Following intracerebral inoculation of the BeAn strain of Theiler's murine encephalomyelitis virus the course of the acute infection and persistence of virus in the CNS varies between individual CBA mice. On the basis of clinical signs, virus distribution, virus titres, histopathology and Southern blot hybridization analysis of virus specific RT-PCR amplified products from total brain and spinal cord RNA, individual CBA mice could be placed into one of three groups. The first group were those animals which died of acute encephalitis. The second group were animals with or without clinical signs which had early high CNS virus titres, and in addition to scattered foci of infection had spread of virus in specific neuronal nuclei followed by destruction of these areas and thereafter persistence of virus in the CNS. The third group had no clinical signs, low CNS virus titres, small foci of CNS infection and were negative for virus after 28 days. This third pattern of infection was also seen in BALB/c mice. Between 50 and 268 days post-infection 53% of CBA mice were positive for viral RNA in the CNS by RT-PCR. No BALB/c mice were positive. In both the acute and persistent infection there was a correlation between serum neutralizing antibody titre and clinical signs. During the acute infection BeAn RNA could be detected in neurons and astrocytes. Oligodendrocytes were negative. In those CBA mice with persistence, viral RNA was observed in scattered individual or small foci of cells, predominantly oligodendrocytes, in both the brain and spinal cord.


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