Abstract / Summary
In older adults, respiratory viral infections should not be viewed solely as isolated acute events, but as part of a broader vaccine-modifiable clinical burden shaped by immunosenescence, multimorbidity and frailty. These interconnected factors increase susceptibility to respiratory viral infection, reduce vaccine-induced immune responses and contribute to more severe disease. Additional immune compromise, including haematological malignancy, solid organ transplantation and immunosuppressive therapy, may further increase vulnerability. Respiratory viral infections and non-communicable diseases interact bidirectionally. Chronic conditions such as diabetes, cardiovascular disease and chronic obstructive pulmonary disease increase the risk of severe respiratory infection, while infection may in turn precipitate exacerbation or destabilisation of underlying disease. In frail older adults, these effects may extend beyond the acute episode through functional decline and further loss of physiological reserve. Respiratory viruses account for a substantial proportion of community-acquired pneumonia (CAP) and may coexist with or predispose to secondary bacterial infection. Influenza virus, respiratory syncytial virus (RSV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are currently the principal vaccine-modifiable respiratory viral pathogens in older adults. Vaccination provides its strongest and most consistent protection against severe disease, hospitalisation and mortality, while effects on infection and other clinical endpoints vary by pathogen, vaccine and population. Emerging evidence further suggests potential benefits beyond acute respiratory outcomes, including reductions in selected cardiorespiratory complications and chronic disease destabilisation. This narrative review examines viral pneumonia in older adults at the intersection of immunosenescence, frailty, multimorbidity and immune compromise. We propose that vaccination should be considered not only as a means of preventing infection, but as a strategy to modify the broader clinical trajectory of respiratory viral disease, with the potential to reduce severe outcomes and limit downstream loss of health and physiological reserve.