Publication: Acetylsalicylic acid (ASA) blocks influenza virus propagation via its NF-κB-inhibiting activity
Issued Date
2007-07-01
Resource Type
ISSN
14625822
14625814
14625814
Other identifier(s)
2-s2.0-34250783318
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Mahidol University
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SCOPUS
Bibliographic Citation
Cellular Microbiology. Vol.9, No.7 (2007), 1683-1694
Suggested Citation
Igor Mazur, Walter J. Wurzer, Christina Ehrhardt, Stephan Pleschka, Pilaipan Puthavathana, Tobias Silberzahn, Thorsten Wolff, Oliver Planz, Stephan Ludwig Acetylsalicylic acid (ASA) blocks influenza virus propagation via its NF-κB-inhibiting activity. Cellular Microbiology. Vol.9, No.7 (2007), 1683-1694. doi:10.1111/j.1462-5822.2007.00902.x Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/24179
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Title
Acetylsalicylic acid (ASA) blocks influenza virus propagation via its NF-κB-inhibiting activity
Abstract
Influenza is still one of the major plagues worldwide. The statistical likeliness of a new pandemic outbreak highlights the urgent need for new and amply available antiviral drugs. We and others have shown that influenza virus misuses the cellular IKK/NF-κB signalling pathway for efficient replication suggesting that this module may be a suitable target for antiviral intervention. Here we examined acetylsalicylic acid (ASA), also known as aspirin, a widely used drug with a well-known capacity to inhibit NF-κB. We show that the drug efficiently blocks influenza virus replication in vitro and in vivo in a mechanism involving impaired expression of proapoptotic factors, subsequent inhibition of caspase activation as well as block of caspase-mediated nuclear export of viral ribonucleoproteins. As ASA showed no toxic side-effects or the tendency to induce resistant virus variants, existing salicylate-based aerosolic drugs may be suitable as anti-influenza agents. This is the first demonstration that specific targeting of a cellular factor is a suitable approach for anti-influenza virus intervention. © 2007 The Authors; Journal compilation © 2007 Blackwell Publishing Ltd.