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Interaction of hydrophobized antiviral antibodies with influenza virus infected MDCK cells
N S Melik-Nubarov1, Suzdaltseva YuG, E L Priss
1Russian Research Center of Molecular Diagnostics and Therapy (RCMDT), Moscow.
The ability of artificially stearoylated antibodies to influenza virus hemagglutinin and M1 proteins to interfere with influenza infection in MDCK cells has been studied. Both the modified anti-hemagglutinin (polyclonal) and anti-M1 (monoclonal) antibodies neutralize the virus when added before the infection. The effect can be attributed to the interaction of stearoylated antibodies with the virus surface, which is enhanced by fatty acylation (anti-hemagglutinin), or to the antibody uptake in the cell endocytic compartments simultaneously with the virion which permits antibodies to interact with the virus envelope internal antigen (anti-M1). The stearoylated antibodies to hemagglutinin inhibit the virus reproduction being added to the infected cells. This effect is believed to be due to the interaction of the antibodies with newly synthesized hemagglutinin on the cell surface which disturbs the virus budding and assemblage; fatty acylation intensifying this interaction.
The ability of artificially stearoylated antibodies to influenza virus hemagglutinin and M1 proteins to interfere with influenza infection in MDCK cells has been studied. Both the modified anti-hemagglutinin (polyclonal) and anti-M1 (monoclonal) antibodies neutralize the virus when added before the infection. The effect can be attributed to the interaction of stearoylated antibodies with the virus surface, which is enhanced by fatty acylation (anti-hemagglutinin), or to the antibody uptake in the cell endocytic compartments simultaneously with the virion which permits antibodies to interact with the virus envelope internal antigen (anti-M1). The stearoylated antibodies to hemagglutinin inhibit the virus reproduction being added to the infected cells. This effect is believed to be due to the interaction of the antibodies with newly synthesized hemagglutinin on the cell surface which disturbs the virus budding and assemblage; fatty acylation intensifying this interaction.