Identification of genomic regions implicated in susceptibility to Schistosoma mansoni infection in a murine genetic model (backcross)

High levels of infection and severe liver fibrosis in schistosomiasis appear only in a few cases of infected people with high susceptibility. Tissue damage is caused by the inflammatory response to eggs trapped in the liver. The genetic background influences susceptibility to schistosome infection. To assess the genetic basis of susceptibility to schistosomiasis and identify the chromosomic regions involved, we used a backcross strategy to generate a mouse cohort with high variation in schistosomiasis susceptibility. Thus, we crossed the resistant C57BL/6 mouse strain with the susceptible CBA one; and later; the F1 females (C57 x CBA) were backcrossed with CBA males generating the F1BX cohort. The spectrum of phenotypes in the F1BX mice showed gradation from mild to severe disease, lacking a fully resistant group. We differentiated four levels of infection intensity using cluster and principal component analyses and K-means based on parasitological, pathological and immunological trait measurements. Mice were massively genotyped with 961 informative SNPs. We identify 19 new quantitative trait loci (QTL) associated with phenotype indicators of parasite burden, liver lesion, white blood cell populations, and antibody responses evaluated in the backcross cohort. Two QTLs on chromosomes 15 and 18 were simultaneously linked to the number of granulomas, grade of liver lesion and IgM levels. The human syntenic regions are located in chromosomes 8 and 18. None of the significant QTL identified coincided with previously reported mice association or were syntenic with human chromosomes. ### Competing Interest Statement The authors have declared no competing interest.