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Rabies virus quasispecies: implications for pathogenesis

K Morimoto1, D C Hooper, H Carbaugh

  • 1Center for Neurovirology, Department of Microbiology and Immunology, Thomas Jefferson University, 1020 Locust Street, Philadelphia, PA 19107-6799, USA.

Proceedings of the National Academy of Sciences of the United States of America
|April 18, 1998
PubMed
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Rabies virus strain CVS-24 rapidly selects distinct variants (CVS-B2c and CVS-N2c) in different cell types. These variants exhibit varied neurotropism and pathogenicity in mice, influencing viral spread.

Area of Science:

  • Virology
  • Molecular Biology
  • Pathogenesis

Background:

  • Rabies virus strains can harbor diverse genetic variants.
  • Cell culture passage can lead to the selection of specific viral variants.
  • Understanding variant selection is crucial for rabies virus research.

Purpose of the Study:

  • To characterize the genotypic and phenotypic differences between rabies virus variants selected in different cell types.
  • To investigate the neurotropism and pathogenicity of these variants in vivo.
  • To explore the factors influencing variant selection during infection.

Main Methods:

  • Passaging the mouse-adapted rabies virus strain CVS-24 in BHK cells and mouse brain/neuroblastoma cells.
  • Genotypic and phenotypic analysis of selected variants (CVS-B2c and CVS-N2c).

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  • In vitro and in vivo studies of neurotropism and pathogenicity in mice.

    • Main Results:

    • BHK cell passage selected for CVS-B2c, differing from CVS-N2c found in mouse-passaged virus, with 10 glycoprotein amino acid substitutions.
    • CVS-N2c showed higher neurotropism and pathogenicity in adult mice, while CVS-B2c replicated better in non-neuronal cells and was more pathogenic in neonatal mice.
    • Differential selection of variants occurred in adult versus neonatal mice, suggesting a role for host immune and nervous system maturation.

    Conclusions:

    • Rabies virus strains contain subpopulations that can be selectively amplified by host cell type.
    • Variant-specific neurotropism and pathogenicity contribute to differential disease outcomes and host-specific selection.
    • Viral variant diversity may enhance rabies virus adaptability and interspecies transmission.