Exacerbation of experimental autoimmune encephalomyelitis in rodents infected with murine gammaherpesvirus-68.

Academic Article


  • Viral infections have long been suspected to play a role in the pathogenesis of multiple sclerosis. In the present study, two different rodent models of experimental autoimmune encephalomyelitis (EAE) were used to demonstrate the ability of murine gammaherpesvirus-68 (gammaHV-68) to exacerbate development of neurological symptoms. SJL mice received UV-inactivated gammaHV-68 or intranasalgammaHV-68, followed by immunization against proteolipid-protein peptide 139-151. Infected mice became moribund within 10 days post-immunization, whereas mice exposed to UV-inactivated gammaHV-68 recovered. In the second model, Lewis rats were exposed to UV-inactivated gammaHV-68 or to gammaHV-68, followed by passive transfer of encephalitogenic T lymphocytes specific for myelin basic protein. Consistently, infected rats had higher clinical scores, and this result was observed during acute or latent gammaHV-68 infection. It is unlikely that this gammaHV-68-induced exacerbation was due to significant viral replication within the central nervous system since nested PCR, viral plaque assays, and infectious-centers assays demonstrated no detectable virus in spinal cords or brains of infected rodents undergoing EAE. Taken together, these studies demonstrate increased clinical symptoms of EAE in rodents infected by a gammaherpesvirus that has a limited ability to invade the central nervous system.
  • Authors

  • Peacock, James W
  • Elsawa, Sherine
  • Petty, Cynthia C
  • Hickey, William F
  • Bost, Kenneth L
  • Status

    Publication Date

  • July 2003
  • Published In


  • Animals
  • DNA, Viral
  • Encephalomyelitis, Autoimmune, Experimental
  • Herpesviridae Infections
  • Mice
  • Rats
  • Rhadinovirus
  • Tumor Virus Infections
  • Digital Object Identifier (doi)

    Start Page

  • 1849
  • End Page

  • 1858
  • Volume

  • 33
  • Issue

  • 7