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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

dc.contributor.authorNongluk Sriwilaijaroenen_US
dc.contributor.authorPrapon Wilairaten_US
dc.contributor.authorHiroaki Hiramatsuen_US
dc.contributor.authorTadanobu Takahashien_US
dc.contributor.authorTakashi Suzukien_US
dc.contributor.authorMorihiro Itoen_US
dc.contributor.authorYasuhiko Itoen_US
dc.contributor.authorMasato Tashiroen_US
dc.contributor.authorYasuo Suzukien_US
dc.contributor.otherFaculty of Medicine, Thammasat Universityen_US
dc.contributor.otherChubu Universityen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherUniversity of Shizuokaen_US
dc.contributor.otherNational Institute of Infectious Diseasesen_US
dc.date.accessioned2018-09-13T06:40:11Z
dc.date.available2018-09-13T06:40:11Z
dc.date.issued2009-11-09en_US
dc.description.abstractBackground: 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.en_US
dc.identifier.citationVirology Journal. Vol.6, (2009)en_US
dc.identifier.doi10.1186/1743-422X-6-124en_US
dc.identifier.issn1743422Xen_US
dc.identifier.other2-s2.0-70350692276en_US
dc.identifier.urihttps://repository.li.mahidol.ac.th/handle/20.500.14594/27632
dc.rightsMahidol Universityen_US
dc.rights.holderSCOPUSen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=70350692276&origin=inwarden_US
dc.subjectImmunology and Microbiologyen_US
dc.subjectMedicineen_US
dc.titleMechanisms of the action of povidone-iodine against human and avian influenza A viruses: Its effects on hemagglutination and sialidase activitiesen_US
dc.typeArticleen_US
dspace.entity.typePublication
mu.datasource.scopushttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=70350692276&origin=inwarden_US

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