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. 2012 Jan;86(2):1059–1068. doi: 10.1128/JVI.06202-11

Fig 4.

Fig 4

(A) The γ134.5 null mutant triggers phosphorylation of p65/RelA and IKKβ. Immature CD11c+ DCs were mock infected or infected with R3616 (5 PFU per cell). At the indicated time points, lysates of cells were processed for Western blot (WB) analysis with antibodies against p65/RelA, phosphorylated p65/RelA, IKKβ, phosphorylated IKKβ, and β-actin. (B) The γ134.5 null mutant stimulates p65/RelA nuclear translocation in DCs. Cells were infected as described for panel A, and the cytoplasmic and nuclear fractions were prepared for Western blot analysis with antibodies against p65, GRP78, and histone H3. (C) Growth of R3616 in DCs. Immature CD11c+ DCs were infected with R3616 as described above, and viral titers were measured at the indicated time points. (D) Viral gene expression. Immature CD11c+ DCs were infected with R3616, and the expression of ICP27, UL30, and UL44 was determined by quantitative real-time RT-PCR. The results are from triplicate samples with standard deviations.