Publikationsdatenbank

Viral genes and cellular markers associated with neurological complications during herpesvirus infections (2017)

Art

Zeitschriftenartikel / wissenschaftlicher Beitrag

Autoren

Holz, Carine L

Nelli, Rahul K

Wilson, M Eilidh

Zarski, Lila M

Azab, Walid (WE 5)

Baumgardner, Rachel

Osterrieder, Nikolaus (WE 5)

Pease, Anthony

Zhang, Liangliang

Hession, Sarah

Goehring, Lutz S

Hussey, Stephen B

Soboll Hussey, Gisela

Quelle

The journal of general virology

Bandzählung: 98

Heftzählung: 6

Seiten: 1439 – 1454

ISSN: 0022-1317

Sprache

Englisch

Verweise

DOI: 10.1099/jgv.0.000773

Pubmed: 28631601

Kontakt

Institut für Virologie

Robert-von-Ostertag-Str. 7-13
14163 Berlin
+49 30 838 51833
virologie@vetmed.fu-berlin.de

Abstract / Zusammenfassung

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.