We transiently induced aberrant N-linked glycosylation in cultured cells with an oligosaccharyltransferase inhibitor, NGI-1. Here, we investigate the consequences of aberrant cellular glycosylation for the glycome and the biology of influenza virus. Individuals with metabolic dysregulation of cellular glycosylation often experience severe influenza disease, with a poor immune response to the virus and low vaccine efficacy. Differences between NGI-1-treated and untreated samples were not significant ( P > 0.05). Data represent the average (± SD) of the results from one representative experiment (of two total). Viral titers were assessed at the indicated time points. (c) MDCK cells with normal N-glycosylation were infected with untreated or NGI-treated MDCK cells grown with virus at MOI 0.01. (a) MDCK cell monolayers or (b) 10-day-old embryonated chicken eggs with unmodified N-glycosylation were infected with A(H3N2)2013 IAV from untreated or NGI-treated NHBE cells at MOI 0.01 (in the case of MDCK cells) or with 4 HA (in the case of embryonated chicken eggs). Virus-containing apical culture supernatants were collected 24 h postinfection, and viral titers were determined. NHBE or MDCK cell monolayers were untreated or pretreated with 10.0 μM NGI-1 1 h prior to infection with A(H3N2)2013 IAV. H3N2 IAV from NGI-1-treated cells exhibits normal growth at conditions of unmodified N-glycosylation.
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