Abstract

The nucleoside analogue virazole (1-β- d-ribofuranosyl 1,2,4-triazole-3-carboxamide) at a concentration of 150 μg/ml inhibited the production of Sindbis virus (SV) and prevented virus-induced cytopathic effect (CPE) in Aedes albopictus LT C-7 cells. The drug had no effect on net viral RNA synthesis, the production of infectious RNA, or on nucleocapsid assembly. All viral structural proteins (E 1, E 2, and C) were synthesized and glycosylated in apparently normal amounts in the presence of virazole (Vz). However, most cells contained little or no reactive viral antigens as measured by an indirect immunofluorescent test. In contrast to the minimal effect on the synthesis of viral RNA and proteins, Vz markedly inhibited host macromolecular synthesis, as well as the growth of mosquito cells. In BHK21 cells the situation was different. As in C-7 cells, the drug caused a marked reduction in host macromolecular synthesis. However, CPE was not prevented and virus production was not inhibited. It is suggested that certain host functions may be required in the late stages of viral maturation and for expression of CPE and that these host functions are inhibited by Vz.

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