Plasma proteome analysis in HTLV-1-associated myelopathy-tropical spastic paraparesisReport as inadecuate




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Retrovirology

, 8:81

First Online: 12 October 2011Received: 19 July 2011Accepted: 12 October 2011

Abstract

BackgroundHuman T lymphotropic virus Type 1 HTLV-1 causes a chronic inflammatory disease of the central nervous system known as HTLV-1-associated myelopathy-tropical spastic paraparesis HAM which resembles chronic spinal forms of multiple sclerosis MS. The pathogenesis of HAM remains uncertain. To aid in the differential diagnosis of HAM and to identify pathogenetic mechanisms, we analysed the plasma proteome in asymptomatic HTLV-1 carriers ACs, patients with HAM, uninfected controls, and patients with MS. We used surface-enhanced laser desorption-ionization SELDI mass spectrometry to analyse the plasma proteome in 68 HTLV-1-infected individuals in two non-overlapping sets, each comprising 17 patients with HAM and 17 ACs, 16 uninfected controls, and 11 patients with secondary progressive MS. Candidate biomarkers were identified by tandem Q-TOF mass spectrometry.

ResultsThe concentrations of three plasma proteins - high β2-microglobulin, high Calgranulin B, and low apolipoprotein A2 - were specifically associated with HAM, independently of proviral load. The plasma β2-microglobulin was positively correlated with disease severity.

ConclusionsThe results indicate that monocytes are activated by contact with activated endothelium in HAM. Using β2-microglobulin and Calgranulin B alone we derive a diagnostic algorithm that correctly classified the disease status presence or absence of HAM in 81% of HTLV-1-infected subjects in the cohort.

Electronic supplementary materialThe online version of this article doi:10.1186-1742-4690-8-81 contains supplementary material, which is available to authorized users.

Paul DW Kirk, Aviva Witkover contributed equally to this work.

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Author: Paul DW Kirk - Aviva Witkover - Alan Courtney - Alexandra M Lewin - Robin Wait - Michael PH Stumpf - Sylvia Richardson -

Source: https://link.springer.com/







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