Premium
Simian‐virus‐40 footprints in human lymphoproliferative disorders of HIV − and HIV + patients
Author(s) -
Martini Fernanda,
Dolcetti Riccardo,
Gloghini Annunziata,
Iaccheri Laura,
Carbone Antonino,
Boiocchi Mauro,
Tog Mauro
Publication year - 1998
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19981209)78:6<669::aid-ijc1>3.0.co;2-b
Subject(s) - virology , virus , lymphoma , biology , lymphoproliferative disorders , context (archaeology) , polymerase chain reaction , in situ hybridization , viral disease , immunology , gene , gene expression , genetics , paleontology
SV40 sequences were investigated by PCR DNA amplification followed by filter hybridization in a series of human lymphoproliferative disorders obtained from human‐immunodeficiency‐virus (HIV)‐seronegative and HIV‐infected patients. Our PCR and filter‐hybridization conditions enabled us to detect SV40 sequences in the range of 10 −4 to 10 −2 genome equivalents per cell. In non‐Hodgkin's lymphomas (NHL) from HIV − patients, SV40 footprints were found in 11 out of 79 (13.9%) samples, while in NHL from HIV + patients SV40 DNA sequences were detected in 2/16 (12.5%). In Hodgkin's disease (HD), SV40 sequences were found in 7/43 (16.3%) and 1/12 (8.3%) in HIV − and HIV + patients respectively. A slightly higher prevalence of SV40 footprints was observed in reactive lympho‐adenopathies both in HIV − (3/9, 33.3%) and in HIV + (6/17, 35.3%) patients. Sequence analysis of 2 NHL and 2 HD DNA samples established that the amplified PCR products belong to the SV40 sequences. SV40 prevalence and load were similar in samples from HIV‐seronegative and HIV‐infected individuals, suggesting that SV40 probably does not undergo strong reactivation phenomena in the context of HIV‐related immunosuppression. Moreover, the large T‐antigen(Tag) expression was detected by immunohistochemistry in 5/18 SV40‐DNA‐positive samples analyzed; however, few tumor cells (<1%) in 3/5 samples displayed positivity for SV40 Tag, while this viral oncoprotein was revealed in several reactive histiocytes present in all 5 SV40‐positive tissues. These results suggest that the lymphoid tissue could represent a reservoir for SV40 and may constitute the first step in understanding whether this DNA tumor polyomavirus has a role in the pathogenesis of human lymphoproliferative disorders. Int. J. Cancer 78:669–674, 1998. © 1998 Wiley‐Liss, Inc.