Dissertations / Theses: 'Epstein-Barr virus. Epstein-Barr virus'

1

Kalla, Markus. "Epigenetik von Epstein-Barr Virus." Diss., lmu, 2008. http://nbn-resolving.de/urn:nbn:de:bvb:19-90227.

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2

Pattle, Samuel Benjamin. "Epstein-Barr virus EBER RNAs." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.430939.

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3

Al-Mozaini, Maha Ahmed. "Epstein-Barr virus BART gene products." Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.479170.

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4

Bosshard, Rachel. "Epstein-Barr virus encoded EBER RNAs." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9698.

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Epstein-Barr virus (EBV) establishes a lifelong latent infection in 95% of the world’s population and is associated with several human cancers. Some of the most abundant viral products in latent infection are the functional EBV-encoded RNAs EBER1 and EBER2. The aim of this thesis was the identification of distinct functions of EBER1 and EBER2 during EBV infection. Epstein-Barr virus bacterial artificial chromosomes with deletion of either EBER1 or EBER2 and corresponding revertant viral genomes were constructed to analyse broad range effects of EBER1 or EBER2 on host cell gene expression. The resulting recombinant viruses were used to infect primary B lymphocytes and establish lymphoblastoid cell lines (LCLs). Microarray expression profiling revealed clear changes in host cell gene expression correlating with EBER expression and significant differences between gene sets regulated with EBER1 and EBER2. Functions of EBER target genes include membrane signalling, regulation of apoptosis and the interferon response. In additional studies, the interaction of EBER1 with ribosomal protein L22 (RPL22), a component of the large ribosomal subunit, was demonstrated in LCL extracts. Using recombinant viruses and EBER expression vectors, the nuclear redistribution of RPL22 by EBER1 was investigated. The delocalisation of RPL22 from nucleoli into the nucleoplasm upon EBV infection was demonstrated in HEK 293, nasopharyngeal carcinoma and gastric carcinoma-derived cell lines. EBER1 was identified as the only viral component necessary for the delocalisation of RPL22. In contrast to the cancer-derived cell lines, LCLs showed a predominantly cytoplasmic expression of RPL22, which was not significantly changed by EBER1. Subsequently, a possible role of RPL22 and EBER1 in p53-dependent stress responses was explored. The data presented in this thesis provide further understanding of the role of EBERs in EBV infection and several of the EBER-regulated genes might be used as markers to elucidate the mechanism of EBER action.

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5

McDonald, Carol Marie. "Regulation of Epstein-Barr virus BZLF1." Thesis, Imperial College London, 2009. http://hdl.handle.net/10044/1/4430.

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Epstein-Barr virus (EBV) establishes a latent infection in the human host. In order to produce infectious virus particles EBV must reactivate from latency and enter its lytic cycle. BZLF1 is the immediate early gene in EBV that mediates the switch between latency and the lytic cycle. The BZLF1 gene is under the control of the Zp promoter. Reactivation from latency is studied in EBV positive Akata cell lines where EBV can be reactivated by crosslinking the B-cell receptor (BCR) using antibodies to mimic antigen binding. This system uses stably transfected reporter plasmids to study Zp regulation. Mutagenesis identified additional regions of the promoter that contribute to regulation and the ZID MEF2 binding site was demonstrated to be functionally important during the initial stages of Zp activation. XBP-1 splicing, previously implicated in Zp reactivation, was found to occur rapidly in this system in response to BCR crosslinking and parallels the transient induction of Zp. Chromatin remodelling also plays an important role in Zp regulation. An inducible BZLF1 expression system, independent of BCR signalling, was developed in Akata cells that accurately mimics BZLF1 activity and provides a novel approach to study repression at Zp. The BZLF1 protein is related to the bZIP family of transcription factors. BZLF1 contains a bZIP motif in which C-terminal residues fold back against a zipper region that forms an a-helical coiled-coil. The 208SSENDRLR215 sequence in the zipper region is conserved between BZLF1 and C/EBP. Point mutagenesis in this sequence revealed the importance of individual residues for transactivation and progression to DNA replication. The restoration of BZLF1 DNA replication activity by complementation of two deleterious mutations (S208E and D236K) indicated that the interaction of the C-terminal tail and the core zipper region is required for DNA replication, identifying a functional role for this structural feature unique to BZLF1.

