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Query: UNIPROT:P06889 (Mol)
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We have studied four cases of fatal B-cell lymphoproliferative syndrome (LPS) developing among 333 patients (incidence 1.2%) treated with allogeneic bone marrow transplantation (BMT). All four patients had received a T-cell depleted graft. Onset of the first clinical symptoms (palpable lymph node enlargement in three and IgA-lambda paraproteinemia in two patients) occurred between 41 and 188 days post-BMT (median 76 days). The course of the LPS was rapidly progressive in all cases, leading to death in 2-5 weeks. The peripheral blood showed progressive pancytopenia with disproportionally high numbers of activated NK cells, apparently compensating for the T-cell deficiency. Post-mortem histological studies disclosed polymorphic B-cell proliferations, most pronounced in the lymph nodes, spleen, liver, lungs and kidneys. Lymphohemopoietic cells were of donor origin in three patients. In the fourth patient, graft failure suggested a host origin for the proliferating cells. Immunophenotyping and gene rearrangement analysis revealed polyclonal proliferation in one patient, monoclonal proliferation in another patient, and an oligoclonal pattern in the other two patients. The clinical behavior of the LPS was independent of clonality. Immunohistologically, the proliferating cells showed characteristics of relatively mature B-cells in three cases, and pre-B-cell features in one case. Epstein Barr virus (EBV) serology indicated seroconversion (primary infection) in one child, and chronic active EBV infection in both adults. EBV DNA as well as EBV nuclear antigen (EBNA) were detected in infiltrated tissues of all four patients. The labeling pattern on in situ hybridization suggested a replicative EBV infection comparable to that in lymphoblastoid cell lines. We conclude that EBV-associated LPS developing as a result of post-transplant immunodeficiency is a distinct clinicopathologic entity, differing from non-Hodgkin's lymphoma (including Burkitt's lymphoma) and infectious mononucleosis of the immunocompetent host.
Virchows Arch B Cell Pathol Incl Mol Pathol 1991
PMID:Fatal B-cell lymphoproliferative syndrome in allogeneic marrow graft recipients. A clinical, immunobiological and pathological study. 168 38

A newly described herpes virus, human herpes virus 6, (HHV-6), has been linked to exanthema subitum but beyond this its pathogenetic impact remains to be determined. A large body of evidence links it to various lymphoproliferative disorders and this study was conducted to identify forms of lymphoproliferation linked to HHV-6. We studied biopsy samples from 32 patients with disorders of the lymphatic system for the presence of HHV-6, both by polymerase chain reaction (PCR) and in-situ hybridization (ISH) methods, as well as Epstein-Barr virus (EBV) viral DNA, clonal rearrangements of the antigen receptor genes and bcl-2 genes. All the specimens were studied morphologically and a clinical follow-up of up to 4 years was obtained. Seven of the 32 patients were positive for HHV-6 DNA and the remainder were negative. Two of these HHV-6 positive specimens, both from elderly persons, showed a similar distinct histological pattern diagnosed as malignant B-cell lymphoma of high grade malignancy. Two other HHV-6-positive specimens were reactive lymphadenopathies occurring in younger adults. In addition, one further specimen with evidence of EBV-involvement was from a patient who died 3 months after biopsy with fatal infectious mononucleosis (IM). These five samples had HHV-6 DNA by PCR and ISH. Two specimens without specific histologic abnormalities showed evidence of HHV-6 only by PCR but not by ISH. Both high grade malignant lymphomas showed clonal proliferations, one of monoclonal B-cells and the other of clonal T-cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Virchows Arch B Cell Pathol Incl Mol Pathol 1991
PMID:Lymphadenitis and lymphoproliferative lesions associated with the human herpes virus-6 (HHV-6). 168 79

We designed synthetic oligonucleotide primers and hybridization probe for use in polymerase chain reaction (PCR) amplification and hybridization detection of Epstein-Barr virus (EBV) nucleic acid sequences. Primer sequences were chosen from the coding region for the Epstein-Barr virus nuclear antigen-1 (EBNA-1). PCR amplification and hybridization with these oligonucleotides was carried out on standard laboratory cell lines including African Burkitt's lymphoma and infectious mononucleosis derived cell lines, as well as cell lines recently established from clinical EBV isolates from bone marrow transplant recipients. All EBV cell lines tested were positive. No false-positives were detected with uninfected cell lines, human placental DNA or with other viruses. The sensitivity of the detection procedure was such that four copies of the EBV genome could consistently be detected in a background of 1 microgram of placental DNA. EBV was detected in DNA extracts from the peripheral blood mononuclear cells of two patients with infectious mononucleosis and one patient with viral-associated hemophagocytic syndrome. Three of 18 EBV seropositive patients without known ongoing EBV-associated illness undergoing ambulatory surgery also had EBV detected in DNA extracts from their peripheral blood mononuclear cells. EBV was detected in DNA extracts from lymphoma tissue from two patients with post-transplant lymphomas and two AIDS patients with primary CNS lymphomas. EBV was not detected in 12 B-cell lymphoma specimens from patients without history of immunocompromise. DNA extracts from formalin-fixed paraffin-embedded Hodgkin's tissues previously shown to be EBV positive by Southern blot were also demonstrated to be EBV positive by PCR. Thus, with the oligonucleotides described, PCR is applicable to the detection of EBV in a spectrum of clinical isolates. The broad specificity of these oligonucleotides for all strains of EBV tested is probably a function of the highly conserved sequence of the EBNA-1 DNA binding domain.
Mol Cell Probes 1990 Oct
PMID:Oligonucleotides for polymerase chain reaction amplification and hybridization detection of Epstein-Barr virus DNA in clinical specimens. 217 46

