Mechanisms of HTLV-1 transformation

Front Biosci. 2004 Sep 1;9:2347-72. doi: 10.2741/1401.


HTLV-1 is the etiological agent of the fatal disease adult T-cell leukemia. The virus encodes many proteins including several accessory proteins, p12I, p13II, p27I, and p30II, whose roles have recently begun to be elucidated. These accessory proteins are important in T-cell activation, transcriptional regulation, viral persistence, and virus assembly. The viral oncogene Tax is thought to be largely responsible for tumorigenesis, although the precise mechanisms underlying transformation are not completely understood. Tax has a profound impact on transcription, cell growth regulation, genomic stability and apoptosis. This review will provide possible contributions of the accessory proteins to transformation as well as highlight the alterations of the above-mentioned cellular events by Tax. Animal models of both Tax and the accessory proteins are also included based on the essential information on the transformation process in vivo that they provide.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Apoptosis
  • Cell Cycle
  • Cell Proliferation
  • Cell Transformation, Neoplastic
  • Cell Transformation, Viral
  • DNA Repair
  • Disease Models, Animal
  • Gene Expression Regulation, Viral
  • Gene Products, tax / metabolism
  • Human T-lymphotropic virus 1 / metabolism*
  • Human T-lymphotropic virus 1 / physiology*
  • Humans
  • Leukemia, T-Cell / virology
  • Lymphocyte Activation
  • Mitosis
  • Oncogene Proteins, Viral
  • Transcription, Genetic
  • Viral Regulatory and Accessory Proteins / physiology*
  • Virus Replication


  • Gene Products, tax
  • Oncogene Proteins, Viral
  • Viral Regulatory and Accessory Proteins