Frequent detection of Epstein-Barr virus DNA by the polymerase chain reaction in lymph node biopsies from patients with Hodgkin's disease without genomic evidence of B- or T-cell clonality

Knecht, Hans; Odermatt, Bernhard; Bachmann, Elias; Teixeira, Silvana; Sahli, Roland; Hayoz, Daniel; Heitz, Philipp U.; Bachmann, Fédor

doi:10.1182/blood.v78.3.760.760

Cited by 71 publications

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“…Several studies have investigated the possible involvement of viral agents in HD, and particular attention has been directed to evaluate the potential role of herpesviruses. Past and recent studies, carried out with different techniques, have demonstrated the presence of Epstein‐Barr virus (EBV) DNA and RNA, as well as the expression of specific gene products in a high percentage of HD cases ( Herbst et al , 1990 ; Herbst & Niedobitek, 1993; Pallesen et al , 1991 ; Knecht et al , 1991 ; Jarrett et al , 1991 ; Valente et al , 1996 ). However, a direct pathogenetic role of EBV in HD has not been definitively demonstrated.…”

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confidence: 99%

Human herpesvirus type 7 in Hodgkin's disease

et al. 1998

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Summary. Several lines of evidence have pointed to the involvement of a viral agent in the pathogenesis of Hodgkin's disease (HD). Therefore we investigated the presence of human herpesvirus type 7 (HHV-7) in 53 cases of HD by polymerase chain reaction (PCR), DNA in situ hybridization (ISH) and immunohistochemistry. HHV-7 DNA was frequently detected (68% of the cases) in HD biopsies by PCR independently of the histological type, whereas only 32% (P < 0·05) of positive cases were found in 19 reactive lymph nodes. However, by applying the quantitative PCR technique, the majority of the samples showed a low level of viral load.Moreover, ISH for HHV-7 DNA was positive in a low number of small T lymphocytes and consistently negative in Hodgkin and Reed-Sternberg (HRS) cells, which appeared negative for HHV-7 also at immunohistochemistry.These results indicate that the high frequency of HHV-7 infection in HD: (i) is probably non-productive, (ii) mainly involves small lymphocytes belonging to the T-lineage, and (iii) is probably due to the recruitment of non-malignant reactive cells in HD tissue.

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confidence: 99%

Human herpesvirus type 7 in Hodgkin's disease

et al. 1998

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“…Immunohistochemical analysis was performed on formalin‐fixed, paraffin‐embedded lymphoma lesions . EBV investigations on formalin‐fixed, paraffin‐embedded tissue sections were performed using: (1) immunohistochemical analysis with monoclonal antibodies to LMP1 and EBNA2 (Dako); (2) in situ hybridization (ISH) using fluorescein‐labelled oligonucleotides complementary to EBER 1 and 2 (Dako); (3) PCR amplification of the Bam W region of the EBV genome (Knecht et al , 1991). B‐cell clonality was assessed using PCR analysis of IgH gene rearrangements, using a sense primer directed at IgH variable region consensus sequence, framework III (FR3A), and an antisense primer directed at a consensus sequence at the IgH joining regions (VLJH), according to previously described protocols (Födinger et al , 1999).…”

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confidence: 99%

Epstein–Barr virus‐positive aggressive lymphoma as a consequence of immunosuppression after multiple salvage treatments for follicular lymphoma

Orlandi

Paulli²,

Viglio³

et al. 2001

Br J Haematol

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Summary. We report on a patient with follicular nonHodgkin's lymphoma (NHL) who developed a fatal high-grade Epstein±Barr virus (EBV)-positive NHL after conventional chemotherapies. The sudden onset of the high-grade lymphoma was accompanied by increasing circulating EBV genome copies and was complicated by spontaneous rupture of the spleen. Splenic tissue was diffusely infiltrated by large B cells. In situ hybridization for Epstein±Barr-encoded RNA (EBER) 1±2 was positive in 70% of cells, and molecular analysis revealed the presence of EBV DNA and a monoclonal IgH gene rearrangement. This case shows that the immunosuppression of multiple treatments may induce uncontrolled reactivation of a latent EBV infection, contributing to high-grade transformation in heavily treated lymphoma patients.

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“…Proliferating activity in the AILD cases ranged from 4% to 34%. Rearrangement studies were performed as described (Knecht et al, 1991). The TcRB genes were clonally rearranged in one AILD and one T-ALC case.…”

Section: Methodsmentioning

confidence: 99%

Expression of human recombination activating genes (RAG‐1 and RAG‐2) in angioimmunoblastic lymphadenopathy and anaplastic large cell lymphoma of T‐type

et al. 1993

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In order to determine the genotypic maturation status of the proliferating lymphoid cells in angioimmunoblastic lymphadenopathy (AILD) and in anaplastic large cell lymphoma of T-type (T-ALC), recombinase activating gene (RAG-1 and RAG-2) expression was assessed in six AILD and five T-ALC cases using a sensitive reverse transcriptase (RT) and competitive (C) polymerase chain reaction (PCR). RAG transcripts were not detectable in nine cases with high proliferating activity, suggesting that in most cases the proliferating cells are derived from mature (rearranged) lymphocytes. However, low levels of RAG transcripts were detected in one AILD and one T-ALC case and are consistent with either an involvement of immature lymphoid precursors in the proliferating pool or a deregulated T-cell maturation pathway with persistence of RAG expression. An association between RAG gene expression and poor response to therapy is possible but has to be tested in larger prospective series.

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Frequent detection of Epstein-Barr virus DNA by the polymerase chain reaction in lymph node biopsies from patients with Hodgkin's disease without genomic evidence of B- or T-cell clonality

Cited by 71 publications

References 0 publications

Human herpesvirus type 7 in Hodgkin's disease

Human herpesvirus type 7 in Hodgkin's disease

Epstein–Barr virus‐positive aggressive lymphoma as a consequence of immunosuppression after multiple salvage treatments for follicular lymphoma

Expression of human recombination activating genes (RAG‐1 and RAG‐2) in angioimmunoblastic lymphadenopathy and anaplastic large cell lymphoma of T‐type

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