Responses to booster hepatitis B vaccination are significantly correlated with genotypes of human leukocyte antigen (HLA)-DPB1 in neonatally vaccinated adolescents.

Genome-wide association studies have identified single nucleotide polymorphisms (SNPs) near the human leukocyte antigen (HLA)-DP loci that were significantly correlated with outcomes of hepatitis B virus (HBV) infection. We performed a case-control study nested in a well-characterized cohort of booster recipients to assess whether genetic variants of HLA-DPB1 are also associated with response to hepatitis B (HB) vaccination. The cases and controls were 171 and 510 booster recipients whose post-booster titers of antibodies against HBV surface antigen (anti-HBs) were undetectable and detectable, respectively.

HLA and response to booster hepatitis B vaccination in anti-HBs-seronegative adolescents who had received primary infantile vaccination.

To explore contemporarily genetic and non-genetic determinants of long-term immunological memory to hepatitis B (HB) vaccination, we conducted a case-control study nested in an adolescent cohort of booster recipients who had received primary infantile HB vaccination but with residual anti-HBs titers <10 mIU/mL at 15-18 years of age. High-resolution phenotypes of human leukocyte antigen (HLA)-A, -B, and -DRB1 loci were determined by sequence-specific oligonucleotide probe hybridization. After controlling for pre-booster anti-HBs levels, the absences of HLA-A*02 and -DRB1*08, simply expressed as A*02(-) and -DRB1*08(-), and the presence of B*15 were significantly associated with elevated risks of non-response (post-booster anti-HBs titers<10 mIU/mL) to booster vaccination.

Risk of betel quid chewing on the development of liver cirrhosis: a community-based case-control study.

Purpose: The role of betel quid on the development of liver cirrhosis is unclear; we thus designed a community-based case-control study to evaluate the association between betel quid chewing and liver cirrhosis.

Methods: A total of 42 cases of liver cirrhosis and 165 matched controls were included for analysis. Questionnaires were administered to obtain histories of betel quid chewing, alcohol consumption, smoking, and family history of liver disease.