Actin-independent maturation of rabies virus in neuronal cultures

Abstract

This study outlines the effects of a modification of the actin-based cytoskeleton on the maturation of rabies virus in human neuroblastoma cell and primary rat cortical neuron cultures. In a Ca(2+)-depleted or an EGTA-containing medium, disruption of microfilaments did not affect intracellular viral nucleoprotein synthesis, as demonstrated by dual-immunofluorescence microscopy, and caused no change in the extracellular titre of rabies virus. Furthermore, the continuous presence of the anti-calmodulin drugs trifluoperazine (1 to 20 microM) and chlorpromazine (1 to 30 microM), or the L-type Ca2+ channel antagonist nifedepine (1 to 10 microM) or the Ca(2+)-specific ionophore A23187 (0.05 to 1.0 microM), did not modify the extracellular titre of rabies virus significantly over a 48 h period. The inference from these studies is that the maturation of rabies virus is independent of the integrity of the microfilament structures and calmodulin-dependent processes of neuronal cells.