H1N1 influenza viruses emerged as a result of a presumed or documented reassortment of segments from viruses of zoonotic origin with human-adapted influenza virus to cause pandemic spread in 1918 and again in 2009. The 2009 appearance of a swine-origin reassortant virus led to the first pandemic of the 21st century. During earlier pandemics, records indicate that certain individuals or populations appeared to be more susceptible to severe disease, but the 2 Clinical and Developmental Immunology ability to conduct studies in order to understand the immune mechanisms that underlay the increased propensity for complications was limited. The 2009 H1N1 (pH1N1) pandemic was accompanied by improved surveillance, thereby facilitating better estimation of disease severity and methods to examine the immune mechanisms behind complicated disease [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] . This surveillance allowed for the identification of several novel risk factors among various populations, but with a limited understanding of the genetic variation that may contribute to those risk factors.