| First Author | Rosato PC | Year | 2015 |
| Journal | PLoS Pathog | Volume | 11 |
| Issue | 7 | Pages | e1005028 |
| PubMed ID | 26153886 | Mgi Jnum | J:245954 |
| Mgi Id | MGI:5914561 | Doi | 10.1371/journal.ppat.1005028 |
| Citation | Rosato PC, et al. (2015) Neuronal Interferon Signaling Is Required for Protection against Herpes Simplex Virus Replication and Pathogenesis. PLoS Pathog 11(7):e1005028 |
| abstractText | 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 IFNbeta 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, gamma34.5, 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. |
