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Loss of actin-based motility impairs ectromelia virus release in vitro but is not critical to spread in vivo

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Duncan, ML, Horsington, J, Eldi, P, Al Rumaih, Z, Karupiah, G ORCID: 0000-0001-6306-4405 and Newsome, TP 2018 , 'Loss of actin-based motility impairs ectromelia virus release in vitro but is not critical to spread in vivo' , Viruses, vol. 10, no. 3 , pp. 1-14 , doi: 10.3390/v10030111.

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Abstract

Ectromelia virus (ECTV) is an orthopoxvirus and the causative agent of mousepox. Like other poxviruses such as variola virus (agent of smallpox), monkeypox virus and vaccinia virus (the live vaccine for smallpox), ECTV promotes actin-nucleation at the surface of infected cells during virus release. Homologs of the viral protein A36 mediate this function through phosphorylation of one or two tyrosine residues that ultimately recruit the cellular Arp2/3 actin-nucleating complex. A36 also functions in the intracellular trafficking of virus mediated by kinesin-1. Here, we describe the generation of a recombinant ECTV that is specifically disrupted in actin-based motility allowing us to examine the role of this transport step in vivo for the first time. We show that actin-based motility has a critical role in promoting the release of virus from infected cells in vitro but plays a minor role in virus spread in vivo. It is likely that loss of microtubule-dependent transport is a major factor for the attenuation observed when A36R is deleted.

Item Type: Article
Authors/Creators:Duncan, ML and Horsington, J and Eldi, P and Al Rumaih, Z and Karupiah, G and Newsome, TP
Keywords: actin-based motility, viral release, A36, Arp2/3 complex, virus transport
Journal or Publication Title: Viruses
Publisher: MDPI
ISSN: 1999-4915
DOI / ID Number: 10.3390/v10030111
Copyright Information:

Copyright 2018 The Authors. Licensed under Creative Commons Attribution 4.0 International (CC BY 4.0) https://creativecommons.org/licenses/by/4.0/

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