Intracerebral administration of recombinant rabies virus expressing GM-CSF prevents the development of rabies after infection with street virus

PLoS One. 2011;6(9):e25414. doi: 10.1371/journal.pone.0025414. Epub 2011 Sep 28.

Abstract

Recently it was found that prior immunization with recombinant rabies virus (RABV) expressing granulocyte-macrophage colony-stimulating factor (GM-CSF) (LBNSE-GM-CSF) resulted in high innate/adaptive immune responses and protection against challenge with virulent RABV (Wen et al., JVI, 2011). In this study, the ability of LBNSE-GM-CSF to prevent animals from developing rabies was investigated in mice after infection with lethal doses of street RABV. It was found that intracerebral administration of LBNSE-GM-CSF protected more mice from developing rabies than sham-treated mice as late as day 5 after infection with street RABV. Intracerebral administration of LBNSE-GM-CSF resulted in significantly higher levels of chemokine/cytokine expression and more infiltration of inflammatory and immune cells into the central nervous system (CNS) than sham-administration or administration with UV-inactivated LBNSE-GM-CSF. Enhancement of blood-brain barrier (BBB) permeability and increases in virus neutralizing antibodies (VNA) were also observed in mice treated with LBNSE-GM-CSF. On the other hand, intracerebral administration with UV-inactivated LBNSE-GM-CSF did not increase protection despite the fact that VNA were induced in the periphery. However, intracerebral administration with chemoattractant protein-1 (MCP-1, also termed CCL2) increased significantly the protective efficacy of UV-inactivated LBNSE-GM-CSF. Together these studies confirm that direct administration of LBNSE-GM-CSF can enhance the innate and adaptive immunity as well as the BBB permeability, thus allowing infiltration of inflammatory cells and other immune effectors enter into the CNS to clear the virus and prevent the development of rabies.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Adaptive Immunity / drug effects
  • Animals
  • Antibodies, Neutralizing / metabolism
  • B-Lymphocytes / drug effects
  • B-Lymphocytes / immunology
  • Blood-Brain Barrier / drug effects
  • Blood-Brain Barrier / metabolism
  • Brain / drug effects
  • Brain / immunology
  • Brain / metabolism
  • Brain / virology
  • Chemokine CCL2 / administration & dosage
  • Chemokine CCL2 / pharmacology
  • Chemokines / metabolism
  • DNA, Recombinant / genetics*
  • Dendritic Cells / drug effects
  • Dendritic Cells / immunology
  • Female
  • Gene Expression
  • Gene Expression Regulation / drug effects
  • Gene Expression Regulation / immunology
  • Granulocyte-Macrophage Colony-Stimulating Factor / administration & dosage*
  • Granulocyte-Macrophage Colony-Stimulating Factor / genetics
  • Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology*
  • Immunity, Innate / drug effects
  • Mice
  • Neutrophil Infiltration / drug effects
  • Permeability / drug effects
  • Rabies / prevention & control*
  • Rabies virus / genetics*
  • Rabies virus / immunology
  • Rabies virus / pathogenicity*
  • Time Factors
  • Ultraviolet Rays

Substances

  • Antibodies, Neutralizing
  • Chemokine CCL2
  • Chemokines
  • DNA, Recombinant
  • Granulocyte-Macrophage Colony-Stimulating Factor