Non-Secretor Status Due to FUT2 Stop Mutation Is Associated with Reduced Rotavirus Infections but Not with Other Enteric Pathogens in Rwandan Children

Enteric pathogens remain a health threat for children in low-income countries. A single nucleotide polymorphism (SNP) in the <i>FUT2</i> gene that precludes the expression of fucosyltransferase 2 has been reported to influence the susceptibility to rotavirus and norovirus infections. The aim of this study was to investigate the association between G428A at <i>rs601338</i> (stop codon variant) in the <i>FUT2</i> gene and a range of enteric pathogens in children under 5 years of age. Rectal swab samples from 668 children (median age 13.6 months, 51% males, 93% rotavirus vaccinated, 468 with diarrhea) from Rwanda were analyzed via PCR for pathogen detection and SNP genotyping. A <i>FUT2</i> stop codon ('non-secretor' status) was found in 19% of all children. Rotavirus was detected in 5.3% of non-secretors compared with in 13% of secretors (OR = 0.39, <i>p</i> = 0.019). Rotavirus P[8] was the predominant genotype and was found in 2.3% of non-secretors compared with 8.8% of secretors (<i>p</i> = 0.009). There was no association with any other pathogen, including noroviruses, of which 2 of 14 GII.4 infections were detected among non-secretors. Thus, the <i>FUT2</i> stop codon variant was associated with rotavirus but not with any other pathogen.