32Lower respiratory viral infections, such as influenza virus and severe acute respiratory syndrome 33 coronavirus 2 (SARS-CoV2) infections, often cause severe viral pneumonia in aged individuals. 34Here, we report that influenza viral pneumonia leads to chronic non-resolving lung pathology 35 and exaggerated accumulation of CD8 + tissue-resident memory T cells (TRM) in the respiratory 36 tract of aged hosts. TRM accumulation relies on elevated TGF-b present in aged tissues. Further, 37we show that TRM isolated from aged lungs lack a subpopulation characterized by expression of 38 molecules involved in TCR signaling and effector function. Consequently, TRM cells from aged 39 lungs were insufficient to provide heterologous protective immunity. Strikingly, the depletion of 40 CD8 + TRM cells dampens persistent chronic lung inflammation and ameliorates tissue fibrosis in 41 aged, but not young, animals. Collectively, our data demonstrate that age-associated TRM cell 42 malfunction supports chronic lung inflammatory and fibrotic sequelae following viral pneumonia 43 in aged hosts. 44 45 46 47 48