Vesicular stomatitis virus infection and neuropathogenesis in the murine model are associated with apoptosis

J. H. Sur, R. Allende, A. R. Doster

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

This study examines apoptosis and viral neuropathogenesis in a murine model infected with vesicular stomatitis virus (VSV). VSV induces apoptotic cell death in cultured cell lines, raising the possibility that apoptosis of infected neurons and other target cells may contribute to disease and mortality. To determine whether or not VSV induces apoptosis in neural tissues, mice were inoculated intranasally with VSV. At 24, 48, 72, 96, and 120 hours postinfection, brain tissues were assayed for the presence of viral RNA by in situ hybridization and viral antigen by immunohistochemistry. Apoptosis was identified by in situ terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling and electron microscopy. Viral replication and lesions were observed predominantly in central nervous system neurons. Apoptotic cell death was restricted to the same regions of the brain in which infected cells and tissue injury were identified. Results suggest that VSV-induced apoptosis is a mechanism causing cell death, tissue injury, and mortality in VSV-infected mice.

Original languageEnglish (US)
Pages (from-to)512-520
Number of pages9
JournalVeterinary pathology
Volume40
Issue number5
DOIs
StatePublished - Sep 2003

Keywords

  • Apoptosis
  • Immunohistochemistry
  • In situ hybridization
  • Neuropathogenesis
  • New Jersey virus
  • Swiss Webster mice
  • TUNEL
  • Vesicular stomatitis

ASJC Scopus subject areas

  • veterinary(all)

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