Rotavirus is a segmented double stranded ribonucleic acid virus with typical surface antigens, viral protein 7 and viral protein 4. Almost 5 million children all over world are reported to be infected with this virus. In vitro studies have shown binding of rhesus rotavirus surface protein with 'Sia' groups of a histo blood group antigens (HBGAs). In case of humans, rotavirus type A is more prevalent. The precise genomic diversity of ABO (H) and Lewis Blood Group System in various ethnic populations may provide plausible explanation for prevalence of specific P genotypes. Present study aims to identify role of Single Nucleotide Polymorphisms in the host FUT-2 gene in the host susceptibility to risk of rotavirus infection of P genotypes.The study indicates that null allele at certain loci of fucosyltransferase-2 (FUT2) gene, also known as secretor (Se) gene leads to lack of functionally active enzyme. This results in absence of α-1/2 fucosylated glycan and may protect the child against rotavirus infection of specific strain. FUT2 gene alleles at loci 428 (AA) and 302 (TT) are found to be associated with group A rotaviruses. Both these alleles were frequent in population under study. Presence of any of these allele in children of Indian origin leads to non-secretor phenotype and hence if exposed to P[4] and P[8] genotypes of rotavirus, can resist the infection.

Recent report of WHO shows 113000 children in India succumb to death due to Rotavirus diarrhea. Lack of knowledge about pathogenesis of virus has led to lack of therapy for severely infected patients. Previous studies have found that, animal rotavirus requires sialyl glycan moieties on cell surface for pathogenesis. Present study states that human rotaviruses also follows same path and this specificity of virus leads to host genetic predisposition for the infection as well as the disease. Two hundred children less than 5 years of age clinically suspected of viral diarrhea were screened for rotavirus infection. EDTA blood was processed for analyzing DNA sequences of various fucosyltransferase genes. Lewis antigens which are secretory form of ABO Histo Blood Group Antigens were correlated with the genotype of patient. Genetics of HBGA secretion, particularly, basis of Le b expression manifested by fucosyltransferase-2 enzyme was studied in healthy individuals and was compared in cases of rotavirus positive and negative diarrhea. Positive clinical isolates with various genotypes were purified from stool samples and gene for VP4surface spike protein was sequenced. Using Bioinformatics interphase, three dimensional protein structures were modeled and their functional domains were analyzed. All these modeled proteins were docked with Le b HBGA (Lewis-b Histo Blood Group Antigens) using molecular docking software. In present study, to investigate possible association of the rotavirus with host genome, we screened highly suspected genes involved in expression of glycoproteins on enterocytes. This study performed for prevalent Indian strains of rotaviruses provides possible evidence that, VP8 domain of VP4 spike protein utilizes Le b surface antigen for attachment and entry to enterocytes in the intestine. The FUT2 and FUT3 gene has been found to show significant association with the rotavirus infection hence can serve as a biomarker for genetic predisposition to Rotavirus diarrhea. Knowledge of molecular biology of the Rotavirus pathogenesis may open up new paths for vaccines and therapy. Data presented here is first of its kind which deciphers Host-Rotavirus interaction by parallel experiments of epidemiological study and In Silico study.