Abstract: Characterization of a pandemic 2009 H1N1 influenza virus isolated from a fatal case patient (F-IAV), showed the presence of three different mutations; potential determinants of its high pathogenicity that were located in the polymerase subunits (PB2 A221T and PA D529N) and the hemagglutinin (HA S110L).
Abstract: Recombinant viruses containing individually or in combination the polymerase mutations in the backbone of A/California/04/09 (CAL) showed that PA D529N was clearly involved in the increased pathogenicity of the F-IAV virus.
Adaptive Mutations in Influenza A/California/07/2009 Enhance Polymerase Activity and Infectious Virion Production.
Discussion: The PA A638R mutation was previously linked to an increase in the production of DVGs, while the D529N mutation was shown to decrease DVG accumulation.
Reduced accumulation of defective viral genomes contributes to severe outcome in influenza virus infected patients.
Result: To confirm that the PA D529N mutation in F-IAV has a major effect on the ability to produce low DVGs numbers, we generated recombinant CAL viruses bearing mutations in genes other than polymerase subunits, such as matrix 1 (M1) and matrix 2 (M2) viral genes (M1 S30N + M2 V86S).
Discussion: We tested this hypothesis genetically by analyzing recombinant viruses bearing mutations identified in a fatal-outcome virus (F-IAV, mutations PB2 A221T and PA D529N) or described elsew
IV mutation literature information.
PMID: 
2019
Frontiers in immunology
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