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Query: UMLS:C1396851 (Epstein)
 24,119 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Epstein-Barr virus (EBV), carried by the majority of the world's adult human population, is closely associated with three known human diseases; infectious mononucleosis IM), Burkitts lymphoma (BL) and nasopharyngeal carcinoma (NPC). It is now generally accepted that EBV plays an active role in the etiology of BL and NPC rather than simply being a "passenger". Considerable evidence also argues for the participation of "co-factors" in these two diseases. Environmental co-factors appear needed to explain the peculiar geographical distribution of BL. Among various possibilities that must be considered are insect-transmitted agents that could lead to eventual immunosuppression and/or stimulate further proliferation of EBV-transformed cells, thereby permitting an additional cytogenetic evolution towards malignancy. Recent studies have uncovered a possible cytogenetic co-factor in the ethiology of BL; the 8-14 chromosomal translocation. Genetic co-factors, on the other hand, are likely to be involved in the etiology of NCP. EBV is a B-cell associated virus. Carrier lymphoid cell lines obtained either by in vitro "immortalization" of human cord-blood lymphocytes or by explants from IM and African BL donors harbor multiple copies of the EBV genome, and viral genetic sequences have also been directly detected in biopsies of African BL. The state of the viral genomes in the carrier cell appears to be such that some are integrated into the cellular DNA while others exist as free, covalently closed circular molecules.
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PMID:The biology and serology of Epstein-Barr virus (EBV) infections. 18 69

Seven patients with a clinical diagnosis of infectious mononucleosis (IM) and detectable heterophil antibodies were found to have peripheral blood lymphocytes that were cytotoxic for lymphoid cells containing Epstein-Barr virus from a patient with Burkitt's lymphoma. The cytotoxic lymphocytes persisted in the peripheral circulation for up to 45 days. Patients who had had IM 1 to 5 years previously lacked such cytotoxic lymphocytes. Patients who had signs and symptoms of IM but no detectable heterophil antibodies lacked cytotoxic lymphocytes. The lymphocytes of one patient with IM showed progressive diminution of cytotoxic ability after prednisone treatment.
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PMID:Cytotoxic lymphocytes in infectious mononucleosis. 18 10

Defective T-lymphocyte E rosette (ER) function associated with viral hepatitis A and B may be due to mechanisms extrinsic or intrinsic to the target lymphocyte. The extrinsic defect is induced by an immunoregulatory plasma lipoprotein (RIF) and has the capacity to regenerate ER function in vitro. The intrinsic defect is refractory to regeneration and is not associated with RIF. Although both mechanisms occur with high frequency during the acute phase of viral hepatitis they tend to segregate in accordance with progression of hepatocellular injury at later stages of the disease. The extrinsic defect was observed in 7 out of 8 patients with longstanding chronic active hepatitis and in 10 out of 10 patients with unresolved hepatitis 12 wk after the onset of jaundice. In contrast, none of nine patients with resolved hepatitis had extrinsically defective ER function 12 wk after the onset of jaundice whereas eight of them displayed an intrinsic defect of ER function at that time. Among the various viral and liver diseases studied RIF appeared to be specific for hepatitis A and B viral infections. None of 64 sera from a variety of viral infections including Epstein-Barr virus cytomegalovirus mononucleosis with associated hepatitis nor 15 sera from patients with several chronic nonviral liver diseases were positive for RIF. RIF and its associated extrinsic defect in ER function therefore appear to correlate with a particular type of hepatocellular injury initiated by the hepatitis A and B viruses that may have a propensity for persistence and(or) progression to an aggressive form of chronic hepatitis.
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PMID:Extrinsic modulation of human T-lymphocyte E rosette function associated with prolonged hepatocellular injury after viral hepatitis. 18 20

