SARS-CoV-2 pneumonia—receptor binding and lung immunopathology: a narrative review

Abstract

The current pandemic of COVID-19 caused thousands of deaths and healthcare professionals struggle to properly manage infected patients. This review summarizes information about SARS-CoV-2 receptor binding dynamics and intricacies, lung autopsy findings, immune response patterns, evidence-based explanations for the immune response, and COVID-19-associated hypercoagulability.

Diurnal Variation in SARS-CoV-2 PCR Test Results: Test Accuracy May Vary by Time of Day

“…Interactions of the immune system with viruses such as influenza, herpes, hepatitis B, and dengue has been shown to lead to diurnal variation in viral shedding and symptoms (Cermakian et al, 2013;Edgar et al, 2016;Scheiermann et al, 2018), and they influence vaccine effectiveness (Long et al, 2016;de Bree et al, 2020). For SARS-CoV-2, recent research suggests that levels of angiotensin-converting enzyme 2 (ACE2) receptors in the lung, which bind to the spike protein, are cyclical and that their disregulation is closely tied to cyclical viral entry and infection severity (Mehrabadi et al, 2021;Menezes et al, 2021;Zhuang et al, 2021b). Other work suggests that SARS-CoV-2 replication may be blocked by a circadian clock-modulating molecule (Sultan et al, 2021).…”

Pulmonary surfactant as a versatile biomaterial to fight COVID-19

“…As briefly mentioned above, infection with SARS-CoV-2 occurs through binding of the viral spike protein to the ACE-2 receptor, mainly expressed in the pulmonary system on endothelial cells and type II pneumocytes. Of note, the ACE-2 receptor is also expressed in other organs such as the intestine, heart and kidney, explaining the extrapulmonary symptoms such as diarrhea, nausea, cardiac injury and acute kidney injury [ 51 , 58 , 59 ]. As shown in Fig.…”

ACE2 and Innate Immunity in the Regulation of SARS-CoV-2-Induced Acute Lung Injury: A Review

“…Chen et al [ 88 ] found that the spike protein of SARS-CoV-2 mediated viral entry through the binding to ACE2 on the cell surface. Menezes et al [ 89 ] and Li et al [ 90 ] hypothesized that immune cells, including monocytes, neutrophils, lymphocytes, and natural killer cells, could travel to infected areas after breaking endothelial and epithelial barriers. These immune cells could eliminate infected cells as well as alveolar exudates, leading to uncontrolled inflammation [ 89 , 90 ].…”

“…Menezes et al [ 89 ] and Li et al [ 90 ] hypothesized that immune cells, including monocytes, neutrophils, lymphocytes, and natural killer cells, could travel to infected areas after breaking endothelial and epithelial barriers. These immune cells could eliminate infected cells as well as alveolar exudates, leading to uncontrolled inflammation [ 89 , 90 ]. Patel et al [ 91 ] found that patients who died from SARS-CoV-2 manifested massive infiltration of various immune cells in their alveolus, which formed a cytokine storm and resulted in lung failure ( Figure 2 ).…”