Present address: Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK
Endocytic tubules regulated by Rab GTPases 5 and 11 are used for envelopment of herpes simplex virus
Article first published online: 18 SEP 2012
Copyright © 2012 European Molecular Biology Organization
This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
The EMBO Journal
Volume 31, Issue 21, pages 4204–4220, November 5, 2012
How to Cite
Hollinshead, M., Johns, H. L., Sayers, C. L., Gonzalez-Lopez, C., Smith, G. L. and Elliott, G. (2012), Endocytic tubules regulated by Rab GTPases 5 and 11 are used for envelopment of herpes simplex virus. The EMBO Journal, 31: 4204–4220. doi: 10.1038/emboj.2012.262
- Issue published online: 5 NOV 2012
- Article first published online: 18 SEP 2012
- Manuscript Accepted: 24 AUG 2012
- Manuscript Received: 10 FEB 2012
- trans-Golgi network
Enveloped viruses employ diverse and complex strategies for wrapping at cellular membranes, many of which are poorly understood. Here, an ultrastructural study of herpes simplex virus 1 (HSV1)-infected cells revealed envelopment in tubular membranes. These tubules were labelled by the fluid phase marker horseradish peroxidase (HRP), and were observed to wrap capsids as early as 2 min after HRP addition, indicating that the envelope had recently cycled from the cell surface. Consistent with this, capsids did not colocalise with either the trans-Golgi network marker TGN46 or late endosomal markers, but showed coincidence with the transferrin receptor. Virus glycoproteins were retrieved from the plasma membrane (PM) to label wrapping capsids, a process that was dependent on both dynamin and Rab5. Combined depletion of Rab5 and Rab11 reduced virus yield to <1%, resulting in aberrant localisation of capsids. These results suggest that endocytosis from the PM into endocytic tubules provides the main source of membrane for HSV1, and reveal a new mechanism for virus exploitation of the endocytic pathway.