Immunochemical comparisons were made of the reactivity of membrane glycoproteins from horse, bovine, sheep and goat erythrocytes with heterophile antibodies of infectious mononucleosis. The four receptors were tested as competitive inhibitors of a sandwich-type solid-phase radioimmunoassay and of agglutination of glycoprotein-latex reagents by infectious mononucleosis serum. The results of this study showed that the bovine glycoprotein had a superior reactivity with this heterophile antibody system and sheep erythrocyte glycoprotein was the least reactive. The latter had negligible ability to displace 125I-bovine glycoprotein and was a very poor inhibitor of the agglutination of a bovine glycoprotein-latex reagent by infectious mononucleosis serum. Horse and goat glycoproteins were more efficient inhibitors than sheep glycoprotein but less active than the preparation from bovine red cells. All of the inhibitory activity of sheep, horse and goat glycoproteins, and a major portion of that of the bovine glycoprotein was destroyed by neuraminidase treatment. We have termed this receptor--shared by all four species--the Paul-Bunnell receptor, since by definition Paul-Bunnell antibody is a sheep erythrocyte agglutinin which is also reactive with horse, bovine and goat erythrocytes. The neuraminidase (and alkaline borohydride) resistant receptor of bovine glycoprotein has been designated the Bo receptor because it is not common to the other three species.
Mol Immunol 1983 Jan
PMID:Immunochemical studies of infectious mononucleosis--XI. comparison of heterophile antibody inhibitors from the erythrocyte membranes of four mammalian species. 640 39

A highly purified preparation of horse erythrocyte glycoprotein was prepared from an aqueous ethanolic extract of hemoglobin-free membranes. The subunit apparent mol. wt was 30,000. In aqueous solution the glycoprotein formed globular aggregates of 93 +/- 16 A diameter. The glycoprotein had a receptor for the Paul-Bunnell antibody of infectious mononucleosis which was associated with an O-glycosidically linked oligosaccharide and dependent on the presence of N-glycolylneuraminic acid. In addition the glycoprotein had a neuraminidase-sensitive receptor for human peripheral blood lymphocytes. Fifty per cent inhibition of the rosetting of sheep red cells by 4 x 10(5) lymphocytes was caused by 30 microgram of glycoprotein.
Mol Immunol 1982 Jun
PMID:Immunochemical studies of infectious mononucleosis--X. Characterization of a glycoprotein from horse erythrocytes which reacts with Paul-Bunnell antibody. 681 Jan 2

We observed a potentially misinterpretable polymerase chain reaction (PCR) amplification product generated with standard primers used to detect the major breakpoint region (mbr) of chromosomal translocation t(14;18). This unexpected phenomenon was initially detected during attempts to transform follicular lymphomas in vitro with Epstein-Barr virus (EBV). Additional studies were performed using the EBV-producing cell line MCUV5, cell lines from EBV-transformed normal B-lymphocytes, and an excised lymph node from a patient with documented EBV-associated infectious mononucleosis. These samples consistently produced a 167-base pair product, which was indistinguishable from a t(14;18) lymphoma product when viewed on ethidium bromide-stained gels. Through DNA sequencing and gene bank analysis, the product was identified as a portion of the EBV genome. A mbr-specific 20-base oligonucleotide probe was able to discriminate between true translocations and the EBV-related amplifications. These results underscore the importance of employing a specific detection system, and comprehensively screening primers when working with PCR.
Diagn Mol Pathol 1994 Mar
PMID:Primers frequently used for detecting the t(14;18) major breakpoint also amplify Epstein-Barr viral DNA. 816 50

