Publication: Mechanisms of the action of povidone-iodine against human and avian influenza A viruses: Its effects on hemagglutination and sialidase activities
Issued Date
2009-11-09
Resource Type
ISSN
1743422X
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2-s2.0-70350692276
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Mahidol University
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SCOPUS
Bibliographic Citation
Virology Journal. Vol.6, (2009)
Suggested Citation
Nongluk Sriwilaijaroen, Prapon Wilairat, Hiroaki Hiramatsu, Tadanobu Takahashi, Takashi Suzuki, Morihiro Ito, Yasuhiko Ito, Masato Tashiro, Yasuo Suzuki Mechanisms of the action of povidone-iodine against human and avian influenza A viruses: Its effects on hemagglutination and sialidase activities. Virology Journal. Vol.6, (2009). doi:10.1186/1743-422X-6-124 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/27632
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Title
Mechanisms of the action of povidone-iodine against human and avian influenza A viruses: Its effects on hemagglutination and sialidase activities
Abstract
Background: Influenza virus infection causes significant morbidity and mortality and has marked social and economic impacts throughout the world. The influenza surface glycoproteins, hemagglutinin (HA) and neuraminidase (NA), act cooperatively to support efficient influenza A virus replication and provide the most important targets for anti-influenza chemotherapy. In this study, povidone-iodine (PVP-I), which has a broad-spectrum microbicidal property, was examined for its inhibitory effects against influenza virus infection in MDCK cells and the mechanisms of PVP-I action on HA and NA were revealed. Results: Results obtained using a novel fluorescence- and chromogenic-based plaque inhibition assay showed that 1.56 mg/ml PVP-I inhibited infections in MDCK cells of human (8 strains) and avian (5 strains) influenza A viruses, including H1N1, H3N2, H5N3 and H9N2, from 23.0-97.5%. A sialidase inhibition assay revealed that PVP-I inhibited N1, N2 and N3 neuraminidases with IC50values of 9.5-212.1 g/ml by a mixed-type inhibition mechanism. Receptor binding inhibition and hemagglutinin inhibition assays indicated that PVP-I affected viral hemagglutinin rather than host-specific sialic acid receptors. Conclusion: Mechanisms of reduction of viral growth in MDCK cells by PVP-I involve blockade of viral attachment to cellular receptors and inhibition of viral release and spread from infected cells. Therefore, PVP-I is useful to prevent infection and limit spread of human and avian influenza viruses. © 2009 Sriwilaijaroen et al; licensee BioMed Central Ltd.