Abstract: The present invention provides compositions and means to identify compositions that increase ?1 PRF programmed ribosomal frameshift (?1PRF) efficiencies and/or decrease peptidyltransferase activity in a cell, and thus directly affect viral replication or assembly of viral particles. Compositions identified in accordance with the invention specifically inhibit the interaction between ribosomal protein L41 and the ribosomes thereby resulting in decreased peptidyltransferase activity of the ribosomes. Decreases in peptidyltransferase activity have been associated with increased ?1 PRF efficiencies, which in turn interfere with self assembly of ?1PRF dependent viruses thereby interfering with virus propagation. Compositions in accordance with the invention are useful as antiviral therapeutics for treating a viral infection in a patient.

Abstract: The invention is directed to a method of stimulating PRF in a viral cell by administering an aminoglycoside antibiotic to said cell. In another embodiment, the invention is directed to a method of inhibiting viral replication by administering an aminoglycoside antibiotic to a viral cell. The invention is also directed to method of treating a viral infection in a patient suffering therefrom comprising administering to said patient an aminoglycoside antibiotic.

Abstract: The present invention provides compositions and means to identify compositions that increase ?1 PRF programmed ribosomal frameshift (?1PRF) efficiencies and/or decrease peptidyltransferase activity in a cell, and thus directly affect viral replication or assembly of viral particles. Compositions identified in accordance with the invention specifically inhibit the interaction between ribosomal protein L41 and the ribosomes thereby resulting in decreased peptidyltransferase activity of the ribosomes. Decreases in peptidyltransferase activity have been associated with increased ?1 PRF efficiencies, which in turn interfere with self assembly of ?1PRF dependent viruses thereby interfering with virus propagation. Compositions in accordance with the invention are useful as antiviral therapeutics for treating a viral infection in a patient.

Abstract: Disclosed are transgenic plants containing an exogenous nucleic acid encoding an L3 protein. The plant exhibits increased resistance to viruses and/or fungi that infect plants. The L3 proteins include wild-type proteins, spontaneously occurring mutants and non-naturally occurring L3 mutants. Also disclosed are methods of reducing the toxicity of single-chain ribosome inhibitory proteins in cells, e.g., yeast, plant and animal cells, by co-administering the L3 protein with the RIP. Further disclosed are non-naturally occurring L3 mutants that (a) substantially fail to bind single-chain RIPs that bind endogenous L3 proteins, (b) are unable to maintain M1 killer virus, (c) promote altered programmed ribosomal frameshift efficiency, (d) exhibit resistance to peptidyltransferase inhibitors, and combinations of any of (a)–(d).

Abstract: An isolated multiprotein complex of S. cerevisiae components is provided that is effective to modulate peptidyl transferase activity during translation. This complex includes a Modulator of Translation Termination protein (Mtt1p, also referred to as helicase B), a Upf1 protein, a peptidyl eukaryotic release factor 1 (eRF1) and a peptidyl eukaryotic release factor 3 (eRF3).

Abstract: This invention provides a method of modulating translation termination efficiency of mRNA and/or promoting degradation of abberant transcripts. Also, this invention provides a method of screening for a drug active involved in enhancing translation termination and a method for identifying a disease state involving defective the protein complex.

Abstract: This invention provides a method for modulating the efficiency of translation termination of messenger RNA. Also provided are methods of screening for compositions and agents capable of modulating translation termination.