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6

Cameron, Barbara Medical Sciences Faculty of Medicine UNSW. "Immunological and virological correlates of persistent illness following primary Epstein-Barr virus infection." Awarded by:University of New South Wales. School of Medical Sciences, 2005. http://handle.unsw.edu.au/1959.4/22373.

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Primary Epstein-Barr virus (EBV) infection in childhood is typically asymptomatic, but infection later in life results in a mononucleosis with the illness severity ranging from asymptomatic to requiring hospitalisation. The illness is generally short-lived (four to six weeks following onset of symptoms), but persistent disabling symptoms (lasting up to 6 months or longer) are well described in around ten percent of individuals. The aim of this work was to characterise immunological and virological parameters in the peripheral blood, which correlate with persistence of symptoms following EBV-induced mononucleosis. Subjects were recruited prospectively following confirmed primary EBV infection, to allow blood samples and clinical data to be collected at multiple timepoints (baseline, 2 weeks, 4 weeks, 3 months and at least 12 months later). Subjects with 6 months or more of disabling symptoms were defined as ???cases??? with control subjects being those whose illness resolved within 6 weeks of enrolment. Cases were compared with control subjects in terms of: cellular EBV viral load in the peripheral blood by PCR; development of antibodies against EBV VCA (IgG and IgM) and EBNA-1 (IgG) by ELISA; proportions of peripheral blood leucocyte subsets and their activation status by flow cytometry; the magnitude, kinetics of development, and breadth of the CD8+ cytotoxic cell response by interferon-?? Elispot; cytokine levels in serum, and production by peripheral blood mononuclear cells ex vivo; and gene expression patterns in peripheral blood mononuclear cells by microarray. With the exception of gene expression, none of these parameters correlated with early resolution of symptoms or predicted clinical outcome following primary EBV infection. Antibody patterns suggest a tendency to Th2 type immune response may be associated with persistent illness. Preliminary analysis of the gene expression studies indicates that there are many genes involved in this complex disease requiring further investigation. Persistent illness following EBV infection is not associated with uncontrolled viral replication, or chronic immune activation due to an aberrant primary immune response.

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7

Kwok, Hin. "Characterization of Epstein-Barr Virus (EBV) strains in primary EBV infection." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/b40203293.

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8

Kwok, Hin, and 郭軒. "Characterization of Epstein-Barr Virus (EBV) strains in primary EBV infection." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B40203293.

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9

Schmaus, Susanne. "Das BPLF1-Gen des Epstein-Barr-Virus." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=965095282.

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10

Patsos, Georgios. "Epstein-Barr virus latent membrane protein 2A." Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399923.

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11

Traylen, Christopher. "To elucidate the Epstein-Barr virus replisome." Thesis, University of Sussex, 2016. http://sro.sussex.ac.uk/id/eprint/59420/.

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Epstein-Barr virus (EBV) is a member of the γ-herpesvirus subfamily of Herpesviridae. EBV is a double stranded DNA virus infecting humans causing a variety of disease from asymptomatic infection to association with certain tumours including Burkitts lymphoma, Hodgkin's disease and nasopharyngeal carcinoma. EBV encodes an immediate-early protein called Zta (BZLF1, EB1, ZEBRA), which is an important transcription factor and replication factor direct in disrupting latency. EBV encodes viral proteins that assemble as a replisome at the viral lytic origin recognition site (Ori-Lyt). Zta binds Ori-Lyt and it is unclear how Zta interacts and recruits the complex to the site of DNA replication, while coordinating and recruiting host factors. After a mutation to three alanines (ZtaAAA) data implicates that the extreme C-terminus of Zta is essential for replication. The question posed is how does Zta assemble the replisome? Identification of the lytic changes that contribute to lytic replication, including cellular components that may contribute to EBV replication is attempted. Transfected control, Zta and ZtaAAA in HEK293-BZLF1-KO cells was compared. Size exclusion chromatography identified a higher molecular weight complex containing Zta during viral replication. SILAC (Stable isotope labelling by amino acids in cell culture) coupled to proteomics analysis identified the elution fraction composition. An interpretation of these cellular components in the context of lytic replication is explored. Identification of interactions of Zta with cellular proteins was attempted by SILAC histidine tagged Zta with pull down assay. Quantitative data was returned and a confirmation of interactions was attempted. A global proteomics approach was also performed. An enrichment method to isolate SILAC labeled Burkitts Lymphoma cells undergoing EBV lytic replication was coupled to mass spectrometry analysis to identify changes in host and viral proteins. Overall, cellular targets that may interact with Zta are to be confirmed. The global proteomics study recognized for the first time by proteomic analysis the identification of three EBV lytic replication cycle proteins.

