 Genetic predisposition to a severe infection form particularly primary infection was demonstrated for several infectious diseases Casanova JL, Science 317:617-619, 2007; Casanova JL, EMBO J 26:915-922, 2007. It usually corresponds to deficiencies in genes involved in the hosts immune response, the transmission of which being Mendelian. Genetic factors affect the ability of enteroviruses and other viruses to damage beta cells and to induce diabetes. Recently, Nejentsev et al have demonstrated a link between enteroviruses and diabetes genes: they have indeed identified 4 rare IFIH1 polymorphisms that reduce the T1D risk. However, this gene encodes an enzyme recognizing the DNA enterovirus, causing immunity activation; mutations inhibit gene activation. Except one study on HIV-1, there is to our knowledge no genome wide association studies GWAS in humans on the role of hosts genetic polymorphisms in the risk of infection, clinical expression, duration of viral shedding, or response to therapy or to anti-viral vaccines. 