Article Figures & Data
Figures
- FIG. 1.
Host gene expression regulated by VV. Host genes which were differentially induced during infection with all VV constructs are shown. Genes were sorted based on a threefold (P < 0.01) or greater level of induction for wtVV at 6 hpi and were also significantly induced by VVE3LΔ83N, VVE3LΔ26C, and VVΔE3L. Red boxes represent genes which were significantly induced. Changes (n-fold) in expression levels relative to those of mock-infected cells are shown within each box. TGFB, transforming growth factorβ .
- FIG. 2.
Host gene expression regulated by the C-terminal dsRNA-binding domain of E3L. Host genes which were differentially expressed during infection with VV constructs lacking the C-terminal dsRNA-binding domain of E3L (VVE3LΔ26C and VVΔE3L) are shown. In the left panel, genes were sorted based on a threefold (P < 0.01) or greater level of induction for VVE3LΔ26C at 6 hpi and were unaltered during wtVV infection. The right panel represents genes which were induced during infection with all VV constructs (yellow boxes) but much more highly induced during infection with VVE3LΔ26C (red boxes). Changes (n-fold) in expression levels relative to those of mock-infected cells are shown within each box.
- FIG. 3.
Host gene expression regulated by the N-terminal Z-DNA-binding domain of E3L. Host genes which were differentially expressed during infection with VV constructs lacking the N-terminal Z-DNA-binding domain of E3L (VVE3LΔ83N and VVΔE3L) are shown. Genes were sorted based on a twofold (P ≤ 0.01) or greater level of induction or repression for VVE3LΔ83N at 2 hpi and were unaltered during wtVV infection. Red boxes represent genes which were significantly induced. Changes (n-fold) in expression levels relative to those of mock-infected cells are shown within each box.
- FIG. 4.
VV regulation of the host inflammatory response. Cells were infected with wtVV, VVE3LΔ83N, VVE3LΔ26C, or VVΔE3L, and the differential expression levels of host genes involved in several proinflammatory responses are shown. Shades of red indicate host gene induction, and shades of green indicate host gene repression. Gray represents cDNA sequences that were not present on all arrays used.
- FIG. 5.
VV regulation of signal transduction. Cells were mock infected or infected with wtVV, VVE3LΔ83N, VVE3LΔ26C, or VVΔE3L. Extracts were prepared at 6 hpi and 12 hpi and analyzed for the presence of phosphorylation, nuclear translocation, or degradation of key components of several host signal transduction cascades by Western blot analysis. During gel electrophoresis, equal protein amounts were loaded into each lane. Chemiluminescent bands corresponding to each protein were quantified using ImageQuant software and graphed. Extracts were assayed in duplicate, and graphs illustrate representative results. Nuclear accum., nuclear accumulation.
- FIG. 6.
VV regulation of the host IFN response. (A) Cells were infected with wtVV, VVE3LΔ83N, VVE3LΔ26C, or VVΔE3L, and the differential expression levels of host genes involved in the IFN response are shown. Shades of red indicate host gene induction, and shades of green indicate host gene repression. Gray represents samples which were eliminated due to chip errors. (B) Cells were mock infected or infected with wtVV or VVΔE3L. At 3 hpi, cells were treated with 100 IU/ml IFN-α for 15 min. Extracts were prepared and analyzed for activation (phosphorylation) of STAT1 by Western blot analysis. During gel electrophoresis, equal protein amounts were loaded into each lane. Chemiluminescent bands corresponding to STAT1 were quantified using ImageQuant software and graphed. ISRE, interferon-stimulated response element; GAS, gamma interferon-activated site.