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12

Tsang, Chi-man. "Epstein-barr virus infection in nasopharyngeal epithelial cells." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41508592.

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13

Chen, Fu. "Epstein-Barr virus (EBV) latent membrane protein LMP2A /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-589-5/.

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14

Shao, Zhouwulin. "Characterization of Epstein-Barr virus BALF0/BALF1 proteins." Electronic Thesis or Diss., Sorbonne université, 2019. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2019SORUS358.pdf.

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L'autophagie est un processus catabolique essentiel qui dégrade les composants cytoplasmiques assurant ainsi la survie des cellules et l'homéostasie. Un nombre croissant de virus comprenant des membres de la famille des Herpesviridae se sont avérés capable de manipuler l'autophagie pour faciliter leur persistance ou optimiser leur réplication. Des travaux antérieurs ont montré que le virus d'Epstein-Barr (EBV), un γ-herpesvirus oncogène humain, détournait l'autophagie au cours de la phase lytique de son cycle pour favoriser la formation de particules virales. Cependant, les protéines virales responsables de la manipulation des voies autophagiques restent à caractériser. Nous montrons ici que le cadre ouvert de lecture BALF0/1 code deux protéines, à savoir BALF0 et BALF1, qui sont exprimées au cours de la phase précoce du cycle lytique. BALF1 stimule le flux autophagique, une activité partiellement limitée par BALF0. Une région supposée d'interaction avec LC3 (LIR) a été identifiée, qui est nécessaire à la fois pour que BALF1 puisse se localiser avec les autophagosomes et pour stimuler l'autophagie. Nous avons aussi contribué à démontrer que BHRF1, un orthologue viral de Bcl-2 bien connu pour ses fonctions anti-apoptotiques, stimule la mitophagie, un processus qui empêche l'initiation de la réponse immunitaire innée médiée par les voies mitochondriales. Enfin, nous montrons que les protéines BALF0, BALF1 et BHRF1 sont au cœur d’un réseau de régulation complexe
Autophagy is an essential catabolic process that degrades cytoplasmic components within the autolysosome therefore ensuring cell survival and homeostasis. A growing number of viruses including members of the Herpesviridae have been shown to manipulate autophagy to facilitate their persistency or to optimize their replication. Previous works have shown that Epstein-Barr virus (EBV), a human γ-herpesvirus, hijacked autophagy during the lytic cycle possibly to favor the formation of viral particles. However, the viral proteins that are responsible for EBV-mediated subversion of the autophagy are still to be characterized. Here we provide first evidences that EBV BALF0/1 open reading frame encodes for two proteins, namely BALF0 and BALF1, that are expressed during the early phase of the lytic cycle. BALF1 stimulates the autophagic flux which, in turn, was limited in the presence of BALF0. A putative LC3-interacting region (LIR) was identified that is required both for BALF1 to colocalize with autophagosomes as well as to stimulate autophagy. BHRF1, one of the well-characterized Bcl-2 homologs of EBV, has been described as an anti-apoptotic modulator in different experimental cell systems. In this thesis, it also shown that BHRF1 stimulates mitophagy, a process that prevents the initiation of the innate immune response mediated by mitochondrial pathways. Co-expression of both BHRF1 and BALF1 resulted in a slight blockage in the degradative step of autophagy. Finally, we demonstrated that the accumulation of BHRF1, BALF0 and BALF1 resulted from a complex interplay

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15

Tsang, Chi-man, and 曾智敏. "Epstein-barr virus infection in nasopharyngeal epithelial cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41508592.

