摘要轮状病毒(rotavirus，RV)是当前全球婴幼儿严重腹泻的首要原因，已发现RV通过其结构蛋白VP8识别并结合人类组织血型抗原(histo-blood group antigens，HBGAs)，FUT2基因决定了HBGAs在上皮组织的表达及体液中的分泌。由于FUT2基因突变导致功能酶活性丧失的个体，称为非分泌者，不能在黏膜及体液表达和分泌HBGAs，研究发现非分泌者可抵抗RV引起的腹泻。微生物组成受宿主遗传调控，数百个基因位点参与调控人体肠道微生物组成，其中包括FUT2。无菌动物模型可降低RV感染率，提示肠道细菌与RV感染过程相关。这些研究揭示了分泌状态直接影响个体对RV的易感性，而其对肠道微生物组成的影响也会间接调节人体对RV的敏感性。该文综述了FUT2和肠道微生物组成与RV易感性的相关性，以期为RV感染个性化防治开辟新途径。

abstractsRotavirus(RV) is currently the leading cause of severe diarrhea in infants and young children worldwide, and RV has been found to recognize and bind to histo-blood group antigens(HBGAs) through its structural protein VP8, and the FUT2 gene determines the expression of HBGAs in epithelial tissues and secretion in body fluids.Individuals with loss of functional enzyme activity due to mutations in the FUT2 gene, called non-secretors, are unable to express and secrete HBGAs in the mucosa and body fluids, and non-secretors have been found to be resistant to diarrhea caused by RV.Studies have shown that microbial composition is genetically regulated by the host, and hundreds of genetic loci are involved in regulating the composition of human gut microbes, including FUT2.Sterile animal models reduce the rate of RV infection, suggesting that intestinal bacteria are associated with the process of RV infection.These studies reveal that secretory status directly influences individual susceptibility to RV, and its effect on gut microbial composition indirectly modulates human susceptibility to RV.This article reviews the correlation between FUT2 and gut microbial composition with RV susceptibility, with the aim of opening new avenues for personalized prevention and treatment of RV infection.