Executive summary

Scanning electron microscopy of AKR cells chronically infected with AKR mouse leukaemia virus revealed that the number of budding virions was greatly increased in interferon-treated c lls. These results, together with previous biochemical findings, suggest that in this system, interferon i hibits a late stage of virus assembly or release. When mouse cells of the AKR, C + line, chronically infected by and producing a mouse leukaemia virus, were treated with interferon for 16 h or 9 days, virus yields were reduced by 90 to 95 ~o but levels of mouse leukaemia virus group-specific antigen (internal non-glyco-sylated protein, p 30) and reverse transcriptase activity were not decreased (Friedman & Ramseur, I974; Friedman et al. I975). Thus, interferon appeared to inhibit a late step in virus assembly, and/or a step or steps involved in virus release. To complement these pre-vious biochemical studies, we have now used (a) transmission electron microscopy (TEM) to study ultracellular structures and the mode of virus assembly and extrusion, and (b), scanning electron microscopy (SEM) to examine the cell surfaces, a technique already used to study oncornavirus extrusion (de Harven, Lampen & Sato, I973; Panem & Kirste