Pathogenesis of Acute Respiratory Distress in SARS-CoV-2 Infection: Molecular and Clinical Investigation

Acute respiratory distress syndrome (ARDS) is a life-threatening condition with high mortality, often triggered by severe lung infections such as those caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). By disrupting immune regulation and inducing excessive cytokine release, SARS-CoV-2 plays a key role in the onset and progression of ARDS. Approximately 10.4% of intensive care unit (ICU) admissions are due to ARDS, with mortality rates ranging from 30% to 50% depending on severity. Viral entry occurs when the spike (S) protein binds to the angiotensin-converting enzyme 2 (ACE2) receptor and is primed by transmembrane protease serine 2 (TMPRSS2), enabling penetration into respiratory epithelial cells. Subsequent viral replication and immune hyperactivation trigger a “cytokine storm,” leading to alveolar and capillary membrane damage, increased pulmonary permeability, and alveolar edema, hallmark features of ARDS. This study reviews the SARS-CoV-2 life cycle, structural and functional characteristics, ARDS pathophysiology, diagnostic approaches including real-time polymerase chain reaction (RT-PCR) and inflammatory biomarkers, and emerging therapeutic strategies. Understanding the molecular pathways underlying viral invasion, immune dysregulation, and lung injury may facilitate the development of targeted therapies for affected patients.