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1 Department of Genetics and Microbiology, University of Geneva Medical School (CMU), 9 Ave Champel, CH1211 Geneva, Switzerland
2 Department of Viral Infection, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108, Japan
Several years ago, we reported that a Sendai virus (SeV) defective genome (DIH4UV) could be rescued in vivo with human parainfluenza virus type 1 (hPIV1) and bovine PIV3 but not by measles virus or vesicular stomatitis virus. It was concluded that the cis-acting RNA sequences were conserved within the SeV/PIV1/PIV3 group but that interactions between the polymerase complex (P-L) and the template protein N were unique for each virus. We have re-examined these conclusions using proteins expressed from cloned N, P and L genes for SeV and PIV3. The results demonstrate the specificity of the protein-protein interactions between polymerase and template, and confirm the prediction of the earlier work that PIV3 N, P and L proteins are capable of assembling and replicating SeV minigenomes also expressed from a cDNA clone.
Received 6 March 1996;
accepted 17 June 1996.
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