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Oligoclonal proliferation of human T‐cell leukaemia virus type 1 bearing T cells in adult T‐cell leukaemia/lymphoma without deletion of the 3′ provirus integration sites
Author(s) -
Leclercq India,
Cavrois Marielle,
Mortreux Franck,
Hermine Olivier,
Gessain Antoine,
Morschhauser Franck,
Wattel Eric
Publication year - 1998
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1998.00743.x
Subject(s) - provirus , biology , virology , southern blot , clone (java method) , superinfection , monoclonal , lymphoma , virus , microbiology and biotechnology , dna , genetics , monoclonal antibody , immunology , antibody , genome , gene
We report a new case of an asymptomatic carrier with a deletion of a 3′ HTLV‐1 integration site. We further investigated whether these 3′ deletions of flanking sequences may explain the oligoclonal pattern of HTLV‐1 replication, evidenced by inverse PCR (IPCR) analysis of tumourous samples from patients with adult T‐cell leukaemia (ATLL). 48 HTLV‐1 3′ integration sites, derived from tumourous DNA of five ATLL patients were sequenced. One dominant flanking sequence was obtained in the four samples harbouring a unique band after Southern‐blotting. In one sample, which harboured two signals after Southern‐blotting, IPCR amplification of diluted tumourous DNA revealed that these two sequences corresponded to one clone harbouring two integrated proviruses rather than to two distinct cellular clones, a result consistent with superinfection of the tumourous sample. In addition to integration sites corresponding to malignant clones, two to six oligoclonal forms were sequenced in four samples. No flanking sequence homology was found between clones derived from each patient, indicating that integration sites deletion in the vicinity of the provirus is a rare event in ATLL. The oligoclonal pattern of HTLV‐1 replication in ATLL may result from clonal expansion of non‐malignant HTLV‐1‐bearing clones within the sample and partly from HTLV‐1 superinfection of monoclonal tumour cells.