Inflammatory polyarthropathy and bone remodeling in HTLV-I Tax-transgenic mice

J Acquir Immune Defic Syndr Hum Retrovirol. 1997 Mar 1;14(3):272-80. doi: 10.1097/00042560-199703010-00012.


Transgenic mice carrying the tax gene of human T-cell lymphotropic virus type I displayed a high prevalence of arthropathy. The percentage of affected animals increased with age, reaching a peak of 43% at 20 months. Southern analysis of deoxyribonucleic acid (DNA) from tissue samples indicated that disease development was related to tax copy number. Histopathologic evaluation of the ankle joints disclosed deep erosion of the synovial lining, fibrous tissue proliferation together with angiogenesis, mononuclear cell infiltration, and activation of osteoclasts. Radiologic examination confirmed joint involvement and revealed bone architecture modifications. The phenotype exhibited by the affected animals closely resembles that of seronegative arthritis in humans, and may indicate tax protein as a causal agent of arthropathy observed in HTLV-I infected individuals.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Age Factors
  • Amino Acid Sequence
  • Animals
  • Ankle / pathology
  • Arthritis / diagnostic imaging
  • Arthritis / etiology*
  • Base Sequence
  • Bone Remodeling*
  • Gene Dosage
  • Gene Products, tax / biosynthesis*
  • Hindlimb / pathology
  • Human T-lymphotropic virus 1 / genetics*
  • Mice
  • Mice, Transgenic
  • Radiography
  • Synovial Membrane / pathology
  • Tail / pathology


  • Gene Products, tax