Amphotericin B increases influenza A virus infection by preventing IFITM3-mediated restriction
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Authors
Lin, Tsai-YuChin, Christopher R.
Everitt, Aaron R.
Clare, Simon
Perreira, Jill
Savidis, George
Aker, Aaron M.
John, Sinu P.
Sarlah, David
Carreira, Erick M.
Elledge, Stephen J.
Kellam, Paul
Brass, Abraham L.
UMass Chan Affiliations
Department of Microbiology and Physiological SystemsDocument Type
Journal ArticlePublication Date
2013-11-27Keywords
AcetylcholineAmphotericin B
Animals
Anti-Bacterial Agents
Antifungal Agents
Antigens, Differentiation
Biological Transport
COS Cells
Cell Fusion
Cell Line
Cell Membrane
Cercopithecus aethiops
HeLa Cells
Humans
*Immunocompromised Host
Influenza A Virus, H1N1 Subtype
Influenza, Human
Interferons
Membrane Proteins
Mice
Mice, Inbred C57BL
Mice, Knockout
Nystatin
Orthomyxoviridae Infections
RNA Interference
RNA, Small Interfering
Sodium
Tetraethylammonium
Virus Internalization
Virus Replication
Immunology of Infectious Disease
Immunopathology
Immunoprophylaxis and Therapy
Influenza Humans
Virology
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Show full item recordAbstract
The IFITMs inhibit influenza A virus (IAV) replication in vitro and in vivo. Here, we establish that the antimycotic heptaen, amphotericin B (AmphoB), prevents IFITM3-mediated restriction of IAV, thereby increasing viral replication. Consistent with its neutralization of IFITM3, a clinical preparation of AmphoB, AmBisome, reduces the majority of interferon's protective effect against IAV in vitro. Mechanistic studies reveal that IFITM1 decreases host-membrane fluidity, suggesting both a possible mechanism for IFITM-mediated restriction and its negation by AmphoB. Notably, we reveal that mice treated with AmBisome succumbed to a normally mild IAV infection, similar to animals deficient in Ifitm3. Therefore, patients receiving antifungal therapy with clinical preparations of AmphoB may be functionally immunocompromised and thus more vulnerable to influenza, as well as other IFITM3-restricted viral infections.Source
Cell Rep. 2013 Nov 27;5(4):895-908. doi: 10.1016/j.celrep.2013.10.033. Epub 2013 Nov 21. Link to article on publisher's siteDOI
10.1016/j.celrep.2013.10.033Permanent Link to this Item
http://hdl.handle.net/20.500.14038/30529PubMed ID
24268777Related Resources
Link to Article in PubMedRights
Copyright © 2013 The Authors. Published by Elsevier Inc. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-No Derivative Works License, which permits non-commercial use, distribution, and reproduction in any medium, provided the original author and source are credited.Distribution License
http://creativecommons.org/licenses/by-nc-nd/3.0/ae974a485f413a2113503eed53cd6c53
10.1016/j.celrep.2013.10.033
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Except where otherwise noted, this item's license is described as Copyright © 2013 The Authors. Published by Elsevier Inc. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-No Derivative Works License, which permits non-commercial use, distribution, and reproduction in any medium, provided the original author and source are credited.