Impact of SNPs interplay across the locus of MBL2, between MBL and Dectin-1 gene, on women’s risk of developing recurrent vulvovaginal infections

BACKGROUND: analysis and for the possible non-linear interaction analysis of two PRRs that may impact RVVI susceptibility. METHODS: blocks, (3) gene-gene interaction analyses between two PRRs, using multifactor dimensionality reduction. RESULTS: G, rs7084554C, rs36014597G, and rs11003123A were observed as the minor alleles in the representative North Indian cohort. RVVI cases and its types showed an appreciably high frequency of C allele, its homozygosity and heterozygosity, explaining the observed dominant mode of inheritance of rs7084554 polymorphism in contributing 1. 81 fold risk of RVVI. The rs36014597 polymorphism showed the overdominant mode of inheritance, which further depicts that the carrier of a heterozygous genotype of this polymorphism had more extreme phenotype than either of its homozygous carriers in developing 4. 07 fold risk of RVVI. sMBL levels significantly varied for rs11003124, rs36014597 and rs11003123 polymorphisms in bacterial vaginosis, while for rs7084554 polymorphism in mixed infection. Independent analysis of 5' and 3' haplotype blocks suggested the risk-modifying effect of all the 5' additional variants, Y/X secretor polymorphism and 3'-UTR SNP i. e. rs10824792. Combined 5'/3' haplotype analyses depicted the importance of rs36014597; an additional 5' variant, Y/X and rs10824792 polymorphisms from both the blocks in regulating sMBL levels and RVVI risk. Three gene-gene interaction models involving uni-variant, bi-variant and tri-variant appeared as significant predictors of RVVI risk with cross-validation consistency of 10/10, 9/10 and 5/10, respectively. CONCLUSIONS: in association with RVVI risk. The preliminary data will establish the foundation for the investigation of within gene and between genes interaction analyses towards RVVI susceptibility.