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West Nile virus (WNV) is a re-emerging pathogen that can cause fatal encephalitis. In mice, susceptibility to WNV has been reported to result from a single point mutation in  oas1b , which encodes 2′–5′ oligoadenylate synthetase 1b, a member of the type I interferon-regulated  OAS  gene family involved in viral RNA degradation. In man, the human ortholog of  oas1b  appears to be  OAS1 . The ‘A’ allele at SNP rs10774671 of  OAS1  has previously been shown to alter splicing of  OAS1  and to be associated with reduced OAS activity in PBMCs. Here we show that the frequency of this hypofunctional allele is increased in both symptomatic and asymptomatic WNV seroconverters (Caucasians from five US centers; total n = 501; OR = 1.6 [95% CI 1.2–2.0],  P  = 0.0002 in a recessive genetic model). We then directly tested the effect of this SNP on viral replication in a novel  ex vivo  model of WNV infection in primary human lymphoid tissue. Virus accumulation varied markedly among donors, and was highest for individuals homozygous for the ‘A’ allele ( P <0.0001). Together, these data identify  OAS1  SNP rs10774671 as a host genetic risk factor for initial infection with WNV in humans.

Genetic Variation in OAS1 Is a Risk Factor for Initial Infection with West Nile Virus in Man