific Research (C), Section：一般, Research Field：Virology