TABLE 1.
Ability of ICP27 kinase consensus site mutants to complement ICP27 deletion virus growtha
| Plasmid | Viral yield (PFU)
|
Complementation indexb
|
||
|---|---|---|---|---|
| Expt 1 | Expt 2 | Expt 1 | Expt 2 | |
| pGEM | 1.0 × 104 | 4.1 × 105 | 1 | 1 |
| Wild-type ICP27 | 2.0 × 105 | 5.9 × 106 | 20 | 14.3 |
| ΔNES | 4.0 × 104 | 4 | ||
| Δ16–18aa | 1.5 × 105 | 15 | ||
| Δ44–46aa | 1.5 × 105 | 15 | ||
| D2ΔS5 | 5.0 × 105 | 1.2 | ||
| H17 | 2.8 × 105 | 0.7 | ||
| S114A | 2.9 × 106 | 7.1 | ||
RSF cells were transfected with different ICP27 mutant constructs individually as indicated and then infected with an ICP27 deletion virus. The progeny viruses were assayed on the ICP27-complementing cell line 2-2. Average values of two separate transfections for each plasmid are shown.
pGEM-1 vector served as a negative control; its ability to support ICP27 deletion virus growth is arbitrarily defined as an index value of 1. The growth complementation indices of ICP27 mutants were equal to the ratio of the yield of ICP27 deletion virus in RSF cells transfected with a mutant plasmid to the yield in RSF cells transfected with pGEM-1.