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Axonal emetine treatment blocks retrograde RABV infection by a mechanism that does not depend on protein synthesis inhibition.

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posted on 2018-07-20, 17:36 authored by Margaret A. MacGibeny, Orkide O. Koyuncu, Christoph Wirblich, Matthias J. Schnell, Lynn W. Enquist

(A) Cell bodies in the S compartment at 24 h post RABV P-mCherry infection in N. Emetine (100 μM) was added to N, 1 h prior to axonal infection and washed out at 5 hpi (scale bar = 250 μm). (B) Quantification of % infected cell bodies at 24, 48, and 72 hpi (+/-) 100 μM emetine in N. (C) Quantification of % infected cell bodies at 24 hpi (+/-) 100 μM emetine, 100 μg/ml CHX, or 10 μg/ml puromycin added to N or S, 1 h prior to infection in N. Inhibitors were washed out at 5 hpi. Black dots in (B) and (C) represent individual tri-chambers (from four (B) and three (C) independent replicates). Horizontal lines and errors bars represent mean ± SD for each condition with ****p < 0.0001 using two-way (B) or one-way (C) ANOVA (ns = not significant). (D) Levels of phosphorylated eIF2α (P-eIF2α) in dissociated SCG (+/-) 100 μM emetine, 100 μg/ml CHX or 10 μg/ml puromycin (6 h post treatment).

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