Morphological changes were extensive following infection of murine neuroblastoma N-18 cells with a temperature-sensitive () mutant of vesicular stomatitis virus (VSV), G31 (complementation group III), and incubation at 39 °C, a non-permissive condition for virion maturation. Incubation for 24 h after infection resulted in extensive morphological degeneration of mitochondria with over 80% of the mitochondria having degenerated. Mitochondrial function, as determined by Janus green B supravital staining, was reduced by 81% from that in uninfected cells. Cellular ATP levels were reduced by 50% 12 h after infection. Mitochondrial degeneration still occurred in infected cells after the inactivation of lysosomes with chloroquine. Extensive cell fusion and cytoplasmic vacuole formation also occurred during the non-permissive infection with G31. Loss of plasma membrane integrity was not the cause of vacuole formation since 90% of the cells were able to exclude trypan blue 24 h after infection, nor were the vacuoles the result of inactivation of the mitochondria since cyanide-poisoned cells did not form vacuoles. The cytopathic alterations observed in N-18 cells during the non-permissive infection of N-18 cells with G31 did not occur during the non-permissive infection of N-18 cells with G11 (I), G41 (IV), or u.v.-inactivated G31. However, the non-permissive infection with O45(V) led to mitochondrial degeneration and cytoplasmic vacuole formation, but no cell fusion occurred. These results are discussed in light of the ultrastructural features previously observed in the central nervous system of mice infected with G31 and cells in culture infected with wild-type VSV.


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