Abstract
BackgroundInfluenza 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.ResultsResults 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.ConclusionMechanisms 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.
Highlights
Influenza virus infection causes significant morbidity and mortality and has marked social and economic impacts throughout the world
HA and NA interact with sialic acid receptors on the host cell surface, the former mediating membrane fusion that results in virus infection and the latter possessing sialidase activity that cleaves sialyl linkages between viral HA and cellular receptors to release progeny viruses and separate viruses from HA-mediated self-aggregation, allowing the virus to infect a new host cell for continuing virus replication [3]
PVP-I ranging from 0–1.56 mg/ml, which had no effect on Madin-Darby canine kidney (MDCK) cells, reduced virus yield in MDCK cells in a dose-dependent manner (Figure 1B)
Summary
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. Among the three types (A, B and C) of influenza viruses, A type is the most virulent, infecting various avian and mammalian species and causing human pandemics as a consequence of antigenic change (antigenic shift) in their surface glycoproteins, hemagglutinin (HA) and neuraminidase (NA) [1]. The worldwide circulation of oseltamivir-resistant seasonal H1N1, highly pathogenic avian H5N1 [17,18] and the pandemic (H1N1) 2009 [19] have provided an impetus to develop new antiviral and antiseptic materials
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