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16

Tune, Cathryn E. "The role of Epstein-Barr virus in oncogenesis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ63685.pdf.

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17

Evans, Tracy Jean. "Regulation of Epstein-Barr virus latent gene expression." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309108.

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18

Cannell, Emma Jane. "Cell cycle activation mediated by Epstein-Barr virus." Thesis, Imperial College London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300043.

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19

Binn, Ulrich Klaus. "Lytic cycle gene regulation of Epstein-Barr virus." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271723.

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20

Amon, Wolfgang. "Gene expression in Epstein-Barr virus lytic cycle." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421907.

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21

Amyes, Elisabeth R. "CD4+ T cell responses to Epstein-Barr virus." Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.410621.

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22

McAulay, Karen A. "Studies on immune regulation of Epstein-Barr virus." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/2692.

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Epstein-Barr virus (EBV) is a gammaherpes virus that infects >90% of the adult population worldwide. During childhood infection is generally sub-clinical, however if delayed until adolescence infectious mononucleosis (IM) may develop. The virus has also been aetiologically linked with a number of tumours including B-cell lymphoma following organ transplantation: post-transplant lymphoproliferative disease (PTLD). The symptoms of IM are caused by an expansion of immune cells in response to infection whilst in the transplant situation immunosuppressive drug therapy allows the outgrowth of the tumour. Understanding the immuno-regulatory mechanisms involved in such EBV-associated diseases is crucial for devising new treatment strategies. We undertook 3 separate studies (1-3) investigating different aspects of the immune response to EBV. In a recently reported phase II trial using allogenic, EBV-specific cytotoxic T-cell (CTL) to treat PTLD, tumour response was significantly increased with a high degree of donor/recipient HLA-allele matching suggesting that further refinement of the matching procedure may be important. In study 1 we investigated the epitope specificity and T-cell receptor (TCR) clonality of the infused CTL to identify potential areas for refinement. We found the protein specificity of the CTL to be polyclonal with dominant recognition of Epstein-Barr nuclear antigen-3 proteins and sub-dominant recognition of Latent membrane protein (LMP)-1 and LMP-2 proteins. Where possible, specificity was confirmed at the peptide level. No single TCR family was preferentially used by CTLs. The CTL epitope specificity did not differ between treatment responders and non-responders however the response was improved in those with several CTL HLA-restricted epitope matches and those infused with CTL containing polyclonal TCR families as opposed to monoclonal. CTL/recipient matching based on HLA matching alone was improved when also matched via HLA- restricted epitiope specificity. Therefore mapping CTL peptide epitope specificity prior to CTL infusions may enhance patient responses. In recent years, interest has developed in genetic variation within components of the immune system. Of particular interest are cytokine/cytokine receptor genes and genes of the human leukocyte antigen (HLA), both of which act to regulate the immune response. Variation within these genes could potentially alter the immune response leading to disease. In study 2 we investigated single nucleotide polymorphisms (SNPs) in several cytokine genes (TNF, IL-1, -6, -10) in both IM and PTLD cases and compared with relevant control groups. We found that the frequency of two TNF promoter alleles was significantly increased in PTLD patients compared to controls whilst the frequency of a TNF receptor II allele was increased in IM and EBV seropositive individuals, suggesting a role for this allele in susceptibility to EBV infection. The frequency of a second TNF receptor II allele was increased in both PTLD and IM subjects compared to controls highlighting the possible significance of TNF and its receptor in the development of EBV associated disease. In study 3 we analyzed two microsatellite markers and two SNPs located near the HLA class I locus in IM, PTLD and control subjects to further determine whether the HLA genes may affect development of EBV-associated diseases. Alleles of both microsatellite markers were significantly associated with development of IM. Specific alleles of the two SNPs were also more frequent in IM patients. Moreover IM cases possessing the associated microsatellite allele had significantly fewer lymphocytes, increased neutrophils, and displayed higher EBV titres and milder IM symptoms relative to IM cases lacking the allele. The results indicate that HLA class I polymorphisms may predispose patients to development of IM upon primary EBV infection and suggest that genetic variation in T cell responses can influence the course of EBV infection.

