HTLV-I SEQUENCE IN LYMPHOPROLIFERATIVE DISORDERS

Several recent studies reported the detection of partially deleted HTL V-I provirus in biopsies of lesions from patients with mycosis fungoid es (MF) and T-cell anaplastic large-cell lymphoma. We studied lesions from 59 patients (21 B-cell lymphomas: 16 diffuse and five follicular; 11 cutaneous T-cell lymphomas, including seven MF; one T-immunoblasti c lymphoma; 10 diffuse anaplastic large-cell lymphomas: two B, four T, and four of indeterminate phenotype; three Hodgkin's lymphomas; eight atypical lymphoid proliferations; four other lymphoid lesions, and on e squamous-cell carcinoma) using primers to the gag, pol and pX region s of HTLV-I in the polymerase chain reaction (PCR) to detect relevant sequences. A total of 10 patients showed one or more PCR-amplifiable p roducts, including five of 11 patients with cutaneous T-cell lymphomas (45%) as compared with one of 21 patients with B-cell lymphomas (4.3% ). We did not find a high incidence of positivity in anaplastic large- cell lymphomas, as reported previously. Detectable HTLV-I sequences we re not limited to any subtype of lymphoma, and a pX sequence was detec ted in a squamous-cell carcinoma. Sequence analysis of one amplified p roduct from each of the three regions studied showed a 94.2, 100, and 98.9% homology to the corresponding prototypical gag, pol, and pX HTLV -I sequences, respectively, indicating that the amplified sequences we re derived from HTLV-I or a very closely related virus. HTLV-I sequenc es were detected in a significant proportion of patients with cutaneou s T-cell lymphoma, but their rote in the pathogenesis of the neoplasm is still unclear.