EXPRESSION OF C1Q, A SUBCOMPONENT OF THE RAT COMPLEMENT-SYSTEM, IS DRAMATICALLY ENHANCED IN BRAINS OF RATS WITH EITHER BORNA-DISEASE OR EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS

In situ hybridization, RT-PCR and Northern blot analysis as well immunohistochemistry were used to examine the expression of Clq, a subcomponent of the rat complement system, in brains of rats infected with Borna disease virus (BDV) and rats afflicted with experimental allergic encephalomyelitis (EAE) induced by the adoptive transfer of myelin basic protein specific T cells. Clq mRNA, which was not detected in normal brain, became clearly detectable using RT-PCR analysis by dl4 post infection (p.i.) with BDV. Maximal levels of Clq mRNA were reached 21 days p.i. when inflammatory reactions in the brain were also at a peak. Similarly, Clq mRNA was elevated when the clinical symptoms of EAE became evident 5 days following cell transfer. Clq positive cells, as identified by immunohistology, were preferentially localized in grey and white matter of the hippocampus and basolateral cortex. The Clq positive cells resembled microglial cells in morphology. The correlation of Clq expression with the development of neurological disease as well as the dramatic increase of Clq within brain regions with inflammatory lesions suggest that local biosynthesis of Clq may play a role in the pathogenesis of Borna virus induced and autoimmune encephalomyelitis.