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

Jafari-Sales, Abolfazl; Nozohour-Leilabadi, Elham; Farahnaki-Sadabadi, Maryam; Safari, Maryam; Pashazadeh, Mehrdad

doi:10.33091/amj.2025.160850.2269

	Pathogenesis of Acute Respiratory Distress in SARS-CoV-2 Infection: Molecular and Clinical Investigation
Al- Anbar Medical Journal
Volume 21, Issue 4, October 2025, Pages 214-222 PDF (1.96 M)
Document Type: Review articles
DOI: 10.33091/amj.2025.160850.2269
Authors
Abolfazl Jafari-Sales¹^{, 2}^{, 3}; Elham Nozohour-Leilabadi²^{, 3}; Maryam Farahnaki-Sadabadi²^{, 4}; Maryam Safari²^{, 3}; Mehrdad Pashazadeh^* ²^{, 5}
¹Department of Microbiology, Kaz.C., Islamic Azad University, Kazerun, Iran
²Infectious Diseases Research Center, TaMS.C., Islamic Azad University, Tabriz, Iran
³Department of Microbiology, Ta.C., Islamic Azad University, Tabriz, Iran
⁴Department of Cellular and Molecular Biology, Ta.C., Islamic Azad University, Tabriz, Iran
⁵Department of Laboratory Sciences and Microbiology, TaMS.C., Islamic Azad University, Tabriz, Iran
Abstract
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.
Keywords
Acute respiratory distress syndrome; SARS-CoV-2; Spike protein; Angiotensin-converting enzyme 2; Transmembrane protease serine 2

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