However, given that our cohort was mainly white Australian (82% influenza+, 95% influenza-), we found no differences in the number of “universal” or “risk” alleles based on studies describing HLA-A*02:01/03:01 and HLA-B*08:01/18:01/27:05/57:01 molecules binding universally conserved influenza peptides40 versus HLA-A*24:02/68:01 types positively correlating with pH1N1 mortality15 and morbidity16. The gene discussed is HLA-B; the disease is influenza.