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Influenza B virus M2 protein can functionally replace its influenza A virus counterpart in promoting virus replication
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Document Title
Influenza B virus M2 protein can functionally replace its influenza A virus counterpart in promoting virus replication
Author
Wanitchang A, Wongthida P, Jongkaewwattana A
Name from Authors Collection
Scopus Author ID
25824516500
Affiliations
National Science & Technology Development Agency - Thailand; National Center Genetic Engineering & Biotechnology (BIOTEC)
Type
Article
Source Title
VIROLOGY
ISSN
0042-6822
Year
2016
Volume
498
Issue
5
Open Access
Bronze
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI
10.1016/j.virol.2016.08.016
Format
Abstract
The M2 protein (AM2 and BM2) of influenza A and B viruses function as a proton channel essential for viral replication. They also carry a cytoplasmic tail whose functions are not fully delineated. It is currently unknown whether these proteins could be replaced functionally in a viral context. Here, we generated single-cycle influenza A viruses (scIAV-Delta HA) carrying various M2-2A-mCherry constructs in the segment 4 (HA) and evaluated their growth in complementing cells. Intriguingly, the scIAV-Delta HA carrying AM2 and that bearing BM2 grew comparably well in MOCK-HA cells. Furthermore, while the virus carrying chimeric B-AM2 in which the BM2 transmembrane fused with the AM2 cytoplasmic tail produced robust infection, the one bearing the AM2 transmembrane fused with the BM2 cytoplasmic tail (A-BM2) exhibited severely impaired growth. Altogether, we demonstrate that AM2 and BM2 are functionally interchangeable and underscore the role of compatibility between transmembrane and cytoplasmic tail of the M2 protein. (C) 2016 Elsevier Inc. All rights reserved.
Keyword
AM2 | BM2 | Chimeric protein | Cytoplasmic tail | Proton channel | ScIAV-Delta HA
Industrial Classification
Knowledge Taxonomy Level 1
Knowledge Taxonomy Level 2
Knowledge Taxonomy Level 3
Funding Sponsor
National Science and Technology Development Agency [CPMO-P14-50863]
License
Copyright
Rights
Elsevier Inc.
Publication Source
WOS