This study has explored the hypothesis that viral infection conjoined with chemical toxins may potentiate the development of encephalopathy and visceral fatty degeneration (EVFAD). Of the chemical agents employed in the study, 4-pentenoic acid when associated with mengo virus infection produced the most consistent and significant hepatic steatosis. Medullary vacuolization was common. Livers demonstrated fine vacuolization and glycogen depletion. Hypoglycemia was observed frequently, especially in animals exposed to prolonged pentenoic acid dosage schedules. Electron microscopy revealed fat droplets, cytoplasmic vacuoles, loss of glycogen, swollen mitochondria, and intramitochondrial electron-dense granules. These inclusions measured from 0.1 to 1 μm and on high magnification showed a finely fibrillar structure. The large granules were irregular in shape and probably resulted from the coalescence of smaller units. Their origin remains obscure, but they were found only in animals exposed to pentenoic acid and the virus. The viral-infection-accentuated hepatic steatosis in these animals provides support for the hypothesis that EVFAD may be the result of a hepatic mitochondrial toxin potentiated by viral infection. The observed electron-dense intramitochondrial granules further support altered mitochondrial function.
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