Host genetic factors affecting hepatitis B infection outcomes: Insights from genome-wide association studies

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hepatitis B 71 Title: World Journal of GastroenterologyHost genetic factors affecting hepatitis B infection outcomes: Insights from genome-wide association studiesIzzet Mehmet AkcayDepartment of Molecular
hepatitis B 866 levent.doganay@saglik.gov.trPublication date (ppub): 8/2018Publication date (epub): 8/2018AbstractThe clinical outcome of hepatitis B virus (HBV) infection depends on the success or failure of the immune responses to HBV, and varies widely
hepatitis B 1423 HBV-related traits. In this review, we discuss GWAS for persistence of HBV infection, antibody response to hepatitis B vaccine, and HBV-related advanced liver diseases. HBV persistence is associated with multiple genes
hepatitis B 2599 proven to be very useful in uncovering the host genetic factors that influence the clinical outcomes of hepatitis B virus (HBV) infection. Both class I and class II human leukocyte antigen (HLA) genes were implicated
hepatitis B 5718 than in same-sex dizygotic twins for HBV carrier status[[12]] and for antibody titers in response to hepatitis B vaccine[[13],[14]]. The host genetic factors were investigated in association studies whereby the frequencies
hepatitis B 7608 conducted to identify the risk loci that predisposes to persistence of HBV infection, non-response to hepatitis B vaccine, and progression of liver disease in chronic HBV infections. In this review, we discuss the
hepatitis B 8097 performed in a Japanese population, and published in 2009[[22]]. Seven hundred and eighty-six chronic hepatitis B (CHB) cases and 2201 HBsAg seronegative controls were used in the discovery phase. This GWAS detected
hepatitis B 10562 validated in these populations, too.Table 1Results of genome-wide association studies for persistence of hepatitis B virus infectionRef.StudypopulationSNPIDMinor/major allelesRiskallelePORLocationNearestgeneFunctional
hepatitis B 12818 1Associations within the human leukocyte antigen locus identified by genome-wide association studies for hepatitis B virus-related traits. GWAS hits for HBV-related pathologies are concentrated on the HLA region. Top
hepatitis B 20561 epitope-specific therapeutic interventions.Table 2Human leukocyte antigen classical alleles associated with hepatitis B virus persistence in more than one studyHLA geneAssociated allelesEffect on HBV persistenceStudy populationRef.HLA-C*07:02ProtectiveChinese[24,28,29]HLA-DPA1*01:03ProtectiveJapanese,
hepatitis B 27402 LD relationships among them.GWAS FOR IMMUNE RESPONSE TO HEPATITIS B VACCINEThe standard 3 doses of hepatitis B vaccine (based on recombinant HBs antigen) have been implemented as part of the routine infantile vaccination
hepatitis B 27807 have been observed[[6],[72]]. However, there is a large natural variation in the antibody response to hepatitis B vaccine. Post-vaccination antibody titers range from undetectable levels to higher than 2000 mIU/mL[[73]].
hepatitis B 28418 implemented to date to identify the genetic factors that underlie the variation in the immune response to hepatitis B vaccine (Figure 1, Table 3). The first GWAS was conducted in Indonesians by grouping vaccine recipients
hepatitis B 29721 pinpoint the causal genes[[73]].Table 3Results of genome-wide association studies for non-response to hepatitis B vaccineRef.Study populationSNPIDMinor/major allelesRiskallelePORLocationNearest geneFunctional classPng
hepatitis B 30790 detected within the HLA-DR locus, and HLA-DRB1*07:01 was significantly associated with nonresponse to hepatitis B vaccination[[76]]. Numerous studies previously associated DRB1*07:01 with both vaccine non-response
hepatitis B 32526 with vaccine responsiveness[[84]]. Therefore, the genetic bases of HBV persistence and nonresponse to hepatitis B vaccine overlap considerably, but not completely.GWAS FOR HBV-RELATED ADVANCED LIVER DISEASESHost genetic
hepatitis B 33882 association, possibly due to small sample size.Table 4Results of genome-wide association studies for hepatitis B virus-related advanced liver diseasesRef.Study populationParticipant phenotypesSNPIDMinor/major allelesRisk
hepatitis B 42609 traits. These GWAS provided novel insights into the pathogenesis of HBV persistence and non-response to hepatitis B vaccine. For instance, the association of HLA-DPB1 with HBV persistence was unknown before GWAS. DPB1
hepatitis B 45268 Asia[[22],[113]]. However, most of these susceptible alleles are not frequent in Africa, too, even though chronic hepatitis B is as prevalent in Africa as in Asia. Given that the predominant mode of transmission and HBV genotypes

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