HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Roemer, K. Articles by Friedmann, T. Search for Related Content PubMed PubMed Citation Articles by Roemer, K. Articles by Friedmann, T. Agricola Articles by Roemer, K. Articles by Friedmann, T.

Recombination between a herpes simplex virus type 1 vector deleted for immediate early gene 3 and the infected cell genome

Center for Molecular Genetics, University of California, San Diego, M-0634 La Jolla, California 92093, U.S.A.

We have used a vector derived from a herpes simplex virus type 1 (HSV-1) mutant deleted for 3.6 kbp of the essential immediate early gene 3 to transduce the Tn5 neomycin phosphotransferase (neo^r) gene into rodent and primate cells in culture. The transgene was flanked by genomic sequences from the human hprt gene. We demonstrate in this study that sequences introduced by infection with the replication-defective HSV vector can be stably inserted into the cell genome by recombination. Both the efficiency of stable transduction, measured by the number of neo^r-positive colonies, and the number and length of the transgene sequences inserted into the cell genome were found to be a function of cell type. The transduction efficiency appeared to be influenced, at least in part, by the cytopathic potential of the replication-defective HSV-1 vector, which was more pronounced in primate than in rodent cells.

Received 19 November 1991; accepted 5 February 1992.