The dynamics of antibody-induced redistribution of viral envelope antigens in the plasma membranes of avian tumour virus-infected chick embryo fibroblasts

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Abstract
Avian tumour virus-infected chick embryo fibroblasts express new antigens, identical with the viral envelope antigens, in their plasma membranes. Electron-microscopic examination of carbon-platinum replicas of cells labelled with haemocyanin-marked antibody has shown the distribution of these antigens to be diffuse over the cell surface with an increased concentration on peripheral cell processes. However, antigen–antibody complexes (AAC), resulting from reaction with specific antibody, may be redistributed into a variety of patterns. Observation of the time course of antibody-induced antigen mobility revealed a rapid and a delayed phase of redistribution. During the rapid phase (10 min or less) some of the antigenbearing cells reorganized AAC into patches, while the remainder maintained a diffuse distribution. A fraction of the cells with either diffuse or patchy distribution also redistributed AAC into a pattern of ‘marginal redistribution (MR)’, consisting of linear aggregation of AAC, at the cell edge. During the ‘late’ phase of redistribution (after about 20 min), AAC began to condense into one or more foci of coalescence (FC) on each cell. As the number of cells with FC increased with time, the fraction of cells which were labelled decreased. Electron-microscopic observation of thin sections of ferritin-labelled specimens indicated that AAC were lost by endocytosis and that this process was probably related to FC formation. Inhibitors of oxidative phosphorylation, protein synthesis, RNA synthesis, or microtubule assembly had no significant effect on the patterns or the course of redistribution. lodoacetic acid (IAA), which depletes cellular ATP, and cytochalasin B (CB), which is believed to depolymerize microfilaments, partially inhibited MR and completely prevented FC formation and endocytosis. Paradoxically, IAA or CB-treated cells lost AAC very rapidly by some alternate mechanism not involving FC formation but which may entail a centrifugal migration of complexes to the cell extremities during the process of AAC disposal.