Files
Abstract
Varicella Zoster Virus (VZV) causes chickenpox upon primary infection and establishes latency in ganglia. Reactivation from latency causes herpes zoster, which may be complicated by post-herpetic neuralgia. Innate immunity mediated by interferon and pro- inflammatory cytokines represents the first line of immune defense upon infection and reactivation. VZV is known to interfere with multiple innate immune signaling pathways including the central transcription factor NFĸB. However the role of these inhibitory mechanisms in vivo is unknown. Simian varicella virus (SVV)-infection of rhesus macaques recapitulates key aspects of VZV pathogenesis and this model thus permits examining the role of immune evasion mechanisms in vivo.