RT Journal Article SR Electronic(1) A1 Holz, Carine L. A1 Nelli, Rahul K. A1 Wilson, M. Eilidh A1 Zarski, Lila M. A1 Azab, Walid A1 Baumgardner, Rachel A1 Osterrieder, Nikolaus A1 Pease, Anthony A1 Zhang, Liangliang A1 Hession, Sarah A1 Goehring, Lutz S. A1 Hussey, Stephen B. A1 Soboll Hussey, GiselaYR 2017 T1 Viral genes and cellular markers associated with neurological complications during herpesvirus infections JF Journal of General Virology, VO 98 IS 6 SP 1439 OP 1454 DO https://doi.org/10.1099/jgv.0.000773 PB Microbiology Society, SN 1465-2099, AB Despite the importance of neurological disorders associated with herpesviruses, the mechanism by which these viruses influence the central nervous system (CNS) has not been definitively established. Owing to the limitations of studying neuropathogenicity of human herpesviruses in their natural host, many aspects of their pathogenicity and immune response are studied in animal models. Here, we present an important model system that enables studying neuropathogenicity of herpesviruses in the natural host. Equine herpesvirus type 1 (EHV-1) is an alphaherpesvirus that causes a devastating neurological disease (EHV-1 myeloencephalopathy; EHM) in horses. Like other alphaherpesviruses, our understanding of virus neuropathogenicity in the natural host beyond the essential role of viraemia is limited. In particular, information on the role of different viral proteins for virus transfer to the spinal cord endothelium in vivo is lacking. In this study, the contribution of two viral proteins, DNA polymerase (ORF30) and glycoprotein D (gD), to the pathogenicity of EHM was addressed. Furthermore, different cellular immune markers, including alpha-interferon (IFN-α), gamma-interferon (IFN-γ), interleukin-10 (IL-10) and interleukin-1 beta (IL-1β), were identified to play a role during the course of the disease., UL https://www.microbiologyresearch.org/content/journal/jgv/10.1099/jgv.0.000773