The mechanism of neutralization of a type A influenza virus by polyclonal IgM was similar for both tracheal epithelial and BHK cells. Maximum neutralization was only 90% and most (70%) of the virus failed to attach to inoculated cells. The remainder attached to -acetylneuraminic acid receptors but was not internalized. IgM aggregated virus, but only at an IgM:virus ratio below the level required for neutralization. Failure to detect any loss of infectivity associated with aggregation suggested that aggregates were unstable. Monoclonal polymeric IgA neutralized virus more efficiently on BHK cells (99.9%) than the equivalent amounts of IgM (90%). Otherwise the mechanisms of IgA and IgM neutralization were similar, except that IgA-induced aggregation was coincident with loss of infectivity and may thus have contributed to it. However, IgA-neutralized virus attached to tracheal epithelial cells more efficiently than infectious virus, initially using a neuraminidase-sensitive receptor, but then becoming neuraminidase-resistant. Whether the latter IgA-virus complexes were internalized or attached to a neuraminidase-resistant receptor is not known. This use of differentiated murine cells with murine IgA gave neutralization data that differed qualitatively from those obtained with the same antibody and undifferentiated hamster cells.


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