Document 0292
 DOCN  M95B0292
 TI    Serologic and molecular evidence for a possible pathogenetic role of
       viral infection in CD3-negative natural killer-type lymphoproliferative
       disease of granular lymphocytes.
 DT    9511
 AU    Zambello R; Loughran TP Jr; Trentin L; Pontisso P; Battistella L;
       Raimondi R; Facco M; Sancetta R; Agostini C; Pizzolo G; et al;
       Department of Clinical Medicine, Padua University School of; Medicine,
       Italy.
 SO    Leukemia. 1995 Jul;9(7):1207-11. Unique Identifier : AIDSLINE
       MED/95356572
 AB    We studied a series of 18 patients with CD3- lymphoproliferative disease
       of granular lymphocytes (LDGL) for evidence of chronic viral infection,
       including Epstein-Barr (EBV), hepatitis B (HBV), hepatitis C (HCV),
       human T lymphotropic virus (HTLV), and human immunodeficiency virus
       (HIV). Although all patients tested had serologic evidence for past
       infection with EBV, polymerase chain reaction (PCR) analysis of
       peripheral blood mononuclear cell (PBMC) DNA utilizing specific EBV
       primers demonstrated the presence of EBV-DNA in only six of 17 CD3- LDGL
       cases. A previous history of HBV infection, as defined by the presence
       of circulating IgG anti-HBc antibodies associated with either HBsAg
       positivity or negativity, was documented in seven cases; however, viral
       DNA was not detected in PBMC of these patients using PCR with specific
       HBV primers. Specific anti-HCV antibodies, confirmed by recombinant
       immunoblot assay, were detected in five CD3- LDGL patients; PCR analysis
       demonstrated the presence of viral RNA in PBMC of two of these cases. No
       patient had antibodies to HTLV-I/II or HIV-1/2. Five patients were
       infected by more than one virus (two with HBV and EBV and three with HBV
       and HCV). Our results provide serologic evidence for past viral
       infection in the large majority of CD3- NK-type LDGL patients. These
       data suggest that viral infection may have played a role early in
       disease pathogenesis and may no longer be necessary in sustaining GL
       proliferation in CD3- NK-type LDGL.
 DE    Antigens, CD3/IMMUNOLOGY  Antigens, Viral/BLOOD  Base Sequence  DNA,
       Viral/BLOOD  Hepatitis B/COMPLICATIONS  Hepatitis C/COMPLICATIONS
       Herpesviridae Infections/COMPLICATIONS  Herpesvirus 4,
       Human/GENETICS/IMMUNOLOGY  Human  HIV Infections/COMPLICATIONS  HTLV-BLV
       Infections/COMPLICATIONS  Killer Cells, Natural/IMMUNOLOGY/*PATHOLOGY
       Lymphoproliferative Disorders/IMMUNOLOGY/PATHOLOGY/*VIROLOGY  Molecular
       Sequence Data  Polymerase Chain Reaction  RNA, Viral/BLOOD  Support,
       U.S. Gov't, P.H.S.  Tumor Virus Infections/COMPLICATIONS  Virus
       Diseases/*COMPLICATIONS/IMMUNOLOGY/VIROLOGY  JOURNAL ARTICLE

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