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.

Thermodynamic, kinetic, and dynamic analyses as well as solubility proteome profiling reveal that influenza A virus liquid inclusions may be selectively hardened with promising antiviral activity.

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

Despite the virus' error prone polymerase, influenza virus antigenic evolution is rare, even in previously immune hosts, virus replication occurs before producing new antibodies.

Host protein kinase C family members regulate influenza virus genome replication by phosphorylating the viral nucleoprotein and controlling assembly of the viral replication machinery.

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.

By distributing receptor-binding and receptor-destroying proteins asymmetrically on their surface, filamentous influenza A virus particles create a Brownian ratchet that facilitates their passage through mucus.

Single-cell mRNA sequencing shows that the impact of infection with influenza virus varies dramatically from one cell to another.

Quantification of both viral transcription and progeny production from single influenza-infected cells shows that the cells that produce the most viral RNA often do not produce the most virions.

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.