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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.

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.

An anti-influenza receptor binding site antibody acquires breadth through hierarchical sets of epistatic mutations distributed across the light and heavy chains, demonstrating how mutations can interact to shape the evolution of antibody breadth in various antigen exposure regimens.

CR9114, one of the most broadly neutralizing anti-influenza antibodies characterized to date, acquires affinity to divergent HA subtypes sequentially, due to higher order interactions between the nested sets of mutations required for binding each distinct subtype.

Infection of human cells by influenza A virus induces changes in the alternative splicing of host genes that, in turn, promote viral replication.

Hyperglycaemia increases influenza severity by damaging the pulmonary epithelial-endothelial barrier and increasing pulmonary oedema during Influenza A virus infection.

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.

Endoplasmic reticulum proteostasis factors enhance the mutational tolerance of influenza hemagglutinin, a model secretory pathway protein and therapeutic target, particularly improving the fitness of temperature-sensitive variants.

Identification of transcriptional changes in the hypothalamus during Influenza A virus infection enhances our understanding of mechanisms underlying long-lasting neurological disturbances, potentially informing future therapeutic interventions and improving patient outcomes.

By comparing gene expression in people before and after they received the influenza vaccine, researchers were able to identify genes that contribute to differences in individual responses to vaccination.