Skip to main content

Table 1 Viruses and mice used in this study.

From: ICP0 antagonizes Stat 1-dependent repression of herpes simplex virus: implications for the regulation of viral latency

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

scid e

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

  1. 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).
  2. b The ICP0- null mutant n212 contains a 14 bp insertion, ctag actag tctag, 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.
  3. 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.
  4. d The ICP4- null mutant n12 contains a 16 bp insertion, ggctag ttaa ctag cc, 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.
  5. e SCID: s evere-c ombined i mmunod eficiency 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.
  6. f PML: a protooncogene which, when mutated, is associated with p rom yelocytic l eukemia.
  7. g RAG2: r ecombination-a ctivated gene 2, which encodes a protein necessary to initiate V-D-J recombination of the T cell receptor gene or B cell receptor gene.
Back to article page

Virology Journal

ISSN: 1743-422X