For example, while infection with a WNV attenuated strain prevents PERK-mediated translation and CHOP transcription (Ambrose and Mackenzie, 2010), infection with the highly neurovirulent WNV NY-99 strain upregulates all three pathways of the UPR (Medigeshi et al., 2007) with an early induction of eIF2α phosphorylation and upregulation of downstream apoptotic factors such as CHOP, GADD34, caspase-3, and PARP, which may represent a host defense mechanism to limit viral replication. The gene discussed is EIF2AK3; the disease is infection.