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More MS news articles for June 2003

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

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12811845&dopt=Abstract

Eur J Immunol. 2003 Jul;33(7):1849-58
Peacock JW, Elsawa SF, Petty CC, Hickey WF, Bost KL.
Department of Biology, The University of North Carolina at Charlotte, Charlotte, USA.

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.