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The sodium taurocholate cotransporting polypeptide (NTCP) encoded by  SLC10A1  was recently demonstrated to be a functional receptor for hepatitis B virus (HBV). The role of  SLC10A1  polymorphisms, particularly the Ser267Phe variant (rs2296651) in exon 4, has been frequently investigated in regard to risk of persistent HBV infection. However, these investigations have generated conflicting results. To examine whether common genetic variation at the  SLC10A1  locus is associated with risk of persistent HBV infection, haplotype-tagging and imputed single nucleotide polymorphisms (SNPs) were assessed in two case-control sample sets, totally including 2,550 cases (persistently HBV infected subjects, PIs) and 2,124 controls (spontaneously recovered subjects, SRs) of Southern Chinese ancestry. To test whether rare or subpolymorphic  SLC10A1  variants are associated with disease risk, the gene’s exons in 244 cases were sequenced. Overall, we found neither SNPs nor haplotypes of  SLC10A1  showed significant association in the two sample sets. Furthermore, no significant associations of rare variants or copy number variation covering  SLC10A1  were observed. Finally, expression quantitative trait locus analyses revealed that SNPs potentially affecting  SLC10A1  expression also showed no significant associations. We conclude that genetic variation at the  SLC10A1  locus is not likely a major risk factor of persistent HBV infection among Southern Chinese.

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Comprehensive assessment showed no associations of variants at the SLC10A1 locus with susceptibility to persistent HBV infection among Southern Chinese