Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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)
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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.
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PMID:Oligonucleotides for polymerase chain reaction amplification and hybridization detection of Epstein-Barr virus DNA in clinical specimens. 217 46

A 46-year-old female patient was diagnosed as having a low-grade malignant B-cell lymphoma of the gastric MALT, stage IV, with bone marrow involvement and a leukaemic blood picture. Different from the infiltrate in the gastric mucosa, which consisted mainly of centrocyte-like cells, the leukaemic cells presented with a blood-picture resembling infectious mononucleosis but showing a predominance of plasma cells. Despite these cytological differences, a common clonal origin for both cellular compartments was demonstrated immunophenotypically and genotypically. Low-grade B-cell lymphomas of the MALT may thus initially present with stage IV disease and a leukaemic blood picture.
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PMID:B-cell lymphoma of the mucosa-associated lymphatic tissue (MALT) presenting with bone marrow and peripheral blood involvement. 238 73

Prevention of EBV-associated lymphoproliferative diseases in immune deficient individuals is preferred; however, standard therapy for the B cell lymphomas has been successful. Chemotherapy must be given cautiously lest further immune compromise result in opportunistic infections. Recently, Acyclovir has decreased morbidity of patients with acute infectious mononucleosis in immune competent persons. In contrast, immunodeficient patients with X-linked lymphoproliferative (XLP) syndrome do not seem to respond favorably. Hence, a prospective study is underway using prophylactic immunoglobulin containing (EBV)-specific antibodies. The mortality rate is 85% following EBV infection in XLP due to fatal infectious mononucleosis associated with fulminant hepatitis and virus-associated hemophagocytic syndrome, acquired hypogammaglobulinemia or malignant B cell lymphoma. We can detect XLP by noting failure of switching from IgM to IgG antibody production on secondary challenge with bacteriophage phi X174. Also, linkage studies with the XLP locus using restriction fragment length polymorphisms are being done to detect affected males pre-EBV infection. Our rationale for prevention of phenotypes of XLP is based on observations that infants in tropical Africa and males with XLP do not develop EBV-induced diseases while neutralizing maternal antibodies are present. An EBV vaccine will be used, when available, in seronegative males with XLP. Prevention of acquired immune deficiency by screening blood for human immune deficiency virus, encouraging prudent life styles, development of specific immunosuppressive agents, development of new antiviral agents (i.e., DHPG), and identification of high risk seronegative patients offer possibilities for preventing life-threatening EBV-induced diseases.
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PMID:Prevention and treatment of Epstein-Barr virus (EBV)-associated lymphoproliferative diseases in immune deficient patients. 243 95

Epstein-Barr virus (EBV) displays several biological properties which distinguish it from any other human herpesvirus. The most important of these is that it infects and immortalizes human B lymphocytes, both in vitro and in vivo. These indefinitely growing cells consistently express viral proteins in the nucleus or in the plasma membrane; at least one of these is required for immortalization. In severely immunocompromised hosts such as transplant recipients and AIDS patients, EBV induces B-cell lymphoma. Two strains of EBV (A and B) have recently been recognized; they behave differently in their reaction to EBV-specific cytotoxic T-lymphocytes. Further studies are needed to define more accurately the part played by EBV in Burkitt's lymphoma and nasopharyngeal carcinoma. Besides immortalization, EBV can infect oropharyngeal epithelial cells in vivo, replicating in them at the time of primary infection (infectious mononucleosis) and reactivations. In fact, EBV infects most people throughout the world while rarely causing severe disease.
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PMID:[Biology of the Epstein-Barr virus]. 255 64

The clinical, immunopathologic, and virologic features of the lymphoproliferative diseases occurring after renal transplantation have been characterized. Clinically, patients may present with an infectious mononucleosis-like illness or with localized solid tumor masses. These lymphoproliferative diseases have unique histologic features that can be classified as polymorphic diffuse B-cell hyperplasia (PDBH) or polymorphic B-cell lymphoma (PBL). Immunologic cell-typing studies have shown that the majority are polyclonal B-cell proliferations, but monoclonal B-cell tumors have also been documented. These B-cell proliferations may, however, evolve from a benign polyclonal B-cell hyperplasia to a monoclonal malignant lymphoma. The Epstein-Barr virus (EBV) has been implicated as the cause of these disorders. Serologic studies frequently demonstrate evidence of a primary or reactivation infection, touch imprints from involved tissue may stain for the presence of EBNA (Epstein-Barr nuclear antigen), and EBV DNA hybridization studies demonstrate the presence of EBV-specific DNA sequences within tumor cells. Since EBV induces a polyclonal B-cell proliferation in vitro and in vivo, the polyclonality of these diseases also implicates EBV. Acyclovir, a new synthetic antiviral agent that inhibits EBV DNA replication may be effective in some patients during the polyclonal growth phase but is ineffective once the tumor evolves into a monoclonal lymphoma. We have identified several factors that may be useful in predicting responsiveness to acyclovir therapy.
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PMID:Advances in the diagnosis and treatment of EBV-associated lymphoproliferative diseases in immunocompromised hosts. 300 29

