title: Genetic susceptibility to symptomatic norovirus infection in Nicaragua.
abstract: Host genetic resistance to Norovirus (NoV) has been observed in challenge and outbreak studies in populations from Europe, Asia, and USA. In this study, we have investigated if histo-blood group antigens can predict susceptibility to diarrhea caused by NoV in Nicaragua, Central America, and if this can be reflected in antibody-prevalence and titer to NoV among individuals with different histo-blood group antigen phenotypes. Investigation of 28 individuals infected with NoV and 131 population controls revealed 6% of non-secretors in the population and nil non-secretors among patients infected with NoV, suggesting that non-secretors may be protected against NoV disease in Nicaragua. Surprisingly, 25% of the population was Lewis negative (Le(a-b-)). NoV infections with genogroup I (GI) and GII occurred irrespective of Lewis genotype, but none of the Lewis a positive (Le(a + b-)) were infected. The globally dominating GII.4 virus infected individuals of all blood groups except AB (n = 5), while the GI viruses (n = 4) infected only blood type O individuals. Furthermore, O blood types were susceptible to infections with GI.4, GII.4, GII.7, GII.17, and GII.18-Nica viruses, suggesting that secretors with blood type O are susceptible (OR = 1.52) and non-secretors resistant. The overall antibody-prevalence to NoV GII.3 VLP was 62% with the highest prevalence among blood type B carriers (70%) followed by A (68%) and O (62%). All four investigated individuals carrying blood type AB were antibody-negative. Among secretors, 63% were antibody-positive compared to 33% among non-secretors (P = 0.151). This study extends previous knowledge about the histo-blood group antigens role in NoV disease in a population with different genetic background than North American and European.
authors.affiliation: Department of Microbiology, University of León, Nicaragua (UNAN-León).
authors.forename: Filemon
authors.initials: F
authors.lastname: Bucardo
authors.forename: Elin
authors.initials: E
authors.lastname: Kindberg
authors.forename: Margarita
authors.initials: M
authors.lastname: Paniagua
authors.forename: Ammi
authors.initials: A
authors.lastname: Grahn
authors.forename: Göran
authors.initials: G
authors.lastname: Larson
authors.forename: Malin
authors.initials: M
authors.lastname: Vildevall
authors.forename: Lennart
authors.initials: L
authors.lastname: Svensson
mesh_terms: D000017:ABO Blood-Group System; D000293:Adolescent; D000328:Adult; D000914:Antibodies, Viral / Q000097:blood; D001789:Blood Group Antigens; D017250:Caliciviridae Infections / Q000453:epidemiology / Q000235:genetics* / Q000503:physiopathology / Q000821:virology; D002648:Child; D002675:Child, Preschool; D018389:Codon, Nonsense; D005647:Fucosyltransferases / Q000235:genetics; D005759:Gastroenteritis / Q000453:epidemiology / Q000235:genetics* / Q000503:physiopathology / Q000821:virology; D020022:Genetic Predisposition to Disease; D006801:Humans; D007223:Infant; D007983:Lewis Blood Group Antigens; D008875:Middle Aged; D009527:Nicaragua / Q000453:epidemiology; D029322:Norovirus / Q000145:classification / Q000235:genetics / Q000276:immunology / Q000472:pathogenicity*; D015995:Prevalence; D055815:Young Adult; D000097631:Galactoside 2-alpha-L-fucosyltransferase
chemical_list: D000017:ABO Blood-Group System; D000914:Antibodies, Viral; D001789:Blood Group Antigens; D018389:Codon, Nonsense; D005647:Fucosyltransferases; D007983:Lewis Blood Group Antigens; D000097631:Galactoside 2-alpha-L-fucosyltransferase