Volume 8 Supplement 1

15th International Conference on Human Retroviruses: HTLV and Related Viruses

Open Access

Three plasma biomarkers of HTLV-1-associated myelopathy/tropical spastic paraparesis

  • Paul Kirk1,
  • Aviva Witkover2,
  • Alan Courtney3,
  • Alexandra M Lewin4,
  • Robin Wait5,
  • Michael P Stumpf1,
  • Sylvia Richardson4,
  • Graham P Taylor6 and
  • Charles R Bangham2Email author
Retrovirology20118(Suppl 1):A43


Published: 6 June 2011

The pathogenesis of HAM remains uncertain: the disease is thought to be caused by the immune response to HTLV-1, possibly by bystander damage to neurons in the spinal cord. The strongest correlate of HAM in HTLV-1-infected individuals is the proviral load of HTLV-1, i.e. the percentage of peripheral blood mononuclear cells that carry the provirus. To aid in the differential diagnosis of HAM, and to search for clues as to the pathogenetic mechanisms of the disease, we carried out SELDI mass spectrometry on plasma samples from 68 HTLV-1-positive individuals, 16 uninfected controls and 11 patients with secondary progressive MS. We identified three plasma protein biomarkers that are specifically associated with HAM, independently of proviral load. The three proteins were identified by tandem mass spectrometry as b2-microglobulin, calgranulin B, and apolipoprotein A2. Using the two most strongly associated biomarkers, b2-microglobulin and calgranulin B, we derive a simple algorithm that correctly classified the disease status (presence or absence of HAM) in 81% of HTLV-1-infected subjects in the cohort.

Authors’ Affiliations

Centre for Bioinformatics, Division of Molecular Biosciences, Imperial College
Department of Immunology, Wright-Fleming Institute, Imperial College
Department of Clinical Biochemistry, Imperial Academic Health Sciences Centre, St Mary’s Hospital
Department of Epidemiology and Biostatistics, Imperial College
Kennedy Institute of Rheumatology, Imperial College London
Department of Genitourinary Medicine and Communicable Diseases, Wright-Fleming Institute, Imperial College


© Kirk et al; licensee BioMed Central Ltd. 2011

This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.