Most studies on rabies virus pathogenesis in animal models have employed fixed rabies
viruses, and the results of those employing street rabies viruses have been inconsistent.
Therefore, to clarify the pathogenesis of street rabies virus (1088 strain) in mice,
106 focus forming units were inoculated into the right hindlimb of
ddY mice (6 weeks, female). At 3 days postinoculation (DPI), mild
inflammation was observed in the hindlimb muscle. At 5 DPI, ganglion cells in the right
lumbosacral spinal dorsal root ganglia showed chromatolysis. Axonal degeneration and
inflammatory cells increased with infection progress in the spinal dorsal horn and dorsal
root ganglia. Right hindlimb paralysis was observed from 7 DPI, which progressed to
quadriparalysis. However, no pathological changes were observed in the ventral horn and
root fibers of the spinal cord. Viral antigen was first detected in the right hindlimb
muscle at 3 DPI, followed by the right lumbosacral dorsal root ganglia, dorsal horn of
spinal cord, left red nuclei, medulla oblongata and cerebral cortex (M1 area) at 5 DPI.
These results suggested that the 1088 virus ascended the lumbosacral spinal cord via
mainly afferent fibers at early stage of infection and moved to cerebral cortex (M1 area)
using descending spinal tract. Additionally, we concluded that significant pathological
changes in mice infected with 1088 strain occur in the sensory tract of the spinal cord;
this selective susceptibility results in clinical features of the disease.