Iriterferon-β1a therapy in human T-lymphotropic virus type I-associated neurologic disease

Unsong Oh, Yoshihisa Yamano, Carlos A. Mora, Joan Ohayon, Francesca Bagnato, John A. Butman, James Dambrosia, Thomas P. Leist, Henry McFarland, Steven Jacobson

Research output: Contribution to journalArticlepeer-review

Abstract

Human T-lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is an immune-mediated inflammatory disorder of the central nervous system. Immune activation in the host, which results from high levels of persistent antigenic stimulation and from transactivation of host immunoregulatory genes by HTLV-I, appears important in the pathogenesis of HAM/TSP. In a single-center, open-label trial, 12 patients with HAM/TSP were treated with doses of interferon-β1a of up to 60μg twice weekly, based on its antiviral and immunomodulatory effects. Primary end points were immunological and virological measures that are potential biomarkers for HAM/TSP. Interferon-β1a therapy reduced the HTLV-I tax messenger RNA load and the frequency of potentially pathogenic HTLV-I-specific CD8+ cells. The HTLV-I proviral DNA load remained unchanged. Spontaneous lymphoproliferation, a marker of T-cell activation in HAM/TSP, also was reduced. Some measures of motor function were improved, and no significant clinical progression occurred during therapy. These results indicate that interferon-β1a may beneficially affect the immune mechanisms central to the pathogenesis of HAM/TSP.

Original languageEnglish (US)
Pages (from-to)526-534
Number of pages9
JournalAnnals of Neurology
Volume57
Issue number4
DOIs
StatePublished - Apr 2005
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)

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