Nonactin hinders intracellular glycosylation in virus-infected baby hamster kidney cells

Abstract

Abstract. Potent antiviral agents hinder virus-infected cell machinery, leading to rescue from viral damage. in this study, we aimed to identify selective intracellular glycosylation inhibitor(s) that do not suppress glycoprotein synthesis. our results showed that nonactin is a potent inhibitor of intracellular glycosylation. First, we examined the effects of nonactin on syncytium formation and cytopathic activity in virus-infected baby hamster kidney cells. nonactin effectively inhibited syncytium formation in a concentration-dependent manner, and infectious virus production was markedly reduced. However, glycoprotein synthesis was not affected. in the presence of 5 µg/ml nonactin, we observed the intracellular accumulation of vesicular stomatitis virus-G protein as well as syncytium formation, but no significant effects on newcastle disease virus-hemagglutinin-neuramidase glycoprotein synthesis. our results collectively indicate that nonactin potentially inhibits glycosylation by acting as a suppressor of intracellular glycosylation trafficking.

Influenza A Virus Entry Inhibitors Targeting the Hemagglutinin

“…Binding of these collectins to high mannose oligosaccharides on the hemagglutinin (HA) appears to be most important for viral neutralization [26]. Inspired by reported antiviral activity of glycosylation inhibitors, such as nonactin and N-butyldeoxynojirimycin (NB-DNJ) [27,28], it may be possible to achieve an anti‑influenza activity by appropriate glycosylation inhibition strategy. No clear examples of antibodies targeting glycans on HA have yet been reported, suggesting this may be a fertile area for future discovery efforts.…”