Herpes simplex virus thymidine kinase and specific stages of latency in murine trigeminal ganglia.
From marker rescue, sequencing, transcript, and latency analyses of the thymidine kinase-negative herpes simplex virus mutant dlsactk and studies using the thymidine kinase inhibitor Ro 31-5140, we infer that the virus-encoded thymidine kinase is required in murine trigeminal ganglia for acute replication and lytic gene expression, for increasing the numbers of cells expressing latency-associated transcripts, and for reactivation from latent infection.
Jacobson
J G
JG
Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115.
Ruffner
K L
KL
Kosz-Vnenchak
M
M
Hwang
C B
CB
Wobbe
K K
KK
Knipe
D M
DM
Coen
D M
DM
D000818:Animals; D001483:Base Sequence; D017931:DNA Primers / Q000737:chemistry; D005814:Genes, Viral; D051379:Mice; D008969:Molecular Sequence Data; D018139:Simplexvirus / Q000201:enzymology / Q000254:growth & development*; D013937:Thymidine Kinase / Q000235:genetics*; D012668:Trigeminal Ganglion / Q000382:microbiology*; D015678:Viral Structural Proteins / Q000235:genetics; D017735:Virus Latency; D014779:Virus Replication
D017931:DNA Primers; D015678:Viral Structural Proteins; D013937:Thymidine Kinase