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More MS news articles for February 2003

Neuropathology of experimental autoimmune encephalomyelitis modified by retroviral infection

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12564768&dopt=Abstract

Neuropathology 2002 Dec;22(4):280-9
Fukumitsu H, Takase-Yoden S, Watanabe R.
Institute of Life Science, Soka University, Hachioji, Tokyo, Japan.

The A8 virus is a molecular clone of the neuropathogenic FrC6 virus derived from the Friend murine leukemia virus (F-MuLV).

To elucidate the effects of A8 virus-infection on immune-mediated diseases in the central nervous system, we investigated the development of acute and monophasic experimental autoimmune encephalomyelitis (EAE) in A8 virus-infected Lewis rats.

In EAE rats after A8 virus infection (A8-EAE), many inflammatory cells were found in the gray matter including the frontal lobe, where almost no inflammatory cells were found in rats with EAE alone.

The modified distribution of inflammatory cells was not dependent on the ages of A8 virus-infected rats, although the frequency of the modified distribution was reduced in older rats.

The chimeric virus Rec2, which contains the pol and env genes of 57 virus on the background of A8 and does not induce spongiform degeneration in the CNS, caused the same distributional modification of inflammatory cells in the rats with EAE as in A8-EAE rats.

Furthermore, the incidence and intensity of spongiform degeneration, thymoma and splenomegaly caused by A8 virus were reduced by the induction of EAE.