Hyperinflammation and immunomodulation in influenza, SARS-CoV-2 and syncytial respiratory virus infection in adults: from innate immune responses and biomarkers to clinical and therapeutic implications.

Influenza, SARS-CoV2-2 and syncytial respiratory virus infection in adults are major causes of morbidity and mortality. However, the pathophysiological mechanisms underlying these infections remain incompletely understood. Disease severity results from an interaction between viral factors and host responses. Lung damage and respiratory failure are produced by hyperinflammation. Understanding these mechanisms is necessary to improve risk stratification and may guide therapeutic decisions. C- reactive protein (CRP), IL-6, ferritin, and ApoH are relevant biomarkers which can identify inflammatory phenotypes. Antivirals and supportive care are the main approaches for these viral infections. From a therapeutic perspective, broad immunosuppression is unlikely to be optimal, and strategies should focus on selectively modulating harmful inflammation while preserving antiviral immunity. Nevertheless, there is scarce evidence of the best choice of treatment based on the patient's clinical profile and further studies are needed.