Complete mapping of human-adaptive mutations to the avian influenza PB2 protein shows how selection at key molecular interfaces combines with evolutionary accessibility to shape viral host adaptation.

The global suitability for avian flu H5N1 in poultry is predicted and spatially cross-validated, highlighting areas where the disease can spread in the absence of prevention and control, and represent a public health threat.

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.

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.

Longitudinal monitoring of poultry farms in southern Vietnam reveals that when outbreaks occur with symptoms similar to highly pathogenic avian influenza, farmers respond by sending their chickens to market early.

Influenza transmission among ferrets correlates strongly with transmission among humans, so the ferret model for influenza transmission is a valid tool for pandemic potential in humans.

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

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.

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