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Here we present the dataset used in our study entitled "Identification of genomic regions implicated in susceptibility to Schistosoma mansoni infection in a murine genetic model (backcross)". Thus, we crossed the C57BL/6 mouse strain with the CBA one and then the F1B6CBA females (C57 x CBA) were backcrossed with CBA males generating the F1BX cohort of the study. The study consists of the identification of genetic markers of schistosomiasis. High infection levels and severe liver fibrosis in schistosomiasis appear only in a few highly susceptible infected people. Schistosomiasis could be a complex trait disease and it could be possible to identify genetic markers associated with severity. This study uses a genetically heterogeneous back-cross cohort with genetically unique mice. A backcross (F1BX) mouse cohort was generated after two stages; firstly, we crossed a mouse strain (CBA/2J) susceptible to schistosomiasis with a resistant one (C57BL/6J) to generate the F1B6CBA mice; secondly, the F1BX mice were generated by backcrossing. F1B6CBA female mice with CBA/2J males. F1BX mice were infected with 150 ± 5 S. mansoni cercariae each mouse and nine weeks post-infection were euthanized. We considered 20 variables: granulomas; affected liver surface (mm2/cm2); the number of adult male and female worms; eggs per gram of liver and small intestine; eggs in liver and small intestine per female; CD4, CD8, CD45, CD220 in blood or spleen; IgG, IgG1, IgG2a, IgM antibodies. Multivariate models (cluster and principal component analyses and K-means) identified four levels of infection intensity in the cohort. The genetic regions associated with severity were assessed by massive genotyping and genetic linkage analysis using 961 informative SNPs.

Only a small number of infected people are highly susceptible to schistosomiasis, showing high levels of infection or severe liver fibrosis. The susceptibility to schistosome infection is influenced by genetic background. To assess the genetic basis of susceptibility and identify the chromosomal regions involved, a backcross strategy was employed to generate high variation in schistosomiasis susceptibility. This strategy involved crossing the resistant C57BL/6J mouse strain with the susceptible CBA/2J strain. The resulting F1 females (C57BL/6J × CBA/2J) were then backcrossed with CBA/2J males to generate the backcross (BX) cohort. The BX mice exhibited a range of phenotypes, with disease severity varying from mild to severe disease, lacking a fully resistant group. We observed four levels of infection intensity using cluster and principal component analyses and K-means based on parasitological, pathological, and immunological trait measurements. The mice were genotyped with 961 informative SNPs, leading to the identification of 19 new quantitative trait loci (QTL) associated with parasite burden, liver lesions, white blood cell populations, and antibody responses. Two QTLs located on chromosomes 15 and 18 were linked to the number of granulomas, liver lesions, and IgM levels. The corresponding syntenic human regions are located in chromosomes 8 and 18. None of the significant QTLs had been reported previously.