title: Genetic effects have a dominant role on poor responses to infant vaccination to hepatitis B virus.
abstract: The objective of this study was to investigate the overall contribution of genetic and environmental effects on poor response to hepatitis B virus (HBV) vaccination in Chinese infants. One-year-old healthy twins were recruited from child-care settings. Parental factors, neonates' condition at birth, postnatal infant feeding history and growth measurements during the 12 months were investigated by conducting an interview and checking the medical records. HBV-related markers were examined at 1 year of age. Heritability of surface antibody to HBV (anti-HBs) concentrations (ordinal variable) among twins was estimated using MX software. The role of perinatal environmental factors on poor vaccine response (anti-HBs<100 mIU ml(-1)) was analyzed using XTGEE (fit population-averaged panel-data models by using GEE) programs. Overall, 172 out of 225 recruited twin pairs were analyzed for heritability, including 82 pairs (47.67%) of monozygotic twins and 90 pairs of dizygotic twins, which consisted 43 pairs of (25.0%) opposite sex twins, 29 pairs of male twins and 18 pairs of female twins. Seventy-one (19.9%) of 370 twins showed poor responses to HBV vaccine. An additive genetic (0.91 of the variance)-random environmental (0.09 of the variance)-model best fit the variation of anti-HBs response. Risk factor analysis showed that with a smoking father and low birth weight, the infants were associated with an increased risk of poor response to HBV vaccination (odds ratio (OR)=4.50, 95% confidence interval (CI): 2.52-8.03 and OR=2.55, 95% CI: 1.33-4.87, respectively). Higher Apgar score and gaining more body weight in the first year of life reduced this risk. Genetic factors have a dominant role in determining infant HBV vaccination responses (91%) compared with perinatal environmental factors.
authors.affiliation: Department of Clinical Epidemiology, Children's Hospital of Fudan University, Shanghai, China.
authors.forename: Kai
authors.initials: K
authors.lastname: Yan
authors.forename: Wenping
authors.initials: W
authors.lastname: Cai
authors.forename: Fang
authors.initials: F
authors.lastname: Cao
authors.forename: He
authors.initials: H
authors.lastname: Sun
authors.forename: Shaoke
authors.initials: S
authors.lastname: Chen
authors.forename: Ruiwei
authors.initials: R
authors.lastname: Xu
authors.forename: Xin
authors.initials: X
authors.lastname: Wei
authors.forename: Xiaoxiang
authors.initials: X
authors.lastname: Shi
authors.forename: Weili
authors.initials: W
authors.lastname: Yan
mesh_terms: D004777:Environment; D005260:Female; D059647:Gene-Environment Interaction; D006509:Hepatitis B / Q000235:genetics* / Q000276:immunology / Q000517:prevention & control*; D006510:Hepatitis B Antibodies / Q000097:blood / Q000276:immunology; D017325:Hepatitis B Vaccines / Q000276:immunology*; D006515:Hepatitis B virus / Q000276:immunology*; D006801:Humans; D007223:Infant; D008297:Male; D012307:Risk Factors; D014429:Twins, Dizygotic; D014430:Twins, Monozygotic
chemical_list: D006510:Hepatitis B Antibodies; D017325:Hepatitis B Vaccines