Key result
FUT2 null homozygote (nonsecretor) status was absent in all 51 patients infected by P[8] rotavirus strains, compared to 20% in the control population, indicating resistance to symptomatic infection.
Why the study?
Does FUT2 null homozygote status prevent symptomatic infection by P[8] rotavirus strains?
Case-Control (n=51)
Does FUT2 null homozygote status prevent symptomatic infection by P[8] rotavirus strains?
Absolute Event Rate: 0% vs 20%
The lack of α1,2fucosylated carbohydrate motifs in the gut surface mucosa (FUT2 nonsecretor status) is associated with resistance to symptomatic infection by P[8] rotavirus strains.
FUT2 nonsecretor status may confer P[8] rotavirus resistance; hypothesis-generating and should not yet change practice.
Attachment to carbohydrates of the histo-blood group type of several human Rotavirus strains (RVA) has recently been described. Synthesis of these ligands requires a functional FUT2 enzyme, suggesting that FUT2 null homozygote (ie, nonsecretor) individuals may not be recognized by most human RVA strains. Whereas such individuals represent 20% of the control population, this retrospective study determined that none of 51 patients infected by P[8] rotavirus strains were nonsecretors. The lack of α1,2fucosylated carbohydrate motifs in the gut surface mucosa is thus associated with resistance to symptomatic infection and virus attachment to such motifs is essential to the infection process.
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Imbert‐Marcille et al. (2013) conducted a case-control in Rotavirus A P[8] genotype infection (n=51). FUT2 null homozygote (nonsecretor) status vs. Control population was evaluated on FUT2 null homozygote (nonsecretor) status. FUT2 null homozygote (nonsecretor) status was absent in all 51 patients infected by P[8] rotavirus strains, compared to 20% in the control population, indicating resistance to symptomatic infection.
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