Viruses exploit the function of epidermal growth factor receptor
Version of Record online: 29 MAY 2014
Copyright © 2014 John Wiley & Sons, Ltd.
Reviews in Medical Virology
Volume 24, Issue 4, pages 274–286, July 2014
How to Cite
Zheng, K., Kitazato, K. and Wang, Y. (2014), Viruses exploit the function of epidermal growth factor receptor. Rev. Med. Virol., 24: 274–286. doi: 10.1002/rmv.1796
- Issue online: 4 JUL 2014
- Version of Record online: 29 MAY 2014
- Manuscript Accepted: 16 APR 2014
- Manuscript Revised: 15 APR 2014
- Manuscript Received: 20 JAN 2014
- Twelfth Five-Year National Science and Technology Support Program. Grant Number: 2012BAI29B06
- National Natural Science Foundation of China. Grant Number: 81274170
- Foundation for High-level Talents in Higher Education of Guangdong, China. Grant Number: NO.79
Epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase that regulates cellular homeostatic processes. Following ligand binding, EGFR activates different downstream signalling cascades that promote cell survival, proliferation, motility, and angiogenesis and induces F-actin-dependent EGFR endocytosis, which relocalises the activated receptors for degradation or recycling. The responses that are induced by ligand binding to EGFR, including cell signalling activation, protein kinase phosphorylation and cytoskeletal network rearrangement, resemble those induced by virus infection. Increasing evidence demonstrates that many viruses usurp EGFR endocytosis or EGFR-mediated signalling for entry, replication, inflammation, and viral antagonism to the host antiviral system. In addition, viruses have acquired sophisticated mechanisms to regulate EGFR functions by interrupting the EGFR-recycling process and modulating EGFR expression. In this review, we provide an overview of the mechanisms by which viruses alter EGFR signalling in favour of their continued survival. Copyright © 2014 John Wiley & Sons, Ltd.