Table 1.

Complementation of HSV-1 viruses with mutations in ICP0, ICP4, OBP, or VP16 by adenovirus expression vectors

Complementing vectorNo. of plaques produced bya:
KOS7134n12hr94RP5
Controls
 None (Vero cells)128 ± 21 ± 00 ± 00 ± 03 ± 1
 None (complementing cells)b 62 ± 6 114 ± 6 104 ± 5 148 ± 5
Test vectorsc
 Ad.T-ICP0110 ± 2 90 ± 5 0 ± 00 ± 0186 ± 8
 Ad.T-n212122 ± 101 ± 10 ± 00 ± 09 ± 1
 Ad.T-ICP466 ± 111 ± 1 115 ± 7 0 ± 022 ± 1
 Ad.T-OBP99 ± 71 ± 00 ± 0 454 ± 14 8 ± 0
 Ad.T-OBPΨ97 ± 81 ± 10 ± 00 ± 06 ± 1
 Ad.T-VP16111 ± 20 ± 00 ± 00 ± 0 108 ± 6
 Ad.T-VP16Δ57 ± 10 ± 00 ± 00 ± 06 ± 1
 Ad.C-rtTA only112 ± 120 ± 00 ± 00 ± 04 ± 1
  • a Vero cells in six-well plates were infected with 100 to 200 PFU of wild-type HSV-1 strain KOS or KOS-derived mutant 7134 (ICP0), n12 (ICP4), hr94 (OBP), or RP5 (VP16). Mean numbers of HSV plaques (± standard deviations) observed on untreated Vero cells ( n = 2 per group), on complementing cells ( n = 3 per group), or on Vero cells superinfected with one of eight adenovirus vectors ( n = 2 per group) are given. The values for primary tests in which HSV-1 mutants were complemented with adenovirus vectors that provided the missing gene products intrans are shown in boldface type. Values with asterisks represent a more than 30-fold increase in the number of plaques formed on Vero cells relative to no-vector controls.

  • b Mutant viral inocula were plated on the following complementing cell lines: 7134, on L7 cells; n12, on E5 cells; hr94, on 2B.11 cells; and RP5, on E5 cells treated with 5 mM HMBA.

  • c Vero cells were coinfected with 10 PFU of Ad.C-rtTA/cell and 10 PFU of the indicated TRE adenovirus vector/cell and were overlaid with complete DMEM containing 1% methyl cellulose and 3 μM DOX.