Mechanism of virus occlusion into A-type inclusion during poxvirus infection

The A-type inclusion (ATI), a product as a late function of some poxviruses, has different strain-specific properties, some containing mature viruses (V + ATI) and some without (V − ATI). The properties of virus-occluding factor (VO factor) responsible for the V + trait were examined either employing a cell fusion technique by inactivated Sendai virus or under the cell-free condition. The VO factor was synthesized late in the (V − virus-infection corresponding to the time of ATI formation. A proportion of the VO factor synthesized may rapidly attach to the surface of mature V+ viruses (vaccinia) so as to acquire the ability of occlusion within ATI, and a residual proportion of the VO factor released throughout the cytoplasm may attach similarly to that of (V − viruses carried in by cell fusion or added in vitro. Neither protein synthesis nor energy was required to occlude mature viruses into ATIs, and the V + trait occurred in the presence of rifampicin. Comparison of the electrophoresis distribution of proteins constituting V + and (V − virions revealed that the VO factor was identical with the VP 4c polypeptide located at the surface of vaccinia virion. The polypeptide showing the same mobility on polyacrylamide gel electrophoresis was also found in the postviral supernatant fraction prepared from V + virus-infected cells.