A latent, nonpathogenic HSV-1-derived vector stably expresses β-galactosidase in mouse neurons

Anthony T. Dobson, Todd P. Margolis, Farhad Sedarati, Jack G. Stevens, Lawrence T. Feldman

Research output: Contribution to journalArticle

214 Scopus citations

Abstract

A genetically engineered herpes simplex virus variant was constructed for use as a stable gene vector for neurons. To inhibit replication, the agent possessed a deletion in the immediate early gene ICP4, and to minimize reactivation from the latent state, the gene encoding the latency-associated transcript was deleted. The E. coli β-galactosidase gene under the control of the Maloney murine leukemia virus long terminal repeat promoter was inserted into the ICP4 region. When introduced into the peripheral nervous system, this virus established latent infections and stably expressed β-galactosidase in primary sensory neurons. Expression of β-galactosidase over a more limited time period was observed when the latent infection was established in motor neurons of the hypoglossal nucleus. Agents of this general design have considerable potential for use as gene vectors for studies of neuronal function and correction of genetic defects affecting neurons.

Original languageEnglish
Pages (from-to)353-360
Number of pages8
JournalNeuron
Volume5
Issue number3
DOIs
StatePublished - Sep 1990
Externally publishedYes

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