TABLE 3.
Plaque-forming ability of ICP0 mutant viruses and induction of conjugated ubiquitin at centromeres during infectiona
| Virus | Relative plaque-forming ability on:
|
Detection of conjugated ubiquitin at centromeres by FK2 | ||
|---|---|---|---|---|
| U2OS | BHK | HFL | ||
| 17+ | 1 | 0.60, 0.68 | 0.70, 0.73 | + |
| dl1403 | 1 | 0.08, 0.04 | 0.000, 0.0004* | − |
| FXE | 1 | 0.08, 0.04 | 0.006, 0.008* | − |
| D22 | 1 | 0.05, 0.03 | 0.01, 0.003* | − |
| E32 | 1 | 0.19, 0.31 | 0.20, 0.14 | + |
| K144E | 1 | 0.05, 0.10 | 0.03, 0.08 | − |
| Q148E | 1 | 0.24, 1.08 | 1.00, 1.50 | + |
| N151D | 1 | 0.10, 0.14 | 0.38, 0.68 | − |
| M1 | 1 | 0.05, 0.04 | 0.31, 0.44 | + |
| D12 | 1 | 0.08, 0.24 | 0.25, 0.74 | + |
| E52X | 1 | 0.07, 0.20 | 0.10, 0.47 | + |
Titers of virus stocks were initially determined on U2OS cells, in which HSV-1 requires little ICP0 to stimulate virus growth. Dilutions of these virus stocks were then titrated simultaneously on all three cell lines, and the ratio of the titers in BHK and HFL cells to those in U2OS cells was calculated. The values given represent the results from two totally independent determinations. Asterisks indicate that the data for these viruses in HFL cells were nonlinear (as previously reported for ICP0-deficient viruses). The data in the rightmost column indicate the ability (+) or inability (−) of the ICP0 proteins to induce the formation of conjugated ubiquitin at centromeres in infected cells.