Abstract
Plasmid DNA including the simian virus 40 (SV40) origin of replication undergoes uncontrolled, runaway replication in cos-1 cells owing to the intracellular production of SV40 large T antigen. Covalent linkage of such plasmids with human papillomavirus type 16 (HPV-16) DNA was found to prevent runaway replication. Replication control was found to be dependent on the presence of HPV-16 DNA sequences including the E1 open reading frame and part of the non-coding region.
† Present address: Department of Immunology, U.M.D.S. Guy's Campus, London SE1 9RT, U.K.
‡> Present address: Department of Medical Microbiology, St George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, U.K.
Present address: Department of Microbiology and Immunology, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, New York 14642, U.S.A.