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23

Al-Sheikh, Yazeed A. "Epstein Barr virus nuclear antigen-1 and lymphomagenesis." Thesis, University of Glasgow, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437956.

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24

Davis-Poynter, Nicholas John. "Studies of the Epstein-Barr virus thymidine kinase." Thesis, University of Cambridge, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386028.

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25

Caioni, Massimo. "Epstein-Barr virus subtype distribution in angioimmunoblastic lymphadenopathy /." [S.l : s.n.], 1994. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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26

McClellan, Michael J. "Cellular reprogramming by Epstein-Barr virus nuclear antigens." Thesis, University of Sussex, 2015. http://sro.sussex.ac.uk/id/eprint/54308/.

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Epstein-Barr virus (EBV) is a widespread human B cell virus that is linked to many malignancies. EBV modulates the transcriptome of B lymphocytes to drive immortalisation and viral persistence. This is primarily coordinated by the EBV nuclear antigens (EBNA) 2 and the EBNA 3 family (3A, 3B and 3C), which regulate overlapping sets of cellular genes. Using Chromatin immunoprecipitation (ChIP) coupled to next generation sequencing we found >21000 EBNA 2 and >7000 EBNA 3 binding sites in the human genome, providing the first evidence of EBNA 3 association with the human genome in vivo. Binding sites were predominantly distal to transcription start sites (TSS) indicating a key role in long-range gene control. This was especially pronounced for EBNA 3 proteins (84% of sites over 4kb from any TSS). 56% of genes previously reported to be regulated by these EBNA proteins in micro array experiments were bound by an EBNA. Using ChIP-QPCR we confirmed EBNA 3C bound to and promoted epigenetic silencing of a subset of integrin receptor signalling genes (ITGA4, ITGB1, ADAM28, ADAMDEC1). Indirect silencing of CXCL10 and CXCL11 chemokines by EBNA 3C was also demonstrated. 75% of sites bound by EBNA 3 were also bound by EBNA 2 implicating extensive interplay between EBNA proteins in gene regulation. By examining novel (WEE1, CTBP2) and known (BCL2L11, ITGAL) targets of EBNA 3 proteins bound at promoter-proximal or distal binding sites, we found both cell-type and locus-specific binding and transcriptional regulation. Importantly, genes differentially regulated by a subset EBNA 3 proteins were bound by the same subset, providing a mechanism for selective regulation of host genes by EBNA 3 proteins. In summary, this research demonstrates that EBNA proteins primarily act through long-range enhancer elements and regulate gene expression in a locus and gene-specific manner through differential binding.

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27

Allday, Martin John. "The Epstein-Barr virus nuclear antigen (EBNA) complex." Thesis, Imperial College London, 1989. http://hdl.handle.net/10044/1/47329.

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28

Hopwood, Paul A. "Epstein-Barr virus infection in cardiothoracic transplant recipients." Thesis, University of Edinburgh, 2001. http://hdl.handle.net/1842/22321.

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Epstein-Barr virus (EBV) is a human DNA herpesvirus which establishes a persistent latent infection in vivo in B-lymphocytes. Iatrogenic immunosuppression to prevent rejection of transplanted organs predisposes to EBV positive post-transplant B-lymphoproliferative disease (PTLD). This study followed 96 adult cardiothoracic transplant recipients for up to 1110 days (mean follow up time of 415 days) post-transplant. Blood samples were taken immediately prior to transplant surgery and multiple samples taken at intervals following transplantation (1 to 14 samples per patient, mean of 5 samples). Blood samples were also obtained from normal EBV seropositive individuals and patients with infectious mononucleosis and PTLD. EBV load in peripheral blood mononuclear cells (PBMs) were determined in each sample using a semi-quantitative DNA PCR capable of detecting 1-10 EBV genomes in a total of 10⁶ cells. RT-PCRs were developed to examine whether the pattern of EBV gene expression changed following transplantation due to immunosuppressive therapy and how these changes relate to PTLD development. The results show that post-transplant EBV load significantly increases above that detected in normal EBV seropositives (EBV load in normals ranged from <1 to 200 EBV genomes/ 10⁶ PBMs, median of 10 EBV genomes/ 10⁶ PBMs) in 52% of transplant recipients and reaches levels equivalent to that detected in patients with clinically apparent EBV associated disease (IM or PLTD) in 19%. EBV load pre-transplant in all patients was equivalent to that in normal EBV seropositives (p>0.05). Thus high EBV load is associated with, but not diagnostic of EBV associated disease. EBV gene expression prior to transplantation did not vary from that in normal EBV seropositives, with detection of LMP2a in 20/36 subjects and LMP2a and 2b in 3/36 but no detection of lytic transcripts (gp350) or EBNA3C. In IM, latency III was detected (EBNA3C) in 2/28 subjects, latency III and lytic replication in 4/28 and restricted latency with lytic replication in 5/28.