Epstein-Barr virus (EBV) infects virtually everyone by adulthood, and a lifelong latency is maintained. It infects children silently, whereas the majority of adolescents have infectious mononucleosis (IM). Children who have IM before 5 years of age are often heterophil negative; EBV-specific antibodies are required for diagnosis. On rare occasions the symptoms of IM may persist in a chronic or recurrent form, and fatal infectious mononucleosis occurs rarely. Depending on the type and degree of immune deficiency and the time the EBV infection occurs in the life cycle, various atypical outcomes can occur. Children with primary immune deficiency can have fatal or chronic IM, malignant B cell lymphoma, virus-associated hemophagocytic syndrome, aplastic anemia, or acquired hypogammaglobulinemia. The various outcomes of the EBV infections are likely governed by the immune response of the individual. The increased frequency of B cell neoplasms in immunodeficient patients is likely due, in part, to EBV. Individuals with acquired immune deficiency disorders such as AIDS or allograft recipients may develop malignant B cell lymphomas which tend to be polyclonal, but which may progress through stages of oligoclonality to monoclonality. This conversion likely results from specific reciprocal chromosomal translocations such as t(8;14), which is seen in Burkitt's lymphoma. Detection of EBV in immunodeficient patients is achieved by EBV-specific antibody studies or isolation of virus by obtaining spontaneous lymphoblastoid cell lines from peripheral blood, isolating virus from throat washings, or identifying EBV genome by molecular hybridization techniques. Prevention of primary immune deficiency by early detection and genetic counseling and monitoring of patients for occurrence of EBV infection may lead to early treatment. Acyclovir and immunoglobulin therapy can be of value in some patients with active EBV infection.
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PMID:Epstein-Barr virus: the spectrum of its manifestations in human beings. 303 69

In a double-blind study, sera of 34 patients with acquired immunodeficiency syndrome (AIDS), 19 patients with lymphadenopathy syndrome, and 14 homosexual men with an increased risk of AIDS were screened for antibodies to proteins of the novel human T-lymphotropic retrovirus (leukaemia virus), HTLV-III, recently isolated from cultured T cells of AIDS patients. On a combination of a convenient and rapid enzyme-linked immunosorbent assay and a more sensitive electroblot (Western) assay, 100% of the AIDS sera were scored positive. Similarly, 84% of the lymphadenopathy patients were found to have serum antibodies to HTLV-III. A lower, but significant, proportion (21%) of healthy homosexual men with an increased risk of AIDS were also positive. No heterosexual controls, including those with heterophile antibodies during the course of infectious mononucleosis and patients with T-cell or B-cell lymphoma, had antibodies to HTLV-III. The results strongly indicate that the antibodies to HTLV-III are diagnostic of AIDS or indicate significant risk of the disease, and suggest that HTLV-III is the primary cause of human AIDS.
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PMID:Seroepidemiological studies of human T-lymphotropic retrovirus type III in acquired immunodeficiency syndrome. 614 81

The present report describes two young males with clinically diagnosed infectious mononucleosis (IM) who subsequently were diagnosed as having malignant B-cell lymphoma (i.e., immunoblastic sarcoma of B-cells). Despite these apparent similarities, there were fundamental differences between the two cases. The first patient, who lymphoma was diagnosed 9 months after IM, was one of a well-described kindred with the X-linked lymphoproliferative syndrome (XLP) in which affected young males lack the ability to mount an effective immune response to primary infection with the Epstein-Barr virus (EBV) (i.e., infectious mononucleosis), and subsequently develop fatal lymphoproliferative disorders of the B-cell type. This was in contrast to a second patient, also a young male, who did not have the X-linked lymphoproliferative syndrome, who did develop specific antibodies to the Epstein-Barr virus and whose malignant lymphoma was closely associated in time (i.e., 5 weeks) with the clinical diagnosis of infectious mononucleosis. The comparative immunologic and virologic features are discussed as well as the importance of careful clinicopathologic correlation in young adults and children developing malignant lymphoma both following and in association with infectious mononucleosis.
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PMID:Malignant B-cell lymphoma following and associated with infectious mononucleosis. A comparison of two cases. 626 25

Twelve renal transplant patients with lymphoproliferative disorders (LPDs) were studied. Two clinical patterns were identified: (1) Young patients present with an infectious mononucleosis-like illness with fever, sore throat, and lymphadenopathy soon after transplantation or antirejection therapy. Many organs are ultimately involved, and the clinical course is one of a rapidly fatal LPD. (2) Older patients present a longer time after transplantation with symptoms of solid tumors involving the central nervous system, oropharynx, liver, or small bowel. The clinical course is slower, but it is progressive and fatal. Morphologically these LPDs can all be classified as polymorphic diffuse B-cell hyperplasia (PDBH) or polymorphic diffuse B-cell lymphoma (PBL). Cell marker studies in four patients demonstrated a polyclonal B-cell proliferation. Transition from a polyclonal B-cell proliferation to a monoclonal tumor may occur. Epstein-Barr virus (EBV) specific antibody titers, anticomplement immunofluorescence staining of tumors for the presence of the Epstein-Barr nuclear antigen (EBNA), and EBV complementary ribonucleic acid (cRNA)/deoxyribonucleic acid (DNA) hybridization and vDNA/DNA reassociation analysis implicate EBV as the probable etiologic agent in these disorders. Successful management of these lethal LPDs may depend on discontinuation of immunosuppression and removal of the allograft. Antiviral therapy, however, may prove to be useful.
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PMID:The Epstein-Barr virus in the pathogenesis of posttransplant lymphoproliferative disorders. Clinical, pathologic, and virologic correlation. 626 59


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