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Previous Volume 355:2752-2756 December 28, 2006 Number 26 Next

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SUMMARY

Humans have innate immunity against Trypanosoma brucei brucei that is known to involve apolipoprotein L-I (APOL1). Recently, a case of T. evansi infection in a human was identified in India. We investigated whether the APOL1 pathway was involved in this occurrence. The serum of the infected patient was found to have no trypanolytic activity, and the finding was linked to the lack of APOL1, which was due to frameshift mutations in both APOL1 alleles. Trypanolytic activity was restored by the addition of recombinant APOL1. The lack of APOL1 explained the patient's infection with T. evansi.

Source Information

From the Laboratory of Molecular Parasitology, Institut de Biologie et de Médecine Moléculaires, Université Libre de Bruxelles, Gosselies, Belgium (B.V., P.P., A.P., E.P.); the Institut de Recherche pour le Développement, Unité de Recherche 117 Trypanosomoses Africaines, Montpellier, France (P.T.); the Department of Medicine, Government Medical College, Nagpur, India (P.P.J.); the Directorate of Health Services, Mumbai, India (R.K.); and Communicable Diseases Control, Prevention and Eradication, World Health Organization, Geneva (J.G.J.).

Address reprint requests to Dr. Pays at the Laboratory of Molecular Parasitology, IBMM, Université Libre de Bruxelles, 12 rue des Professeurs Jeener et Brachet, B-6041 Gosselies, Belgium, or at epays{at}ulb.ac.be.

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