Abstract
Noroviruses are the most common etiological agent of acute gastroenteritis worldwide. Despite their high infectivity, a subpopulation of individuals is resistant to infection and disease. This susceptibility is norovirus genotype-dependent and is largely mediated by the presence or absence of human histo-blood group antigens (HBGAs) on gut epithelial surfaces. The synthesis of these HBGAs is mediated by fucosyl- and glycosyltransferases under the genetic control of the FUT2 (secretor), FUT3 (Lewis) and ABO(H) genes. The so-called non-secretors, having an inactivated FUT2 enzyme, do not express blood group antigens and are resistant to several norovirus genotypes, including the predominant GII.4. Significant genotypic and phenotypic diversity of HBGA expression exists between different human populations. Here, we review previous in vivo studies on genetic susceptibility to norovirus infection. These are discussed in relation to population susceptibility, vaccines, norovirus epidemiology and the impact on public health.
Highlights
Infectious diseases have influenced the evolution of the human genome, in part by selecting for host alleles that modify infection and pathogenesis
In spite of the high infectivity and rapid transmission of norovirus, a subpopulation of individuals does not develop symptomatic disease or become infected after exposure. Studies have shown this phenomenon to be largely dependent on human histo-blood group antigens (HBGAs), mainly the types controlled by the FUT2 (Secretor), FUT3 (Lewis), and ABO genes
The clinical outcome of norovirus infection is partly genotype-dependent, with studies demonstrating that the predominant GII.4 genotype causes more severe symptoms and is relatively less prevalent in asymptomatic controls compared to other genotypes [53,60,61,66]
Summary
Infectious diseases have influenced the evolution of the human genome, in part by selecting for host alleles that modify infection and pathogenesis. In spite of the high infectivity and rapid transmission of norovirus, a subpopulation of individuals does not develop symptomatic disease or become infected after exposure. Studies have shown this phenomenon to be largely dependent on human histo-blood group antigens (HBGAs), mainly the types controlled by the FUT2 (Secretor), FUT3 (Lewis), and ABO genes. We review previous in vivo studies on norovirus infections in relation to host genetic susceptibility. These are discussed in the light of population susceptibility, norovirus epidemiology and the impact on public health
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