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A model for persistent murine coronavirus infection involving maintenance via cytopathically infected cell centres.

Abstract
The relatively cell impermeable hygromycin B was found to inhibit viral but not cellular protein synthesis when added to cultures of murine hepatitis virus (MHV)-infected or mock-infected mouse L-2 fibroblasts. Membrane permeability, as judged by influx of sodium ions, has previously been demonstrated to be an MHV E2 glycoprotein-mediated, cytopathic effect of MHV infection in L-2 cells. It is therefore likely that the selective effect of hygromycin B on viral protein synthesis is a reflection of an increased drug penetration into virus-infected cells. Using hygromycin B as a marker for MHV-induced cell membrane cytopathology, the effects of drug treatment on a persistent MHV infection in mouse LM-K fibroblasts were investigated. MHV persistence in LM-K cells, which normally involves a steady state infection of 0.1 to 1% of the cells in culture, was found to be cured by hygromycin B treatment, as measured by the elimination of infectious virus from the supernatant medium. Hygromycin B also resulted in the eradication of MHV-specific RNA from LM-K cells, arguing against the presence of a non-cytopathically or latently infected subpopulation of cells.
AuthorsG Macintyre, F Wong, R Anderson
JournalThe Journal of general virology (J Gen Virol) Vol. 70 ( Pt 3) Pg. 763-8 (Mar 1989) ISSN: 0022-1317 [Print] England
PMID2543759 (Publication Type: Comparative Study, Journal Article)
Chemical References
  • Viral Proteins
  • Hygromycin B
Topics
  • Animals
  • Coronaviridae Infections (drug therapy, etiology, microbiology)
  • Cytopathogenic Effect, Viral (drug effects)
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Hepatitis, Viral, Animal (drug therapy, etiology, microbiology)
  • Hygromycin B (therapeutic use)
  • L Cells
  • Mice
  • Murine hepatitis virus (drug effects, metabolism)
  • Viral Proteins (antagonists & inhibitors, biosynthesis)

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