FIG. 2.

The L segment of LCMV-WE controls the disappearance of PRH from liver cell nuclei. HepG2 cells were infected with LCMV reassortants (ARM/WE or WE/ARM) as described in Materials and Methods. The cells were stained with anti-Z (green) and anti-PRH (red) or anti-PML (blue). All cells were counterstained for DNA with DAPI. The effects of reassortant viruses on PRH expression and localization were determined by confocal microscopy. Hepatic cells infected with LCMV carrying the L RNA segment of WE had the same disruptive effects on PRH distribution as those infected with LCMV-WE (WE/WE) (similar to Fig. 1A and B). However, the hepatic cells infected with LCMV carrying the L RNA segment of ARM had no effect on the subcellular distribution of PRH (similar to Fig. 1). Magnification, ×300. The overlay is shown in yellow (OV), and the overlay of DAPI staining is designated OV+DAPI. FITC and Texas Red channels were recorded independently.