title: LGL leukemia and HTLV.
abstract: Samples were obtained from 53 large granular lymphocytic leukemia (LGLL) patients and 10,000 volunteer blood donors (VBD). Sera were screened in an HTLV-1 enzyme immunoassay (EIA) and further analyzed in peptide-specific Western blots (WB). DNAs were analyzed by HTLV-1, -2, -3, and -4-specific PCR. Forty four percent of LGLL patients vs. 0.12 % of VBD had anti-HTLV antibodies via EIA (p < 0.001). WB and PCR revealed that four LGLL patients (7.5%) vs. one VBD patient (0.01%) were infected with HTLV-2 (p < 0.001), suggesting an HTLV-2 etiology in a minority of cases. No LGLL patient was positive for HTLV-1, -3, or -4, whereas only one EIA-positive VBD was positive for HTLV-1 and none for HTLV-3 or -4. The HTLV EIA-positive, PCR-negative LGLL patients' sera reacted to epitopes within HTLV p24 gag and gp21 env. Other then the PTLV/BLV viruses, human endogenous retroviral element HERV K10 was the only sequence homologous to these two HTLV peptides, raising the possibility of cross-reactivity. Although three LGLL patients (5.7%) vs. none of 110 VBD patients tested positive for antibodies to the homologous HERV K10 peptide (p = 0.03), the significance of the anti-HTLV seroreactivity observed in many LGLL patients remains unclear. Interestingly, out of 36 HTLV-1-positive control subjects, 3 (8%) (p = 0.014) were positive for antibodies to HERV K10; all three had myelopathy. Out of 64 HTLV-2-positive control subjects 16 (25%) (p = <0.001) were positive for HERV K10 antibodies, and 4 (6%) of these had myelopathy. Out of 22 subjects with either HTLV-1 or -2 myelopathy, 7 (31.8%) were positive for HERV K10 antibodies, and out of 72 HTLV-infected subjects without myelopathy, 12 (16.7%) were positive for anti-HERV K10 antibodies (p = 0.11). The prevalence of anti-HERV K10 antibodies in these populations and the clinical implications thereof need to be pursued further.
authors.affiliation: Department of Medicine, State University of New York, Upstate Medical University, Syracuse, 13202, USA.
authors.forename: Anish
authors.initials: A
authors.lastname: Thomas
authors.forename: Raisa
authors.initials: R
authors.lastname: Perzova
authors.forename: Lynn
authors.initials: L
authors.lastname: Abbott
authors.forename: Patricia
authors.initials: P
authors.lastname: Benz
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Poiesz
authors.forename: Syamalima
authors.initials: S
authors.lastname: Dube
authors.forename: Thomas
authors.initials: T
authors.lastname: Loughran
authors.forename: Jorge
authors.initials: J
authors.lastname: Ferrer
authors.forename: William
authors.initials: W
authors.lastname: Sheremata
authors.forename: Jordan
authors.initials: J
authors.lastname: Glaser
authors.forename: Matilde
authors.initials: M
authors.lastname: Leon-Ponte
authors.forename: Bernard J
authors.initials: BJ
authors.lastname: Poiesz
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D000914:Antibodies, Viral / Q000097:blood; D015153:Blotting, Western / Q000379:methods; D003429:Cross Reactions; D020077:Endogenous Retroviruses / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D005260:Female; D015498:HIV-2 / Q000235:genetics / Q000276:immunology / Q000302:isolation & purification*; D015368:Human T-lymphotropic virus 1 / Q000235:genetics / Q000276:immunology / Q000302:isolation & purification*; D015367:Human T-lymphotropic virus 2 / Q000235:genetics / Q000276:immunology / Q000302:isolation & purification*; D056187:Human T-lymphotropic virus 3 / Q000235:genetics / Q000276:immunology / Q000302:isolation & purification*; D006801:Humans; D001909:Leukemia Virus, Bovine / Q000276:immunology; D054066:Leukemia, Large Granular Lymphocytic / Q000821:virology*; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction / Q000379:methods; D016036:Seroepidemiologic Studies; D055815:Young Adult
chemical_list: D000914:Antibodies, Viral