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29

Moquin, Stephanie. "Novel Molecular Insights Into Epstein-Barr Virus Reactivation." Thesis, University of California, San Francisco, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10633481.

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Epstein-Barr Virus (EBV) is a herpesvirus responsible for approximately 1% of cancers worldwide, including African Burkitt lymphoma, Hodgkin lymphoma, lymphomas in immunosuppressed patients, and nasopharyngeal and gastric carcinoma. Interestingly, the development of different cancers is mainly due to expression of the latent EBV proteins, although expression of lytic genes has recently been shown to play a role. Many of the molecular mechanisms behind EBV reactivation have been revealed, however, the contribution of chromatin dynamics to EBV reactivation is not well understood. A better understanding of how the switch between the latent and lytic cycle is regulated could have implications in treating disease. Here we investigate the contribution of chromatin dynamics to EBV reactivation in the context of i) nuclear localization and contacts with the human genome, and ii) the chromatin-reading protein BRD4. We used in situ Hi-C to show that the Epstein-Barr virus associates with repressive compartments of the nucleus during latency, and non-repressive compartments of the nucleus during reactivation. This adds 3D re-localization as a novel component to the molecular events that occur during EBV reactivation. Furthermore, we show that the protein BRD4 plays an important role in EBV lytic reactivation. BRD4 binds to the lytic origins of replication and inhibition of BRD4 by JQ1 inhibits the lytic cycle at two different steps. In summary, this work has led to a better understanding of how the latent-lytic switch of EBV is regulated.

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Chen, Yichen. "The role of dendritic cells in Epstein-Barr virus infection." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B37473396.

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31

Cheung, Wing-yi, and 張詠兒. "Evaluation of immunoblot-based assay for diagnosis of primary EBV infection." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B4515336X.

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32

Xu, Xuequn. "Longitudinal study of Epstein-barr virus (EBV) - specific CD8 + T lymphocyte development in primary EBV infection." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B4163407X.

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33

Zou, Jie Zhi. "Epstein-Barr virus latency in vivo and in vitro /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-968-8/.

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Dümpelmann, Edda. "Die effiziente Transkription des viralen EBER 2-RNA-Gens hängt von der strukturellen Integrität der RNA ab." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=963562215.

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35

Schultheiss, Ute. "Identifizierung von Signaltransduktionskomponenten des latenten Membranproteins 1 des Epstein-Barr-Virus." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=964441853.

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36

黃麗敏 and Lai-man Wong. "A study of the biological effect of Epstein-Barr virus encoded latent membrane protein 1 (LMP1) in human epithelial cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31221932.

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Wong, Lai-man. "A study of the biological effect of Epstein-Barr virus encoded latent membrane protein 1 (LMP1) in human epithelial cells /." Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2130113X.

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38

Chen, Yichen, and 陳以晨. "The role of dendritic cells in Epstein-Barr virus infection." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B37473396.

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39

Herrmann, Heidrun. "Erste Schritte zu einem Mausmodell für Epstein-Barr-Virus." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-74582.

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40

Bergbauer, Martin. "Identifizierung von BZLF1-regulierten Promotoren des Epstein-Barr Virus." Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-127409.

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41

Isaksson, Åsa. "Characterization of non-coding mRNA in Epstein-Barr virus /." Göteborg : Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine, Göteborg University, 2007. http://hdl.handle.net/2077/4444.

