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Epstein Barr Virus (epstein + barr_virus)
Selected AbstractsPrevention of cancer through immunization: Prospects and challenges for the 21st centuryEUROPEAN JOURNAL OF IMMUNOLOGY, Issue S1 2007Abstract Persistent infection by several microbial agents is responsible for at least 15% of cancer globally, including most cancers of the liver, stomach, and cervix. The recent development of vaccines that can prevent infection and premalignant disease caused by human papillomaviruses (HPV), which cause virtually all cases of cervical cancer as well as some other cancers, has focused renewed attention on infection control as a means of reducing the global cancer burden. For vaccines to prevent cancer-causing infection with hepatitis C virus, Helicobacter pylori, or Epstein Barr virus, new vaccine technologies to induce more effective protective responses are required. For the two available cancer control vaccines, designed to prevent infection with HPV and hepatitis B virus, the major challenge is to promote effective vaccine deployment through education programs and increased affordability/accessibility for underserved populations, particularly in the developing world, where the cancer burden attributable to infection by these two viruses is greatest. [source] Patients with Epstein Barr virus-positive lymphomas have decreased CD4+ T-cell responses to the viral nuclear antigen 1INTERNATIONAL JOURNAL OF CANCER, Issue 12 2008Kevin N. Heller Abstract Epstein Barr virus (EBV) causes lymphomas in immune competent and, at increased frequencies, in immune compromised patients. In the presence of an intact immune system, EBV-associated lymphomas express in most cases only 3 or fewer EBV antigens at the protein level, always including the nuclear antigen 1 of EBV (EBNA1). EBNA1 is a prominent target for EBV-specific CD4+ T cell and humoral immune responses in healthy EBV carriers. Here we demonstrate that patients with EBV-associated lymphomas, primarily Hodgkin's lymphoma, lack detectable EBNA1-specific CD4+ T-cell responses and have slightly altered EBNA1-specific antibody titers at diagnosis. In contrast, the majority of EBV-negative lymphoma patients had detectable IFN, expression and proliferation by CD4+ T cells in response to EBNA1, and carry EBNA1-specific immunoglobulins at levels similar to healthy virus carriers. Other EBV antigens, which were not present in the tumors, were recognized in less EBV positive, than negative lymphoma patients, but detectable responses reached similar CD8+ T cell frequencies in both cohorts. Patients with EBV-positive and -negative lymphomas did not differ in T-cell responses in influenza-specific CD4+ T cell proliferation and in antibody titers against tetanus toxoid. These data suggest a selective loss of EBNA1-specific immune control in EBV-associated lymphoma patients, which should be targeted for immunotherapy of these malignancies. © 2008 Wiley-Liss, Inc. [source] Cellular normalization of viral DNA loads on whole blood improves the clinical management of cytomegalovirus or Epstein Barr virus infections in the setting of pre-emptive therapyJOURNAL OF MEDICAL VIROLOGY, Issue 1 2009Céline Bressollette-Bodin Abstract Two quantitative duplex real-time PCR assays were developed for co-amplification of human albumin and cytomegalovirus (CMV) or Epstein Barr virus (EBV) genes after automated extraction on whole blood, and compared two units for expressing viral DNA loads (copies per ml of blood or per 106 peripheral blood leukocytes (PBLs)) on 1,138 positive samples. Both PCRs were characterized by high sensitivity, reproducibility, and linear range. Automated extraction by a MagNA Pure LC Instrument was shown to be more efficient when peripheral blood cell count was inferior to 5,×,109 PBLs/L. Albumin co-amplification allows the detection of PCR inhibitors and normalization of viral load according to the number of cells calculated in the sample. The two ways of expressing viral load results were highly correlated, but quantitative differences varied in relation to variations of blood cell count. As these two viruses are highly cell associated, viral loads can be underestimated in patients with leucopenia. In the setting of pre-emptive strategies during CMV infection, the units in which results are expressed can influence clinical management, as illustrated in this article. J. Med. Virol. 81:90,98, 2009. © 2008 Wiley-Liss, Inc. [source] Postvaccination hyperhemolysis coinciding with remission of Epstein Barr virus (EBV)-associated immune thrombocytopenic purpura (ITP),,AMERICAN JOURNAL OF HEMATOLOGY, Issue 9 2009Christine M. Cserti-Gazdewich No abstract is available for this article. [source] Activation of the JAK/STAT Pathway in Epstein Barr Virus+ -Associated Posttransplant Lymphoproliferative Disease: Role of Interferon-,AMERICAN JOURNAL OF TRANSPLANTATION, Issue 10 2009M. Vaysberg Epstein Barr virus (EBV) is associated with B-cell lymphomas in posttransplant lymphoproliferative disease (PTLD). Latent membrane protein 1 (LMP1), the major oncogenic protein of EBV, promotes tumorigenesis through activation of NF-,B, Erk, p38, JNK and Akt. The Jak/STAT signal transduction pathway is also constitutively active in PTLD-associated EBV+ B-cell lymphomas. Here we determine the mechanism of Jak/STAT activation in EBV+ B-cell lymphomas and the role of LMP1 in this process. Immunoprecipitation studies revealed no direct interaction of LMP1 and JAK3, but known associations between JAK3 and common gamma chain, and between LMP1 and TRAF3, were readily detected in EBV+ B cell lines from patients with PTLD. An inducible LMP1 molecule expressed in EBV, BL41 Burkitt's cells demonstrated STAT activation only after prolonged LMP1 signaling. While LMP1 induced IFN-, production in BL41 cells, IFN-, receptor blockade and IFN-, neutralization prior to LMP1 activation markedly decreased STAT1 activation and expression of LMP1-driven IFN-, inducible genes. Understanding the mechanisms by which EBV induces cellular signal transduction pathways may facilitate development of new treatments for PTLD. [source] Detection of presence or absence of herpes simplex virus, Epstein Barr virus and human cytomegalovirus in infected pulp using a polymerase chain reactionAUSTRALIAN ENDODONTIC JOURNAL, Issue 1 2009Hannah Rosaline mds Abstract The development of methods to amplify nucleic acids has provided a way of identifying and quantifying infectious pathogens in infected pulp and periapical region. Recent studies have detected human herpes virus in periapical pathosis and periodontitis. The aim of this study is to detect the presence or absence of herpes simplex virus, human cytomegalovirus and Epstein Barr virus in an infected pulp. Ten pulp tissue samples from teeth with irreversible pulpitis and eight control samples were subjected to polymerase chain reaction (Perkin , Elmer Gene Amplification System) for detection of human herpes virus. The results of this study did not reveal any human herpes virus in both the control and infected pulp tissue samples. According to this study, human herpes virus may not have an entry through the infected pulp to reach the periapical region and may not be a causative organism in the pulp. [source] | ||||||||||