We devised a quantitative assay for Epstein-Barr-virus-infected mononuclear leukocytes (virocytes) to determine their prevalence in the blood of patients with acute-phase and convalescent-phase infectious mononucleosis and in healthy Epstein-Barr-virus-seropositive controls. Mononuclear peripheral blood leukocyte suspensions were tested for virus-determined cytoproliferative activity by cocultivation with human cord-cell indicator cultures. The highest levels of virocytes among circulating mononuclear leukocytes were found in the early acute phase of infectious mononucleosis (up to 0.05 per cent). Virocytemia decreased to levels comparable with those of healthy controls (less than 0.00001 per cent) by the third month after onset of infectious mononucleosis. These findings provide a quantitative profile of the course of the infection at cellular level and support existing evidence of the efficiency of immune control mechanisms in limiting Epstein-Barr-virus infection during the course of infectious mononucleosis.
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PMID:Quantitative evaluation of Epstein-Barr-virus-infected mononuclear peripheral blood leukocytes in infectious mononucleosis. 18 34

Epstein-Barr virus (EBV)-specific antibody responses were determined in 43 consecutive pediatric patients who had signs and symptoms of inectious mononucleosis (IM) and positive diagnostic tests for mononucleosis (Monspot). Thirty patients gave clear-cut serologic evidence of primary EBV infections; of the remaining 13 patients, seven had no antibodies to EBV in the acute- or convalescent-phase sera and six showed serologic patterns of past EBV infections. Further testing proved that the initial Monospot results were either false-positive or were incorrectly interpreted in all 13 patients with unidentifiable illnesses but in only two of the patients with current EBV infections. The data confirm the occurrence of classical IM in children and show that the disease and the EBV-specific antibody responses can be virtually indistinguishable from adult cases.
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PMID:Infectious mononucleosis in children. Evaluation of Epstein-Barr virus-specific serological data. 18 99

Infection of cells of the Epstein-Barr virus (EBV)-negative human B-lymphoma lines BJAB and Ramos with EBV preparations from P3HR-1 or B 95-8 cells converted these cells to EBV genome carriers expressing Epstein-Barr nuclear antigen (EBNA) in almost 100% of these cells. Induction of these cells as well as of clones from P3HR-1 EBV-converted BJAB cells with iododeoxyuridine, aminopterin, and hypoxanthine resulted in the appearance of a nuclear antigen in about 1-6% of the cells 1-4 days after induction. The antigen is different from known EBV-induced antigens like EBNA, viral capsid antigen (VCA) or the D- and R-subspecificities of the early antigen (EA) complex. It is demonstrated by indirect immunofluorescence and inactivated after acetone fixation. The antigen was not detectable after induction of uninfected BJAB and Ramos cells nor has it been found in noninduced or induced P3HR-1 and Raji cells. Thus, it appears that EBV-infection mediates the expression of this antigen, for which the name TINA (transiently induced nuclear antigen) is suggested. Sera reacting against TINA generally contained high antibody titers against EBV-induced EA. Only a limited number of highly EA-reactive sera, however, were also positive for TINA. Among 200 sera tested thus far, TINA reactivity was most frequently observed in sera of patients with nasopharyngeal carcinoma (7 out of 28), in sera of the only two patients with immunoblastoma tested and occasionally in sera from patients with Hodgkin's disease and chronic lymphatic leukemia. Among 70 sera from nontumor patients, TINA reactivity was observed three times: two patients suffered from "chronic" infectious mononucleosis, the other revealed persistent splenomegaly.
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PMID:Transient induction of a nuclear antigen unrelated to Epstein-Barr nuclear antigen in cells of two human B-lymphoma lines converted by Epstein-Barr virus. 18 13

