Long-term effects of HTLV-1 on brain astrocytes: sustained expression of Tax-1 associated with synthesis of inflammatory mediators

HTLV-1 is the causative agent of a chronic neurological disease, TSP/HAM, The persistently activated CTL response to the viral protein Tax-1 suggests the existence of persistent viral replication with continuous expression of Tax-1. Although CD4+ T-cell is the main target for HTLV-1, previous observations have indicated that the astrocyte, the major neural cell in close contact with blood vessel and thus with HTLV-l-infected T-cells infiltrating the CNS, may also be infected. We tested in vitro the hypothesis of persistent/restricted infection in human and rat astrocytes after transient contact with an infectious T-cell line (C91PL). Long-term analysis showed prolonged expression of Tax-1 in astrocytes, associated with secretion of inflammatory mediators (TNF alpha, IL1 alpha, MMP-2, and MMP-9). These data suggest a possible contribution of Tax-1-expressing astrocytes to TSP/HAM pathogenesis.