Epstein-Barr virus (EBV) has been detected in African Burkitt's lymphoma, posttransplant lymphoproliferative disease, and a variable fraction of Hodgkin's lymphomas. To assess if EBV is associated with other lymphoid proliferations, we evaluated a wide variety of benign and malignant lymphoid lesions, using polymerase chain reaction and a sensitive in situ hybridization method. Abundant EBV+ cells were seen in posttransplant lymphomas, some B cell immunoblastic lymphomas, and in tonsils from patients with infectious mononucleosis. Intermediate numbers of EBV+ cells were seen in a mixed B cell lymphoma, peripheral T cell lymphomas, and in syncytial variants of Hodgkin's disease as well as a lymph node from a patient with infectious mononucleosis. Low numbers of EBV+ cells were detected in normal and reactive lymph nodes, B and T cell lymphomas, and Hodgkin's lymphomas. The variable extent of EBV infection in lymphoid lesions suggests that EBV may play a variety of roles in the development of malignant and nonmalignant lymphoid lesions.
Diagn Mol Pathol 1994 Mar
PMID:Presence of Epstein-Barr virus in many types of benign and malignant lymphoid lesions. Detection by polymerase chain reaction and in situ hybridization. 816 52

Our study describes the comparison of a rapid nested PCR assay to standard serology techniques for the detection of Epstein-Barr virus (EBV) in serum. The sera of 81 patients with suspected EBV infection were analyzed; 54 were positive for one or more of the standard serology markers, i.e., IgM viral capsid antigen (VCA), IgG-VCA, Epstein-Barr nuclear antigen 1 (EBNA-1), and early antigen (EA), and 27 were negative for all serology markers. The sera from 15 normal healthy blood donors were also included. No EBV DNA was detected in any of the 15 blood donor samples or in any of the 27 samples with negative serology results. Eleven samples (20%) of the 54 with positive EBV serology results were positive for EBV DNA. Of these samples, 9 were EBV IgM-VCA positive and anti-EBNA negative, suggesting acute infection. One of the 11 samples had high titers of IgM-VCA, IgG-VCA, anti-EBNA, and anti-EA. The last of the 11 samples was from a patient with acute infectious mononucleosis without sufficient sample volume for EBV serology testing. Seventeen of the total 96 samples from the study were IgM-VCA positive and anti-EBNA negative and 9 of these 17 samples (53%) tested positive for EBV DNA. These data suggest that the detection of EBV DNA by PCR in serum may be a useful indicator of active infection rather than latent virus.
Biochem Mol Med 1997 Apr
PMID:Detection of Epstein-Barr viral DNA in serum using rapid-cycle PCR. 916 98

An in situ polymerase chain reaction (IS-PCR) technique was used to detect and differentiate strains of episomal Epstein-Barr virus (EBV) in infected cells. IS-PCR was performed on cell monolayers in eight-chamber glass slides using EBV type-specific primer pairs conserved within the EBV-encoded nuclear antigen (EBNA) 3C region. The amplicons in the cells were detected by in situ hybridization using EBV type-1 and type-2 specific 5'-biotinylated oligonucleotide probes and avidin-conjugated alkaline phosphatase as secondary reagent. This method was successfully used to identify EBV strains not only in Burkitt's lymphoma cell lines but also in B cells obtained from a patient with infectious mononucleosis. The technique described on this report is a reliable method to detect latently infected EBV-positive cells and can potentially be used to identify and type EBV strains present in clinical specimens.
Mol Cell Probes 1997 Jun
PMID:Detection and differentiation of Epstein-Barr virus strains by in situ polymerase chain reaction. 923 25

EBNA-2 is the first protein to be detected after infection of primary B lymphocytes by Epstein-Barr virus (EBV) and plays an essential role as transcriptional activator in EBV-induced lymphocyte transformation. We analysed by PCR and sequencing regions of the EBNA-2 type 1 gene from isolates from 13 children with infectious mononucleosis (IM), 6 children with tonsillar hyperplasia (TH), and 9 patients with HIV infection followed longitudinally. We found in all three groups of patients frequent non-silent point mutations at positions 48990, 48991, 49021, 49057, 49083, 49089, 49091, 49113, 49119, 49140, 49156, and a triplet insertion at position 49136. While 4 out of 13 samples from patients with IM showed a mosaic pattern suggesting co-existence of more than 1 substrain of EBNA-2 type 1, none of the samples from TH showed this pattern consistent with substrain selection during clinical latency. No sequence changes were noted over time in samples derived from patients with HIV infection. We conclude that in analogy to the coexistence of several subtypes of EBNA-1 in healthy EBV carriers, samples from IM can harbor more than one subtype of the EBNA-2 type 1 gene.
Int J Mol Med 1998 Jun
PMID:Molecular analysis of critical sequences within the EBNA-2 type 1 gene from Epstein-Barr virus isolates from patients with infectious mononucleosis, tonsillar hyperplasia, and HIV infection. 985 35


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