Biological activities of extracellular Epstein-Barr virus (EBV) from two laboratory strains, namely P3J-HR-1 (P-H) from Burkitt's lymphoma and B95-8 (B95) from infectious mononucleosis, were compared. Virus stocks from both sources contained approximately the same number of virions. Virus from the P-H line induced early antigen in six non-producer EBV-genome carrier cell lines; virus from B95 did not induce early antigen. Extracellular virus from B95 regularly caused lymphocytes from human umbilical cords to form continuous lines (immortalization); P-H virus did not cause primary cultures of human lymphocytes to grow continuously. B95 virus stimulated DNA synthesis, as determined by the rate of incorporation of 3H-thymidine into acid-insoluble material; P-H virus did not stimulate DNA synthesis. Pretreatment of lymphocytes with undiluted P-H virus inhibited immortalization and stimulation of DNA synthesis by B95 virus. The inhibitory properties of the P-H virus were sedimented at 100 000 g and inactivated by heat and UV irradiation; interference by the P-H virus was neutralized by human serum with antibody to EBV and not by antibody-negative human serum. The hypothesis most consistent with these results is that the P-H virus is defective in gene(s) needed for initiation of immortalization. We speculate that the absence of this gene allows early antigen to be expressed upon superinfection of non-producer cell lines. The availability of two laboratory strains of two laboratory strains of EBV that differ in biological behaviour provides starting material for analysis of the mechanism of lymphocyte immortalization by EBV and of virus structural differences that affect immortalization.
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PMID:Differences between laboratory strains of Epstein-Barr virus based on immortalization, abortive infection and interference. 19 Jan 45

Studies on virus-induced animal tumors have provided indirect approaches to a search for viruses causing human malignancies. Epstein-Barr virus (EBV), the cause of infectious mononucleosis, served to illustrate the usefulness of these approaches in linking EBV with Burkitt's lymphoma and nasopharyngeal carcinoma. Despite its demonstrated intimate association with these tumors the role of EBV in their causation remains uncertain. While a passenger role seems excluded, it cannot be decided whether EBV is the primary or a secondary agent in the etiology of the tumors. If the primary cause, immunologic, genetic, virologic or other environmental factors are undoubtedly needed for EBV to express its obvious oncogenic potential. The data illustrate the difficulties encountered in proving a viral etiology of human malignancies.
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PMID:Evidence for an etiologic relation of the Epstein-Barr virus to human malignancies. 19 Apr 97

A 35 year old previously healthy physician had clinical manifestations of a mononucleosis illness complicated by arthralgia, vesicular pharyngitis and hepatitis. Initially, the patient had cytomegalovirus (CMV) viremia (predominantly in polymorphonuclear leukocytes) followed by the presence of CMV in the urine, throat and semen. He also had an antibody response to the Epstein-Barr virus which appeared to be a secondary type. During the acute phase of illness, only 7 per cent of the patient's lymphocytes formed spontaneous T cell rosettes as compared to a normal value of 65 to 70 per cent. Concurrently, evidence of abnormal delayed hypersensitivity was manifested by the loss of reactivity to mumps skin test antigen. All clinical and laboratory abnormalities except for the persistence of CMV in the pharynx, urine and semen returned to normal after resolution of the clinical illness.
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PMID:Cytomegalovirus mononucleosis in a healthy adult: association with hepatitis, secondary Epstein-Barr Virus antibody response and immunosuppression. 19 Aug 84

The leukocyte adherence inhibition (LAI) assay was utilized as a test for cellular immunity to Epstein-Barr virus (EBV) antigens in 22 patients with infectious mononucleosis (IM), 47 patients with lymphoma, 101 carcinoma patients, and 84 subjects without cancer. Response to EB virion ("v") antigen was generally present at the time of diagnosis in the IM patients but the response to EB soluble ("S") antigen was delayed. An increased CMI response to "v" antigen was found in patients with IM, Hodgkin's disease and non-Hodgkin's lymphoma as compared to controls with and without cancer. Patients with Hodgkin's disease had depressed responses to the EBV-associated "S" antigen. The finding of increased LAI responses to "v" antigen in Hodgkin's disease patients with high EBV antibody titers conflicts with previous reports attributing high antibody responses against EBV to a generalized depressed cell-mediated immunity.
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PMID:Lymphocyte responses to EBV-associated antigens in infectious mononucleosis, and Hodgkin's and non-Hodgkin's lymphoma patients, with the leukocyte adherence inhibition assay. 19 8


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