An explanation for enhanced virus plaque formation in chick embryo cells.

Abstract

While studying virus neutralization of many togaviruses by antisera raised in chickens, Hawkes and Lafferty1,2 observed a significant increase of plaque counts above controls when virus–antibody mixtures were assayed on chick embryo (CE) cell monolayers, or monolayers derived from other avian embryos. Among those antisera tested, partial neutralizing activity was observed at low dilutions and plaque enhancement at high dilutions above the neutralizing end point. These studies interested us because of the many apparent similarities between plaque enhancement and enhanced replication of dengue virus in mononuclear phagocytes. The latter has been shown to be mediated by anti-dengue IgG at dilutions above neutralization end points. When non-neutralized immune complexes are formed between dengue virus and antibody molecules, the Fc termini attach to cell receptors and complexes are internalized; this facilitates infection and results in enhanced production of virus3,4. The same phenomenon has been extended to West Nile (WN) virus demonstrated on mouse macrophage cell lines by Peiris and Porterfield5. Here, we have examined the infection of CE cells with virus–antibody complexes of another flavivirus, Murray Valley encephalitis (MVE) virus. Our results show that a similar mechanism operates in the antibody-mediated viral plaque enhancement of MVE virus on CE cells.