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. 2011 Aug 25;7(8):e1002157. doi: 10.1371/journal.ppat.1002157

Figure 5. ORF61 SIMs are essential for PML NB disruption in VZV-infected cells but not required for VZV replication in vitro.

Figure 5

(A) Confocal microscopy of melanoma cells that were infected with pOka and ORF61 SIM mutants for 6 h and stained for ORF61 (red), PML (green), and nuclei (blue). The images show association of puncta (indicated by white arrows) formed by ORF61 and SIM mutant proteins with PML NBs. Scale bars: 5 µm. (B) Confocal microscopy of melanoma cells that were infected with pOka and ORF61 SIM mutants for 24 h and stained for ORF61 (red), PML (green), and nuclei (blue). The images show PML NB dispersal in pOka- or SIM mutant-infected cells. Infected nuclei with abundant expression of ORF61 or SIM mutant proteins are outlined by dashed ovals. Scale bars: 10 µm. (C) PML NB frequencies (mean±SEM) in pOka/ORF61 SIM mutants-infected melanoma cells (Mock, N = 213; pOka, N = 206; mSIM-N, N = 212; mSIM-C, N = 202; mSIM-N&C, N = 232) and HELFs (Mock, N = 227; pOka, N = 221; mSIM-N, N = 235; mSIM-C, N = 225; mSIM-N&C, N = 214). (D) Expression of PML in melanoma cells and HELFs that were infected by pOka or ORF61 SIM mutants. VZV gE or IE63 serve as the control for VZV infection. (E) Replication of pOka and ORF61 SIM mutant viruses in melanoma cells over 5 days. Each point represents mean±SEM of virus titers from three replicates.