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Expression of potentially oncogenic HHV‐8 genes in an EBV‐negative primary effusion lymphoma occurring in an HIV‐seronegative patient
Author(s) -
Cobo Francesc,
Hernández Sílvia,
Hernández Lluís,
Pinyol Magda,
Bosch Francesc,
Esteve Jordi,
LópezGuillermo Armando,
Palacín Antonio,
Raffeld Mark,
Montserrat Emilio,
Jaffe Elaine S.,
Campo Elías
Publication year - 1999
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(199910)189:2<288::aid-path419>3.0.co;2-f
Subject(s) - primary effusion lymphoma , virology , biology , gammaherpesvirinae , epstein–barr virus , virus , lymphoma , immunology , herpesviridae , viral disease
Primary effusion lymphoma (PEL) is a novel lymphoproliferative disorder associated with human herpesvirus 8 (HHV‐8) infection. Most PELs develop in HIV‐seropositive individuals and are nearly always positive for Epstein–Barr virus (EBV), a finding which obscures the role of HHV‐8 in lymphomagenesis. However, rare EBV‐negative PEL cases occurring in HIV‐seronegative patients have been reported, suggesting that HHV‐8 may be pathogenetic by itself. To investigate whether HHV‐8 may contribute to PEL development in the absence of EBV, the expression of seven potentially oncogenic HHV‐8 open reading frames (ORFs) (ORF72/viral cyclin D, ORF16/viral bcl ‐2, ORF74/viral G‐protein coupled receptor, ORFK2/viral IL‐6, ORFK13/viral FLICE inhibitory protein, ORFK9/viral interferon regulatory factor, and ORFK1, equivalent to the gene encoding herpesvirus saimiri transforming protein) was assessed by reverse transcriptase‐polymerase chain reaction (RT‐PCR) in an EBV‐negative PEL presenting in an HIV‐negative patient. RNA transcripts were demonstrated for the seven HHV‐8 genes, and this was confirmed by hybridization to specific oligonucleotide probes. The expression of potentially oncogenic HHV‐8 genes in this HIV‐, EBV‐negative PEL case suggests that HHV‐8 may induce malignant transformation of B‐lymphocytes through different molecular pathways in the absence of EBV infection. Copyright © 1999 John Wiley & Sons, Ltd.