Dissociation of Rabies Virus Matrix Protein Functions in Regulation of Viral RNA Synthesis and Virus Assembly

摘要: Recently, we have shown that the rabies virus (RV) matrix (M) protein regulates balance of RNA synthesis by shifting activity from transcription to replication (S. Finke, R. Mueller-Waldeck, and K. Conzelmann, J. Gen. Virol. 84:1613-1621, 2003). Here describe identification an M residue critical for regulation RV synthesis. By analyzing phenotype heterotypic proteins with respect SAD L16, identified ERA PV strains as deficient. Comparison sequences suggested a single residue, arginine 58, was critical. A recombinant having this amino acid exchanged glycine, M(R58G), has lost abilities downregulate stimulate replication. This resulted in increase rate more than 15-fold, previously observed deletion mutants. Most importantly, efficiencies assembly budding were equal wild-type determined assays studying transient complementation M- G-deficient construct, NPgrL. In addition, particle density, composition, specific infectivity L16 M(R58G) viruses identical. Thus, mutations affect function only synthesis, but not budding, providing evidence these functions are genetically separable.