Abstract
Interferon (IFN) responses are critical for controlling herpes simplex virus 1 (HSV-1). The importance of neuronal IFN signaling in controlling acute and latent HSV-1 infection remains unclear. Compartmentalized neuron cultures revealed that mature sensory neurons respond to IFNβ at both the axon and cell body through distinct mechanisms, resulting in control of HSV-1. Mice specifically lacking neural IFN signaling succumbed rapidly to HSV-1 corneal infection, demonstrating that IFN responses of the immune system and non-neuronal tissues are insufficient to confer survival following virus challenge. Furthermore, neurovirulence was restored to an HSV strain lacking the IFN-modulating gene, γ34.5, despite its expected attenuation in peripheral tissues. These studies define a crucial role for neuronal IFN signaling for protection against HSV-1 pathogenesis and replication, and they provide a novel framework to enhance our understanding of the interface between host innate immunity and neurotropic pathogens.
Highlights
Herpes simplex virus type I (HSV-1) is a highly prevalent neurotropic virus that persists for the lifetime of the host
There is no vaccine against HSV, and antiviral drugs can control herpes simplex virus 1 (HSV-1), it persists because it establishes lifelong latent infections in neurons
In this study we sought to elucidate the role of neuronal innate immunity in the control of viral infection
Summary
Herpes simplex virus type I (HSV-1) is a highly prevalent neurotropic virus that persists for the lifetime of the host. Reactivation from latency can occur and HSV-1 travels in an anterograde direction down the axon of sensory neurons to the periphery where it undergoes subsequent rounds of lytic replication, enabling viral shedding and host-tohost spread [2]. While HSE can result from primary infection, mostly in newborns, both disease pathologies can result from reactivation of latent HSV which travels to the eye or CNS [4,5]. Nucleoside analogs such as acyclovir (ACV) reduce HSE mortality significantly, but survivors are often left with long-term neurological sequelae, and ACV cannot eliminate the latent virus reservoir [5]
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