An investigation of herpes simplex virus type 1 latency in a novel mouse dorsal root ganglion model suggests a role for ICP34.5 in reactivation

• DOI: 10.1099/vir.0.000138
• Publication Date: 2015-04-09T03:37:12Z
• Authors: R. K. Mattila; K. Harila; S. M. Kangas; H. Paavilainen; A. M. Heape; I. J. Mohr; V. Hukkanen
• Keywords: Lytic cycle; Dorsal root ganglion; Neurotropic virus; Virus latency; Latent Virus; Immunofluorescence; Trigeminal ganglion; Pseudorabies

After a primary lytic infection at the epithelia, herpes simplex virus type 1 (HSV-1) enters innervating sensory neurons and translocates to nucleus, where it establishes quiescent latent infection. Periodically, can reactivate progeny viruses spread back epithelium. Here, we introduce an embryonic mouse dorsal root ganglion (DRG) culture system, which be used study mechanisms that control establishment, maintenance reactivation from latency. Use of acyclovir is not necessary in our model. We examined different phases HSV-1 life cycle DRG neurons, showed WT could establish both form cells. reactivating stimulus, all markers true reactivation. In addition, deletion γ134.5 gene rendered incapable reactivation, even though was clearly able replicate persist neurons.