Human T cell leukemia virus type 1: the role of Tax in leukemogenesis

Arch Immunol Ther Exp (Warsz). 2005 Jul-Aug;53(4):283-96.

Abstract

Human T cell leukemia virus type 1 (HTLV-1) is a complex human retrovirus which is the causative agent of adult T cell leukemia (ATL). ATL occurs in about 4% of carriers and develops after a long latent period. Although the precise mechanism of HTLV-1 oncogenesis remains unclear, the pathogenesis has been linked to the pleiotropic activity of the viral transcriptional activator protein Tax. Tax has been shown to regulate viral and cellular gene expression and to functionally interfere with proteins involved in cell-cycle progression and DNA repair. This review will focus on the role of Tax in p53 inhibition.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Cycle
  • Cell Proliferation
  • Cyclic AMP Response Element-Binding Protein / metabolism
  • DNA Repair
  • Gene Expression Regulation*
  • Gene Expression Regulation, Neoplastic
  • Gene Expression Regulation, Viral*
  • Gene Products, tax / metabolism*
  • Genome
  • Human T-lymphotropic virus 1 / metabolism*
  • Humans
  • Leukemia / virology*
  • Models, Biological
  • NF-kappa B / metabolism
  • Protein Binding
  • Serum Response Factor / metabolism
  • Transcription, Genetic
  • Transcriptional Activation
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • Cyclic AMP Response Element-Binding Protein
  • Gene Products, tax
  • NF-kappa B
  • Serum Response Factor
  • Tumor Suppressor Protein p53