During adaptation in dogs, H3N2 canine influenza viruses (CIVs) became to recognize human-like SAα2,6-Gal receptor, increased replication ability in human cells, acquired a 100% transmission rate via respiratory droplet in ferret model, and human population lacked immunity to H3N2 CIVs.

The H3N2 canine influenza virus – which originally came from birds – is evolving to become more transmissible between dogs.

A new assay for specific mutational classes provides preciseestimates of the mutation rates and mutational bias for influenza A viruses.

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

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

The abundance and complex genetic diversity of swIAV were documented and the zoonotic potential evaluated.

The intracellular SOCS5 protein has a unique and key role in restraining influenza A infection by regulating epidermal growth factor receptor signaling in airway epithelial cells.

Host protein homeostasis is a critical force shaping influenza evolution, impacting both the nature of selection on the influenza genome and the accessibility of specific mutational trajectories.

N2 neuraminidases from human H3N2 viruses from 2009 until 2017 can be subdivided into four antigenic groups, with amino acid substitutions near the catalytic site more likely impacting neuraminidase inhibition.

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.