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42

Almond, Elizabeth Jennifer Philippa. "Epstein-Barr virus infection of the lower respiratory tract." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1989. http://hub.hku.hk/bib/B31208484.

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43

Flanagan, James Michael. "The immortalisation of B-lymphocytes with Epstein-Barr virus /." St. Lucia, Qld, 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16501.pdf.

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44

Balan, Nicolae. "Analysis of the Epstein-Barr virus transcription factor, Zta." Thesis, University of Sussex, 2014. http://sro.sussex.ac.uk/id/eprint/48903/.

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Epstein-Barr virus (EBV) is a ubiquitous pathogen that infects most of the adult population and persists for life after the initial contact. The extreme success of the virus is attributed to its bipartite life cycle, which consists of a dormant-like state of latency, with periodical reactivation to the virus producing, lytic phase. Zta (BZLF1, Z, Zebra or EB1) is a multifunctional viral protein that belongs to the bZIP family of transcription factors and is known as the master lytic regulator of EBV. Together with transcriptional activation, Zta has been shown to be involved in DNA binding-dependent transcriptional repression, particularly of the host class II major histocompatibility complex transactivator, CIITA. Distinct protein domains, as well as various post translational modifications, like phosphorylation of Serine 209 by the viral protein kinase (VPK), have been linked to different functional roles of Zta. In the present study, it was shown that VPK can partially inhibit SUMOylation of Zta on Lysine 12, in a manner which was not dependent on Serine 209 phosphorylation. However, no direct interaction of VPK and Zta could be observed and no significant effect of either proteins on histone H2AX phosphorylation was seen. Interestingly, in vitro reporter assays revealed that fusion of a SUMO moiety to the amine-terminus of Zta inhibited repression of the CIITA promoter, but not the activation of the viral BHLF1 promoter, pointing at divergent mechanisms of action of transcriptional repression and activation by Zta. Moreover, truncation of the carboxy-terminal dimerisation domain of Zta (crucial for protein-DNA interaction) abrogated BHLF1 transactivation but not CIITA down-regulation, revealing underlying diffe rences in DNA binding requirements for the two processes. Further in silico sequence analysis, coupled with a mutation approach of the CIITA promoter, confirmed that an alternate route to the Zta DNA binding-dependent repression exists. Finally, no single promoter element could be linked to down-regulation of CIITA, suggesting sequestration of a possible, yet unknown cofactor, by Zta.

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Forrest, Calum Philip Gascoyne. "Cytotoxic T lymphocyte immunodominance to Epstein-Barr virus infection." Thesis, University of Birmingham, 2017. http://etheses.bham.ac.uk//id/eprint/7306/.

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EBV lytic replication involves the sequential expression of a large array of antigens that potentially provides a complex antigenic challenge. Despite this number, the primary CD8+ T cell response in infectious mononucleosis (IM) patients appears focused against epitopes found in immediate-early and some early expressed antigens with responses to late antigens typically subdominant. However previous approaches have only focused on a limited number of lytic antigens. To resolve these issues, this study examines the CD8+ T cell repertoire to all EBY lytic antigens in different phases of infection. Polyelonal CD8+ T cell lines were mitogenically expanded from IM patients or expanded in an antigenically unbiased way from post-1M patients and healthy carriers using autologous dendritic cells loaded with lysates of lytically infected cells. Target cells expressing individual lytic antigens along with donor HLA class I molecules were used to challenge polyclonal lines with responses measured by the release of IFNγ. These studies show that the pattern of target antigen choice varies with the phase of infection and is consistent with the idea that CD8+ T cell responses in primary infection are driven by lytically infected B cells. However over time the repertoire of responses may be influenced through antigen cross-presentation.

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Tsai, Ching-Hwa Ann. "Characterization of Epstein-Barr virus (EBV)-specific monoclonal antibodies /." The Ohio State University, 1990. http://rave.ohiolink.edu/etdc/view?acc_num=osu148768178825386.

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Morton, David. "Epstein-Barr virus infection in adult renal transplant recipients." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/epsteinbarr-virus-infection-in-adult-renal-transplant-recipients(bc856b34-7164-45e5-8a64-71693a104912).html.

