DISTRIBUTION OF VIRAL-RNA IN THE SPINAL-CORD OF DBA 2 MICE DEVELOPINGBIPHASIC PARALYSIS FOLLOWING INFECTION WITH THE D-VARIANT OF ENCEPHALOMYOCARDITIS VIRUS (EMC-D)/

DBA/2 mice infected with the D variant of encephalomyocarditis virus ( EMC-D) (10(1)PFU/head) developed biphasic hind limb paralysis. As a fi rst step in clarifying its pathogenesis, we examined the distribution of viral RNA in the spinal cord using in situ hybridization. At 3 days post inoculation (DPI), in the spinal cord of mice showing slight par alysis, viral RNA was observed in capillary endothelial cells and a fe w adjacent glia cells in the funiculus lateralis from thoracic to lumb ar enlargement. At 7 DPI, in the spinal cord of mice showing apparent paralysis, viral RNA was observed in a larger number of glia cells in the demyelinated lesion associated with infiltration of macrophages in the funiculus lateralis and in a small number of degenerated neurons in the cornu ventrale. In the funiculus lateralis, viral RNA could not be observed after 28 DPI. On the other hand, viral RNA was observed i n degenerated neurons in the cornu ventrale of mice showing the second phase paralysis at 42 DPI. Many CD4(+)T cells infiltrated around thes e degenerated neurons. These results suggest that: (1) the viral entry zone was the capillary endothelial cells in the funiculus lateralis; (2) first phase paralysis was due to demyelination caused by EMC-D and associated with macrophage infiltration; (3) second phase paralysis w as due to degeneration of motor neurons bearing viral RNA associated w ith infiltration by CD4(+)T cells.