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American Journal of Pathology, Vol 124, 457-468, Copyright © 1986 by American Society for Investigative Pathology

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Noninflammatory spongiform polioencephalomyelopathy caused by a neurotropic temperature-sensitive mutant of Moloney murine leukemia virus TB

JF Zachary, CJ Knupp and PK Wong

Newborn inbred CFW/D mice were inoculated intraperitoneally with ts1, a neurotropic temperature-sensitive mutant of Moloney murine leukemia virus TB (MoMuLV-TB), with the parental wild type (wt) MoMuLV-TB, or with culture medium. A progressive symmetric hindlimb paresis that progressed to paralysis was observed in ts1-infected mice. Wt-infected mice and control mice had no neurologic signs. The severity and progression of neurologic signs correlated with the location, development, and progression of lesions. Lesions consisted of neuronal and glial cell vacuolization in the brain and the anterior horn of the spinal cord, spongiform change in the associated neuropil, spongiform change in lateral and ventral funiculi, and late fibrillary gliosis in the brainstem. There was no inflammation. Lesions were symmetric, increased in severity with time, and consistently arose at specific times in specific nuclei and areas of the brain and spinal cord. Similar, but less severe, histologic lesions were observed in corresponding areas of the central nervous system from wt-infected mice. Ultrastructurally, neuronal and glial cell vacuolization in ts1- infected mice at 31 days after inoculation was caused by dilatation of the endoplasmic reticulum and Golgi complex. Virions were observed in extremely low numbers predominantly in extracellular space and budding from membranes of neurons and glial cells. Virions were not observed in the endoplasmic reticulum or Golgi complex of neurons, nor were there cytoplasmic vacuoles that contained abnormal virions.

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