Genome sequence data from 58 Mexican swine influenza A viruses resolves the spatial origin of the virus that originated the influenza pandemic of 2009.

The local fitness landscape of an antigenic region in influenza neuraminidase was determined by combinatorial mutagenesis and next-generation sequencing.

Deep mutational scanning was used to comprehensively quantify the effects of mutations to influenza hemagglutinin and shows that the virus possesses a high inherent mutational tolerance at key antigenic sites.

Combined antigenic and genetic analysis shows that different strains of the human influenza virus display dramatically different rates of antigenic drift, and that these differences have a significant impact on the number of new infections in each flu season.

The frequent co-occurrence of two variants of influenza is due to the fact that they cooperate, meaning that a mixed population grows better than either variant alone.

Swine populations worldwide are sporadically infected by influenza viruses from humans and birds leading to geographically heterogeneous swine influenza virus populations that pose epizootic and pandemic threats.

Phylogenetic relationships between viral RNA segments are distinct between subtypes and lineages of seasonal human influenza A viruses and implicate RNA-RNA relationships as novel drivers of influenza virus evolution.

Chicken ANP32A, and not chicken ANP32B, supports influenza polymerase activity and thus editing of this single gene may generate chickens that are resilient to influenza virus infection.

Vaccination has the potential to decrease swine influenza diversification by restricting influenza virus co-infections and reassortment events in pigs.

The analysis of the genomes of two lineages of influenza B virus (Victoria and Yamagata) reveal that their phylodynamics are fundamentally different, and are determined by a complex relationship between virus transmission, age of infection and receptor binding preference.