Journal
TRANSPLANTATION
Volume 75, Issue 1, Pages 102-104Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00007890-200301150-00019
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Background. Human T-cell lymphotropic virus type I (HTLV-I) causes a subacute myelopathy in less than 5% of chronic carriers. However, the risk of neurologlic disease appears to increase in persons infected through blood transfusion. Methods. We report three recipients of solid organ transplants who developed a subacute myelopathy within 2 years after becoming infected with HTLV-I from a single asymptomatic HTLV-I donor. Genetic studies were performed in LTR and tax sequences in proviral DNA, and HTLV-I proviral load was measured by real-time quantitative polymerase chain reaction. Results. HTLV-I sequences were obtained in two of these individuals, and they were almost identical and clustered within the Cosmopolitan A HTLV-I subtype, which indicates a common source. All typical changes in Tax amino acid sequence of the HTLV-I Cosmopolitan A were identified, plus two additional changes were noted. Although taxA has been associated with a greater risk of neurologic disease, both patients were positive for human leukocyte antigen-A*02, which is considered a protective factor. Conclusion. Rapid development of subacute myelopathy may occur in recipients of organ transplants from asymptomatic HTLV-I donors. A particular virulence of the virus strain, the large size of the virus inoculum, and the immunosuppressed condition after transplantation may have contributed to produce this unusual rapid development of HTLV-I associated myelopathy.
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