All in all the two complementary approaches, PSCPL and NetMHCpan, agreed on the specificity of the SLA-1*0401 molecule, as well as of the two chimeric MHC-I molecules. Thus, the specificity of SLA-1*0401 appear to be well established. This specificity has successfully been used to search for foot-and-mouth disease virus (FMDV)specific CTL epitopes in FMDV-vaccinated, SLA-1*0401positive pigs, and the recombinant SLA-1*0401 molecules have been used to generate corresponding tetramers and stain pig CTLs (Patch et al. 2011) . In conclusion, we here present a set of methods that can be used to generate functional recombinant MHC-I molecules, map their specificities and identify MHC-I-restricted epitopes, and eventually generate peptide-MHC-I tetramers for validation of CTL responses. This suite of methods is not only applicable to humans, but potentially to any species of interest. Immunogenetic Factors Associated with Severe Respiratory Illness Caused by Zoonotic H1N1 and H5N1 Influenza Viruses Following the 2009 H1N1 pandemic and ongoing sporadic avian-to-human transmission of H5N1 viruses, an emphasis has been placed on better understanding the determinants and pathogenesis of severe influenza infections. Much of the current literature has focused on viral genetics and its impact on host immunity as well as novel risk factors for severe infection (particularly within the H1N1 pandemic). An understanding of the host genetic determinants of susceptibility and severe respiratory illness, however, is currently lacking. By better defining the role of genetic variability in influenza infection and identifying key polymorphisms that impair the host immune response or correlate with protection, we will be able to better identify at-risk populations and new targets for therapeutic interventions and vaccines. This paper will summarize known immunogenetic factors associated with susceptibility or severity of both pH1N1 and H5N1 infections and will also identify genetic pathways and polymorphisms of high relevance for future study. Transmission of zoonotic influenza A viruses to humans is commonly the cause of new pandemics, which typically result in high disease burden and increased symptomatic severity and mortality. In order to predict which populations may be at highest risk of infection and to develop more effective therapeutic interventions and vaccines, a thorough understanding of both viral and host contribution to pathogenesis is required. In both the recent 2009 H1N1 (pH1N1) pandemic and the on-going rare avian-to-human transmission of H5N1, numerous studies have taken an indepth look at the impact of viral evolution and mutation on viral pathogenesis. Conversely, while both human and animal model studies of the host immune response to infection have identified correlates of severe disease, the contribution of host genetics to these correlates and to variability in susceptibility remains relatively unknown. Identification of host genetic polymorphisms contributing to altered susceptibility or disease severity has several benefits: identification of high-risk populations at greater need of prophylactic intervention, elucidation of host proteins important in virus-host interactions, and new targets for therapeutic interventions or vaccine development [1] . Studies of host genetics have provided important contributions to the study of other infectious diseases, including HIV, SARS, and HCV. This paper will describe what is currently known about the impact of host immunogenetics in both pH1N1 and H5N1 infections and will identify highly relevant polymorphisms and genetic pathways that could be investigated in future work.