Presence of serum anti-human T-lymphotropic virus type I (HTLV-I) IgM antibodies means persistent active replication of HTLV-I in HTLV-I-associated myelopathy.

We investigated serum IgM antibodies against human T-lymphotropic virus type I (HTLV-I) in 29 HTLV-I associated myelopathy (HAM) patients and 34 HTLV-I carriers, using western blot analysis. Anti-HTLV-I IgM was detected in all 6 post-transfusional HAM patients and in 19 of 23 (83%) HAM patients with no history of blood transfusion, but in only 4 of 21 (19%) HTLV-I carriers. In HAM patients, HTLV-I proviral DNA integrated into peripheral blood lymphocyte (PBL) was detected by Southern blot analysis in all of the 6 (100%) and 18 of the 23 (78%). In contrast, it was detected in only 2 of 25 (8%) HTLV-I carriers. For the serum anti-HTLV-I IgM and HTLV-I provirus in PBL, the differences between the HAM and HTLV-I carriers were statistically significant (P less than 0.01). Our data indicate that the increased HTLV-I proviral DNA in PBL is produced by the persistent active replication of HTLV-I in HAM. Furthermore, Southern blot analysis showed intense bands in HAM patients with histories of blood transfusion, in whom the progression of the disease had been rapid. We conclude that the persistent active replication of HTLV-I is an important factor in the pathogenesis of HAM.