The Combined Effect of Infant and Mother Secretor Status on Infant Susceptibility to Viral Gastroenteritis and Celiac Disease

Celiac disease is a prevalent autoimmune disorder with a rising incidence of 7.5% annually during the second half of the 20th century and the 21st century. Not all genetically susceptible individuals that carry the risk alleles HLA DQ2 and DQ8 go on to develop celiac disease, suggesting that there may be other environmental triggers that contribute to the development of celiac disease in genetically susceptible individuals. Gastroenteritis during infancy has been shown to be associated with increased risk of celiac disease. Secretor status, per the FUT2 genotype, and subsequent alterations in the microbiota, is associated with risk of gastroenteritis in infants. This review investigates the literature from January 2010 to June 2022 to determine the combined effect of secretor status and viral gastroenteritis on the development of celiac disease. Mothers with the secretor phenotype and infants with the non-secretor phenotype provided the most protection against particular strains of gastroenteritis and celiac disease. Both the maternal and infant secretor status, as well as the infant’s Lewis status and ABO blood group can influence the infant’s susceptibility to different viral strains, which cause gastroenteritis. Gastroenteritis caused by viral infections can damage intestinal epithelial cells, cause dysbiosis, and affect pro-inflammatory cytokines, which exacerbate celiac disease onset. Understanding the effect of secretor status and gastroenteritis on celiac disease may provide a novel approach to early screening and preventative strategies to reduce risk factors that contribute to the onset of celiac disease.