The US11 gene of herpes simplex virus 1 promotes neuroinvasion and periocular replication following corneal infection

Audra J. Charron, The Geisel School of Medicine at Dartmouth
Stephen L. Ward, Washington University School of Medicine in St. Louis
Brian J. North, The Geisel School of Medicine at Dartmouth
Stacey Ceron, The Geisel School of Medicine at Dartmouth
David A. Leib, Washington University School of Medicine in St. Louis

Abstract

Herpes simplex virus 1 (HSV-1) cycles between phases of latency in sensory neurons and replication in mucosal sites. HSV-1 encodes two key proteins that antagonize the shutdown of host translation, US11 through preventing PKR activation and ICP34.5 through mediating dephosphorylation of the α subunit of eukaryotic initiation factor 2 (eIF2α). While profound attenuation of ICP34.5 deletion mutants has been repeatedly demonstrated, a role for US11 in HSV-1 pathogenesis remains unclear. We therefore generated an HSV-1 strain 17 US11-null virus and examined its properties