{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T20:34:17Z","timestamp":1791146057739,"version":"4.1.0"},"reference-count":34,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2005,3,22]],"date-time":"2005-03-22T00:00:00Z","timestamp":1111449600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2005,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Human T\u2010lymphotropic virus type I (HTLV\u2010I)\u2013associated myelopathy\/tropical spastic paraparesis (HAM\/TSP) is an immune\u2010mediated 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\u2010I, appears important in the pathogenesis of HAM\/TSP. In a single\u2010center, open\u2010label trial, 12 patients with HAM\/TSP were treated with doses of interferon\u2010\u03b21a of up to 60\u03bcg 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\u2010\u03b21a therapy reduced the HTLV\u2010I <jats:italic>tax<\/jats:italic> messenger RNA load and the frequency of potentially pathogenic HTLV\u2010I\u2013specific CD8<jats:sup>+<\/jats:sup> cells. The HTLV\u2010I proviral DNA load remained unchanged. Spontaneous lymphoproliferation, a marker of T\u2010cell 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\u2010\u03b21a may beneficially affect the immune mechanisms central to the pathogenesis of HAM\/TSP. 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