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Mechanisms of the action of povidone-iodine against human and avian influenza A viruses: its effects on hemagglutination and sialidase activities

Nongluk Sriwilaijaroen12, Prapon Wilairat3, Hiroaki Hiramatsu2, Tadanobu Takahashi45, Takashi Suzuki45, Morihiro Ito2, Yasuhiko Ito2, Masato Tashiro6 and Yasuo Suzuki25*

Author Affiliations

1 Faculty of Medicine, Thammasat University (Rangsit Campus), Pathumthani 12120, Thailand

2 Health Science Hills, College of Life and Health Sciences, Chubu University, Kasugai, Aichi 487-8501, Japan

3 Department of Biochemistry, Faculty of Science, Mahidol University, Bangkok, Thailand

4 Department of Biochemistry, University of Shizuoka, School of Pharmaceutical Sciences, Shizuoka 422-8526, Japan

5 Global COE Program for Innovation in Human Health Sciences, Shizuoka 422-8526, Japan

6 Department of Viral Diseases and Vaccine Control, National Institute of Infectious Diseases, Toyama, Shinjuku-ku, Tokyo, 162-8640, Japan

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Virology Journal 2009, 6:124  doi:10.1186/1743-422X-6-124

Published: 13 August 2009

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 IC50 values of 9.5–212.1 μg/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.