Abstract
We have inserted a modified Escherichia coli lacZ gene, placed under the control of herpes simplex virus α4 or ,β8 regulatory signals, into the HSV-1 genome disrupting the viral thymidine kinase gene. Using β-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 β-galactosidase expression in neuronal cells indicates that TK-deficient viruses are capable of invading mouse neuronal cells and expressing up to the β class of gene product.
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