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the REDS investigators*.
*See the Appendix for a complete list of REDS investigators.
From the University of California San Francisco (Drs. Murphy and Engstrom), San Francisco, CA; the Blood Bank of San Bernadino and Riverside Counties (Dr. Fridey), CA; the Oklahoma Blood Institute (Dr. Smith), Oklahoma City, OK; the Georgetown University School of Medicine (Dr. Sacher), Washington, DC; Westat Inc. (Dr. Miller, and R. Thomson and D. Hansma), Rockville, MD; the American Red Cross Chesapeake and Potomac Region (Dr. Gibble), Baltimore, MD; the American Red Cross Southeastern Michigan (Dr. Stevens), Detroit, MI; the Centers for Disease Control and Prevention (Drs. Kaplan and Khabbaz), Atlanta, GA; and the National Heart, Lung, and Blood Institute (Dr. Nemo), Bethesda, MD.
Supported by National Heart, Lung and Blood Institute research contracts N01-HB-97077, -97078, -97079, -97080, -97081, and -97082.
Received February 21, 1996. Accepted in final form July 8, 1996.
Address correspondence and reprint requests to Dr. Edward L. Murphy, Department of Laboratory Medicine, University of California San Francisco, Box 0884, San Francisco, CA 94143-0884.
Article abstract-Objective: HTLV-I-associated myelopathy (HAM) is a slowly progressive spastic paraparesis caused by infection with human T-lymphotropic virus type I (HTLV-I). The prevalence of HAM among those infected with HTLV-I is poorly defined, and the association of a similar myelopathy with HTLV-II infection has not been confirmed. Design: Cross-sectional examination of HTLV-I, HTLV-II, and control subjects from the baseline visit of a cohort study. Setting/subjects: Persons testing HTLV seropositive at the time of blood donation at five U.S. blood centers, their seropositive sex partners, and a matched control group of HTLV seronegative blood donors. Measurements: HTLV-I and HTLV-II were differentiated by serology and/or polymerase chain reaction. All subjects received systematic neurologic screening examinations. Results: A diagnosis of myelopathy was confirmed in four of 166 HTLV-I subjects (2.4%, 95% confidence interval 0.7%, 6.1%) and in one of 404 HTLV-II subjects (0.25%, 95% confidence interval 0.0%, 0.6%). None of the 798 controls had a similar myelopathy, although one had longstanding typical multiple sclerosis. Conclusions: Our data also suggest that HAM occurs more frequently among HTLV-I-infected subjects than reported by previous studies. The HTLV-II infected myelopathy patient identified in this cohort, together with three other case reports in the literature, implies a pathogenic role for this human retrovirus. The diagnosis of HTLV-associated myelopathy should be considered in cases of spastic paraparesis or neurogenic bladder when risk factors for HTLV-I or HTLV-II infection are present.
NEUROLOGY 1997;48: 315-320
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