Beta-galactosidase as a marker in the peripheral and neural tissues of the herpes simplex virus-infected mouse.
We have inserted a modified Escherichia coli lacZ gene, placed under the control of herpes simplex virus alpha 4 or beta 8 regulatory signals, into the HSV-1 genome disrupting the viral thymidine kinase gene. Using beta-galactosidase as an in situ indicator of viral gene expression, we detected expression from these recombinant HSV in dermal and neural tissues of the BALB/c mouse. Our detection of beta-galactosidase expression in neuronal cells indicates that TK-deficient viruses are capable of invading mouse neuronal cells and expressing up to the beta class of gene product.
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Department of Medical Microbiology, Stanford University School of Medicine, California 94305.
Mocarski
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D000818:Animals; D005629:Frozen Sections; D005696:Galactosidases / Q000235:genetics*; D005786:Gene Expression Regulation; D006561:Herpes Simplex / Q000382:microbiology*; D051379:Mice; D008807:Mice, Inbred BALB C; D009474:Neurons / Q000201:enzymology / Q000382:microbiology*; D011401:Promoter Regions, Genetic; D012091:Repetitive Sequences, Nucleic Acid; D018139:Simplexvirus / Q000201:enzymology / Q000235:genetics* / Q000502:physiology; D012867:Skin / Q000382:microbiology; D013937:Thymidine Kinase / Q000235:genetics; D012668:Trigeminal Ganglion / Q000201:enzymology / Q000382:microbiology; D014779:Virus Replication; D001616:beta-Galactosidase / Q000032:analysis / Q000235:genetics*
D013937:Thymidine Kinase; D005696:Galactosidases; D001616:beta-Galactosidase