Microtubule detyrosination links inflammasome activation to apoptotic cell death in macrophages upon influenza A virus infection

Programmed cell death is an essential host response to viral infection, but whether infected macrophages undergo inflammatory or non-inflammatory forms of death has important consequences for disease progression. In this study, we found that influenza A virus infection induces a modification of microtubules known as detyrosination, which stabilizes their structure. This change was driven by the host enzyme vasohibin-1 through activation of the inflammasome, a key signaling complex that normally promotes inflammatory cell death. Remarkably, enhanced detyrosination shifted dying cells away from inflammatory membrane rupture toward apoptosis, an immunologically silent cell death pathway that preserves membrane integrity. Our findings identify microtubule detyrosination as a stress-induced host response during influenza A virus infection, highlighting a novel mechanism by which cytoskeletal modification influences the outcome of infection.