Journal
GENES AND IMMUNITY
Volume 12, Issue 6, Pages 457-465Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/gene.2011.15
Keywords
anthrax vaccines; bacillus anthracis; bacterial vaccines; vaccination; HLA antigens
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Funding
- Centers for Disease Control and Prevention
- National Institute of Allergy and Infectious Diseases [N01-AI40068]
- National Heart, Lung, and Blood Institute [T32 HL072757]
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Host genetic variation, particularly within the human leukocyte antigen (HLA) loci, reportedly mediates heterogeneity in immune response to certain vaccines; however, no large study of genetic determinants of anthrax vaccine response has been described. We searched for associations between the immunoglobulin G antibody to protective antigen (AbPA) response to Anthrax Vaccine Adsorbed (AVA) in humans, and polymorphisms at HLA class I (HLA-A, -B, and -C) and class II (HLA-DRB1, -DQA1, -DQB1, -DPB1) loci. The study included 794 European-Americans and 200 African-Americans participating in a 43-month, double-blind and placebo-controlled clinical trial of AVA (clinicaltrials.gov identifier NCT00119067). Among European-Americans, genes from tightly linked HLA-DRB1, -DQA1, -DQB1 haplotypes displayed significant overall associations with longitudinal variation in AbPA levels at 4, 8, 26 and 30 weeks from baseline in response to vaccination with three or four doses of AVA (global P = 6.53 x 10(-4)). In particular, carriage of the DRB1-DQA1-DQB1 haplotypes *1501-*0102-*0602 (P = 1.17 x 10(-5)), *0101-*0101-*0501 (P-0.009) and *0102-*0101-*0501 (P-0.006) was associated with significantly lower AbPA levels. In carriers of two copies of these haplotypes, lower AbPA levels persisted following subsequent vaccinations. No significant associations were observed amongst African-Americans or for any HLA class I allele/haplotype. Further studies will be required to replicate these findings and to explore the role of host genetic variation outside of the HLA region. Genes and Immunity (2011) 12, 457-465; doi:10.1038/gene.2011.15; published online 3 March 2011
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