Key result
Mutation of residue T157 in the influenza A virus PA protein to alanine reduced cRNA synthesis and viral pathogenesis in mice, while mutation to glutamate was lethal to the virus.
Population
Influenza A virus PA protein mutants and mouse models for viral pathogenesis
Comparison
Mutations in the PA protein (T162A, T157A, T157E) vs Wild-type influenza A virus
Design
Preclinical
Authors
Loading...
Moderate PA protease reductions may spare influenza fitness; leaves open the activity threshold for RNP function in intact viruses.
Residue T157 in the influenza A virus PA protein is critical for the viral polymerase's capacity to synthesize cRNA and for overall viral viability and pathogenesis.
Huarte et al. (2003) studied Influenza A virus infection. T157A and T157E mutations in PA protein vs. Wild-type virus and T162A mutant was evaluated on Viral polymerase capacity to synthesize cRNA, protease activity, and viral pathogenesis. Mutation of residue T157 in the influenza A virus PA protein to alanine reduced cRNA synthesis and viral pathogenesis in mice, while mutation to glutamate was lethal to the virus.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: