How to cite this article: Vet. Res. (2008) 39:36
DOI: 10.1051/vetres:2008013

Slc11a1 (formerly Nramp1) and susceptibility to canine visceral leishmaniasis

Elisenda Sanchez-Robert¹, Laura Altet¹, Mireia Utzet-Sadurni², Urs Giger³, Armand Sanchez¹ and Olga Francino<sup>1

1</sup>  Veterinary Molecular Genetics Service, Department of Animal and Food Science, Veterinary Faculty, Universitat Autonoma de Barcelona, 08193 Bellaterra, Barcelona, Spain
²  Population Genomics Node, National Institute for Bioinformatics, Biomedical Research Park, 08003 Barcelona, Spain
³  Section of Medical Genetics, School of Veterinary Medicine, University of Pennsylvania, 3900 Spruce Street, Philadelphia, PA 19104-6010 USA

(Received 26 July 2007; accepted 18 February 2008; published online 29 February 2008)

Abstract - Visceral leishmaniasis is the most important zoonosis in Europe and it is caused by Leishmania infantum, a protozoan intracellular parasite. Canine visceral leishmaniasis (CVL) is endemic in the Mediterranean basin, Middle East, and South America, and is emerging within non endemic areas such as the United Kingdom and North America. We have analyzed 24 polymorphisms in the canine Slc11a1 (formerly NRAMP1) gene: 19 new polymorphisms characterized by direct sequencing from 40 dogs of different breeds and five polymorphisms previously described. Data analysis in a case-control study including 164 dogs of 19 different breeds revealed that two of the 24 polymorphisms were associated with increased risk for CVL: one intronic single nucleotide polymorphism (SNP) (A4549G in intron 6: odds ratio (OR) = 6.78, P = 0.001) and one silent SNP in exon 8 (C4859T: OR = 13.44, P = 0.004). In silico analysis of the significant SNP revealed that SNP in the promoter region affect putative transcription binding sites and SNP C4859T in exon 8 disrupts a putative exonic splicing enhancer (ESE). These results corroborate that Slc11a1 polymorphisms are associated with increased risk for CVL.

Key words: leishmaniasis / Slc11a1 / polymorphism / dog / susceptibility

Corresponding author: elisenda.sanchez@uab.cat

© INRA, EDP Sciences 2008