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Aims: To explore the clinical significance of EBV infection in adult renal transplant recipients when detected in the late post-transplant period. Methods: (1) A prospective observational study recruiting 499 stable adult kidney transplant recipients with serial blood sampling for EBV DNAemia and assessment of clinical outcomes and associated factors. (2) A retrospective analysis of PTLD incidence, timing and outcomes in relation to EBV infection. Results: EBV DNAemia in stable kidney transplant recipients is common, found in 46% of recruited individuals screened over 1 year, with persistent DNAemia seen in 10%. DNAemia prevalence increased significantly with time from transplant (p<0.0001) from 16% within 1 year of transplant to 66% in those transplanted for 20-24 years. High baseline DNA levels predicted persistence of DNAemia. Time adjusted analyses showed significant association of DNAemia with EBV seronegative status and previous PTLD and low DNAemia rates with Mycophenolate Mofetil (MMF) use and lymphopenia. The mechanism did not appear to be directly linked to MMF induced B cell depletion. Chronic high viral load detection was significantly associated with time from transplant, EBV seronegative status at transplant, ciclosporin use and plasma detection of DNA. No significant differences in overall patient survival at 3 years, clinical symptoms or clinical findings such as anaemia, thrombocytopenia or rate of decline in renal function were seen between stable transplant recipients with and without EBV DNAemia. PTLD incidence also increases with time from transplant and was greatest during the 10th-14th post-transplant years. Disease was EBV positive in 68% cases. No statistically significant differences in overall patient survival, or overall disease complete response rates were seen in relation to recipient EBV serostatus or EBV status of PTLD histology. Conclusions: EBV DNAemia prevalence increases with time from transplant but was not associated with worse patient or graft survival or specific symptoms. PTLD incidence including EBV negative disease also increases with time from transplant but response rates and survival were not influenced by EBV serostatus or histological status.

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Macsween, Karen F. "Epstein-Barr virus infection in the Edinburgh student population." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/24880.

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A longitudinal sero-epidemiological cohort study of Epstein-Barr virus (EBV) in the Edinburgh student population was conducted between 1999 and 2003. During this time 60 cases of infectious mononucleosis (IM) were recruited at the University Health Centre to join a case control study to investigate the symptoms of IM and its impact on daily activities. In the longitudinal cohort study a total of 2006 students (1258 female and 748) commencing four year degree courses in 1999 or 2000 had their EBV serology determined and completed a lifestyle questionnaire. Overall 1499 (75%) were EBV seropositive at recruitment. Female students were more likely than male students to be seropositive (79% vs. 69%, p<0.001), as were, students with siblings (75%, compared to those without 66%, p=0.023), and those reporting prior residence in a tropical country (81%, p=0.003). Students reporting a prior sexual relationship were more likely to be seropositive (83%, p<0.001). Repeat serological testing of 241 initially seronegative students undertaken at the start of their fourth year of study showed that 110 (54%) had seroconverted over the intervening three year period. The proportion experiencing IM was 25%. Of the 60 IM cases recruited to the case control study the great majority 56/60 (93%) had either sore throat or complaints relating to lymphadenopathy when presenting to their GP. Few students complained of fever (13%), and some had presentations that included atypical symptoms including gastrointestinal complaints 8% (predominantly vomiting), headache 10%, fainting 10% or cough 7%. Students with IM are likely to be sexually active, and may therefore have additional health care needs. IM in university students is associated with prolonged clinical, immunological, and social consequences. Female students are more likely than males to experience a protracted fatigue state and to miss university classes.

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McLaren, James Edward. "Regulation of the STAT1 by the Epstein-Barr virus." Thesis, Cardiff University, 2007. http://orca.cf.ac.uk/55169/.

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Hafner, Jonas [Verfasser], and Marcus [Akademischer Betreuer] Panning. "Die Epstein-Barr-Virus-Konzentration im Vollblut und im Plasma von Transplantationspatienten unter dem Gesichtspunkt der Epstein-Barr-Virus-assoziierten Posttransplantations-Lymphoproliferativen Erkrankung." Freiburg : Universität, 2015. http://d-nb.info/1120020581/34.

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Dissertations / Theses on the topic 'Epstein-Barr virus. Epstein-Barr virus'

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