Susceptibility of Children to Sapovirus Infections, Nicaragua, 2005–2006 - - Emerging Infectious Disease journal - CDC

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Susceptibility of Children to Sapovirus Infections, Nicaragua, 2005–2006 - - Emerging Infectious Disease journal - CDC



Table of Contents
Volume 18, Number 11–November 2012

Dispatch

Susceptibility of Children to Sapovirus Infections, Nicaragua, 2005–2006

Article Contents

• The Study
• Conclusions
• Acknowledgments
• References
• Figure 1
• Figure 2
• Table 1
• Table 2
• Suggested Citation

Filemón Bucardo¹, Beatrice Carlsson¹, Johan Nordgren, Göran Larson, Patricia Blandon, Samuel Vilchez, and Lennart Svensson 

Author affiliations: University of León, León, Nicaragua (F. Bucardo, P. Blandon, S. Vilchez); Linköping University, Linköping, Sweden (F. Bucardo, B. Carlsson, J. Nordgren, L. Svensson); and University of Gothenburg, Göteborg, Sweden (G. Larson)

Suggested citation for this article

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.

Human sapovirus (SaV), family Caliciviridae, is a causative agent of gastroenteritis in children and adults. Symptoms of SaV infection seem to be milder than symptoms of rotavirus and norovirus (NoV) infections; thus, SaV infection prevalence is higher in nonhospitalized children than in hospitalized children.
Some calciviruses bind to histo-blood group antigens (HBGA) expressed on cells in the gastrointestinal tract (1). Human NoV strains demonstrate strain-dependent binding patterns to HBGAs (1,2). ABO blood groups and Lewis phenotype also play a role in NoV infections, either as ligands or as restriction factors (2). Moreover, a non-sense mutation in the fucosyltransferase gene 2 (FUT2), which gives rise to the nonsecretor phenotype, has been found to provide almost complete protection from experimental and natural NoV infection (2,3).
Although human NoV susceptibility is highly associated with secretor status, and thus with mutations in 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.