1. ¹McGill Centre for the Study of Host Resistance, and Departments of Human Genetics, Medicine and Biochemistry, McGill University, Montreal, PQ, Canada
2. ²INSERM U550, Human Genetics of Infectious Disease, Necker Medical School, University Paris 5, Paris, France
3. ³Hospital for Dermato-Venereology, Ho Chi Minh City, Vietnam

Correspondence: E Schurr, McGill Centre for the Study of Host Resistance, Montreal General Hospital Research Institute, L11-521, 1650 Cedar Avenue, MONTREAL, PQ, Canada H3G 1A4. E-mail: erwin@igloo.epi.mcgill.ca

Abstract

Each year an estimated 600 000 new leprosy cases are diagnosed worldwide. The spectrum of the disease varies widely from limited tuberculoid forms to extensive lepromatous forms. A measure of the risk to develop lepromatous forms of leprosy is provided by the extent of skin reactivity to lepromin (Mitsuda reaction). To address a postulated oligogenic control of leprosy pathogenesis, we investigated in the present study linkage of leprosy susceptibility, leprosy clinical subtypes, and extent of the Mitsuda reaction to six chromosomal regions carrying known or suspected leprosy susceptibility loci. The only significant result obtained was linkage of leprosy clinical subtype to the HLA/TNF region on human chromosome 6p21 (P_corrected=0.00126). In addition, we established that within the same family different HLA/TNF haplotypes segregate into patients with different leprosy subtypes directly demonstrating the importance of this genome region for the control of clinical leprosy presentation.