title: Apoptotic and necrotic changes in cultured murine neurons infected  with equid herpesvirus 1.
abstract: Equid herpesvirus 1 (EHV-1), like other members of the Alphaherpesvirinae, is a neurotropic virus, that causes latent infections in the nervous system of the natural host. All alphaherpesviruses have developed sophisticated strategies to interfere with the host cell apoptotic mechanisms, but the ability of EHV-1 to induce apoptosis in neurons has not been determined yet. In this study, apoptotic and necrotic changes in cultured murine neurons were methods identifying key stages of apoptosis. These methods have demonstrated characteristic apoptosis features, like DNA fragmentation, chromatin condensation, membrane blebbing and cell shrinkage in the infected cells. It seems likely that apoptosis was the predominant way of cell death in EHV-1-infected murine neurons. However, we showed also that during acute EHV-1 infection the majority of infected neurons remained unchanged and survived for more than eight weeks in culture, suggesting some protective mechanisms induced by the virus. Furthermore, it was shown that infection of neurons with EHV-1 has no significant influence on the level of the caspase 3, 7, and 8. We speculate that the control of apoptosis may be the key mechanism regulating the balance between productive and latent infection at the site of virus persistence.
authors.affiliation: Department of Preclinical Sciences, Warsaw University of Life Sciences, Warsaw, Poland. jcymerys@op.pl
authors.forename: J
authors.initials: J
authors.lastname: Cymerys
authors.forename: A
authors.initials: A
authors.lastname: Słońska
authors.forename: M M
authors.initials: MM
authors.lastname: Godlewski
authors.forename: A
authors.initials: A
authors.lastname: Golke
authors.forename: A
authors.initials: A
authors.lastname: Tucholska
authors.forename: A
authors.initials: A
authors.lastname: Chmielewska
authors.forename: M W
authors.initials: MW
authors.lastname: Bańbura
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics / Q000276:immunology*; D020169:Caspases / Q000235:genetics / Q000378:metabolism; D002478:Cells, Cultured; D053938:DNA Fragmentation; D015870:Gene Expression; D006566:Herpesviridae Infections / Q000276:immunology / Q000821:virology; D004861:Herpesvirus 1, Equid / Q000472:pathogenicity / Q000502:physiology*; D054884:Host-Pathogen Interactions; D020287:In Situ Nick-End Labeling; D051379:Mice; D009336:Necrosis; D009474:Neurons / Q000378:metabolism / Q000473:pathology / Q000821:virology*; D013045:Species Specificity; D017735:Virus Latency; D014779:Virus Replication
chemical_list: D020169:Caspases