Pathogenesis of ross river virus infection in mice. I.ependymal infection, cortical thinning, and hydrocephalus

Newborn mice inoculated sc with a minimally lethal strain of Ross River virus had severe paralysis from days 5 to 6, but only 25% died. Small foci of infection in ependyma and very few infected neurons in the cerebral cortex were detected, but there were no other evidences of acute infection in the central nervous system. From day 10, there was thinning of the cerebral cortex, with appearance of fluid-filled spaces by day 18. Paralysis was apparently due to severe necrosis of muscle; mice recovered and appeared normal by days 25-35, despite persistent cortical lesions still present in apparently healthy mice surviving for one and a half years. Intracerebrally inoculated newborn mice had necrosis of infected ependymal cells; in many instances this resulted in aqueductal stenosis and hydrocephalus. Semliki Forest virus, in contrast to Ross River virus, produced widespread infection and necrosis in the central nervous system, including foci in the retina. Death was attributed to neuronal destruction. Extraneural tissues were also infected, but mice died before there had been time for evolution of pathologic changes seen with Ross River virus.