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Received: Revised: Accepted: Published online: August 04, 2018 October 22, 2018 November 01, 2018 January 24, 2019 Rabies virus (RABV) is a highly neurotropic pathogen that causes neuronal dysfunction and alters the structural morphology of cytoskeleton. Different factors co-participate in regulating dynamic actin-microtubule cytoskeleton. Although RABV infection has been identified to induce microtubule depolymerization, but the relevant or associated molecular mechanism remains unclear. In order to observe the relation between RABV and cytoskeleton, immunofluorescence was performed to observe the structure of actin-microtubule cytoskeleton and associated binding proteins followed by quantification through experiments of Real-time PCR and western blot. The data showed that RABV disrupted the continuity of microtubules in confocal microscopy, and the localization of EB3 was random and varied at 48 hr and 98 hr of post-infection as compared to mock-infected cells. Street (MRV) and fixed (CVS-11) strains of RABV drastically reduced the gene expression of EB3 protein. These results demonstrated that RABV may alter the neuronal morphology by destructing balance of actin-microtubule cytoskeleton. Moreover, EB3 and p140cap play vital roles in inducing microtubule depolymerization during RABV infection. ©2018 PVJ. All rights reserved

In vitro Infection of Street and Fixed Rabies Virus Strains Inhibit Gene Expression of Actin-Microtubule Binding Proteins EB3 and p140cap in Neurons