Table 1.
Viruses and mice used in this study.
| Genetic Background | Virus | Genotype of virus | Phenotype of virus |
| KOS | wild-type | wild-type | |
| KOS-GFPa | CMV-GFP cassette between UL26 and UL27 genes | wild-type [56] | |
| KOS | n212b | ICP0- null | IFN-sensitive [14] |
| 0--GFPc | ICP0- null | IFN-sensitive (Fig. 5B) | |
| n12d | ICP4- null | replication-defective [55] | |
| Genetic Background | Mouse | Immunological status of mouse | |
| BALB/c | BALB/c scide |
immunocompetent lymphocyte-deficient [64] |
|
| Strain 129 | immunocompetent | ||
| PML-/- f | immunocompetent [63] | ||
| rag2-/- g | lymphocyte-deficient [64] | ||
| ifngr-/- | IFN-γ receptor-null [65] | ||
| ifnar-/- | IFN-α/β receptor-null [66] | ||
| Strain 129 | ifnar-/- ifngr-/- | IFN-α/β receptor-null + IFN-γ receptor-null [67] | |
| stat1-/- | Stat 1-null [68] | ||
| rag2-/- stat1-/- | lymphocyte-deficient + Stat 1-null | ||
| rag2-/- ifnar-/- | lymphocyte-deficient + IFN-α/β receptor-null | ||
a The HSV-1 recombinant virus KOS-GFP contains a 2.0 kbp insertion in the intergenic region between the UL26 and UL27 genes of HSV-1 strain KOS, which contains a cytomegalovirus (CMV) IE promoter driving the expression of the green-fluorescent protein (GFP).
b The ICP0- null mutant n212 contains a 14 bp insertion, ctagactagtctag, in codon 212 of the ICP0 gene of HSV-1 strain KOS, which inserts stop codons into all three open-reading frames of the ICP0-encoding DNA strand. Illustrated in Figure 4.
c The ICP0- null mutant 0--GFP contains an ~770 bp insertion in codon 105 of the ICP0 gene of HSV-1 strain KOS, which inserts a GFP coding sequence and 'taa' terminator codon into the ICP0 open-reading frame. Illustrated in Figure 4.
d The ICP4- null mutant n12 contains a 16 bp insertion, ggctagttaactagcc, in codon 262 of the ICP4 gene of HSV-1 strain KOS, which inserts stop codons into all three open-reading frames of the ICP4-encoding DNA strand.
e SCID: severe-combined immunodeficiency is a phenotype that results from any one of dozens of genetic mutations that block lymphocyte maturation. The genetic lesion that accounts for the SCID phenotype of scid mice lies in the gene that encodes the catalytic subunit of the DNA-dependent protein kinase. This protein is necessary to repair double-stranded DNA breaks, and is essential to complete V-D-J recombination of either the T cell receptor gene or the B cell receptor gene.
f PML: a protooncogene which, when mutated, is associated with promyelocytic leukemia.
g RAG2: recombination-activated gene 2, which encodes a protein necessary to initiate V-D-J recombination of the T cell receptor gene or B cell receptor gene.