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patients by ABO blood rotavirus group and Lewis antigen strain, status ([dagger]) patient FUT2 genotype O A B Le+ Le- Le+ Le- Le+ G9P[8] 4 0 1 0 2 Se/Se 0 0 1 0 1 Se/se 4 0 0 0 1 se/se 0 0 0 0 0 G3P[8] 1 0 4 0 2 Se/Se 0 0 2 0 1 Se/se 1 0 1 0 1 se/se 0 0 0 0 0 G1P[8] 4 0 3 0 0 Se/Se 0 0 0 0 0 Se/se 4 0 2 0 0 G4P[8] 1 0 1 0 0 Se/se 0 0 1 0 0 G2P[4] 2 0 0 0 0 Se/Se 1 0 0 0 0 P[8] 0 0 1 0 0 Se/Se 0 0 1 0 0 Total 12 0 10 0 4 Se/Se 1 0 4 0 2 Se/se 9 0 4 0 2 se/se 0 0 0 0 0 Isolated No.
Missense mutation of FUT1 and deletion of FUT2 are responsible for Indian Bombay phenotype of ABO blood group system.
Bombay blood group 211100 FUT1 or FUT2 Para-Bombay blood group 211100 FUT1 Non-secretor blood group 182100 FUT2 Lewis-negative blood group 111100 FUT3 CDG-IIc 266265 FUCT1 CDG-IId 607091 B4GALT1 CDG-IIe 608779 COG7 CMRD 246700 SARA2 Anderson disease 607689 SARA2 CMRD with Marinesco--Sjogren syndrome 607692 SARA2 A.
Previous studies determined that overexpression of FUT2 in natively nonexpressing or low-expressing cell types, or upon differentiation of Caco-2 cells that natively express FUT2, results in a dramatic increase in NV particle binding (5,19,32,37,38).
No nonsecretors who were carrying the G428A FUT2 mutation were infected with NoV (9,14).
Although NoV infections of secretors are well documented (18) and a few cases of infected nonsecretors have been reported (19,20), no virus has been identified in authentic outbreaks that is completely secretor or Lewis antigen independent, where homozygous carriers of the nonsense G428A mutation in FUT2 are at similar or higher risk for infection than are secretors.