ACTIVATION OF BCL-2 EXPRESSION IN HUMAN ENDOTHELIAL CELLS CHRONICALLY EXPRESSING THE HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE I

摘要: Abstract Programmed cell death (PCD) characteristically involves chromatin condensation, membrane blebbing, and DNA oligonucleosomal fragmentation. These events, collectively referred to as apoptosis, represent an active suicide mechanism that eliminates cellular threats including potentially cancerous or virus-infected cells. Various types of programmed can be blocked by the proto-oncogene Bcl-2. Levels this protein are consistently low undetectable in human endothelial cells (EC), which important for immunoregulation through their interactions with circulating lymphocytes potential targets infection virus-bearing T-cells. Accumulating evidence suggests EC may infected vivo play role HTLV-I-associated neuromyelopathy. In present study, we report establishment characterization lines stably transfected HTLV-I-derived molecular clone. We observed constitutive expression HTLV-I genes coinciding activated Bcl-2 expression. Transient transfection viral transactivator Tax a reporter construct promoter-CAT did not result significant increase CAT activity that, EC, second might required activation. Further, Tax-induced apoptosis rat fibroblasts has been shown Thus, HTLV-I-mediated induction provide protection against viral-induced extend survival create reservoir gene