Researchers identified the viral PB1 gene as the determinant allowing avian influenza strains to replicate at fever-range temperatures that suppress human-origin viruses. Mouse experiments confirmed that fever-level heat crippled human-derived strains but not avian strains bearing the PB1 variant. The finding highlights a specific genetic mechanism that could increase zoonotic risk if reassortment transfers PB1 variants into human-adapted influenza backbones. Authors used controlled infection models and sequencing to map the phenotypic effect to PB1. Clarification: PB1 is an influenza polymerase subunit; changes in polymerase function can alter replication efficiency at different host body temperatures, affecting host range and pathogenicity.