Abstract
We describe the genetic diversity of sapovirus (SaV) in children in Nicaragua and investigate the role of host genetic factors and susceptibility to SaV infections. Our results indicate that neither ABO blood group, Lewis phenotype, nor secretor status affects susceptibility to SaV infection in Nicaragua.
Highlights
We describe the genetic diversity of sapovirus (SaV) in children in Nicaragua and investigate the role of host genetic factors and susceptibility to SaV infections
Human NoV susceptibility is highly associated with secretor status, and with mutations in fucosyltransferase gene 2 (FUT2) [4], no information is yet available on whether host genetic factors determine susceptibility to SaV
We describe here the genetic diversity of SaV in a Central American population of hospitalized and nonhospitalized children and investigate the role of host genetic factors and susceptibility to SaV infections
Summary
To investigate whether certain SaV genogroups (GI, GII, GIV, or GV) were associated with clinical severity, we examined 25 SaV-positive symptomatic and asymptomatic children. No association between genogroup and clinical status was observed; GI, GII, and GIV viruses infected symptomatic and asymptomatic children at similar rates (data not shown). To investigate whether HBGAs were associated with SaV susceptibility similar to NoV susceptibility [2,3,11], we examined 22 of 33 SaV-infected children who were either symptomatic (n = 18) or asymptomatic (n = 4) in relation to ABO. We did not find any significant association between ABO blood groups, Lewis phenotypes, or secretor genotype and susceptibility to SaV infection (Table 2). Only 1 report in the literature has explored binding properties of recombinant SaV GI/1 (Mc114) and GV/1 (NK24) to HBGAs and revealed that the recombinant SaV strains investigated showed no specific binding activity to HBGAs from or to synthetic carbohydrates [15]
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