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COVID-19 Usurps Host Regulatory Networks
Colleen S Curran1, Donna R Rivera2, Jeffrey B Kopp3
1Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, MD, United States.
Frontiers in Pharmacology
|September 14, 2020
Summary
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection disrupts key physiological systems, including the renin-angiotensin-aldosterone system (RAAS). Understanding these disruptions may reveal new treatments for COVID-19 and related conditions.
Area of Science:
- Physiology
- Pathophysiology
- Virology
Background:
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19 by binding to angiotensin-converting enzyme 2 (ACE2) on cell surfaces.
- ACE2 normally inhibits inflammatory signals in the renin-angiotensin-aldosterone system (RAAS), complement, coagulation, and kallikrein-kinin system (KKS).
- Dysregulation of these pathways is common in patients with comorbidities like hypertension and diabetes, potentially increasing SARS-CoV-2 susceptibility.
Purpose of the Study:
- To understand the pathophysiological effects of SARS-CoV-2 on RAAS, complement, coagulation, and KKS.
- To explore the link between viral activation of these pathways and COVID-19 manifestations.
- To identify potential therapeutic targets for mitigating COVID-19 symptoms and complications.
Main Methods:
- The study reviews existing literature on SARS-CoV-2 interactions with ACE2 and its downstream effects on major physiological systems.
- It analyzes the role of RAAS, complement, coagulation, and KKS in the pathophysiology of COVID-19.
- It discusses potential pharmacological interventions targeting these pathways.
Main Results:
- SARS-CoV-2 infection can lead to vasoconstrictive, prothrombotic, and pro-inflammatory states through activation of RAAS, complement, coagulation, and KKS.
- Alterations in these pathways may contribute to COVID-19 susceptibility and severity in patients with pre-existing conditions.
- Specific COVID-19 symptoms, including skin, sensory, and CNS manifestations, may be linked to viral pathway activation.
Conclusions:
- Targeting molecules within the RAAS, complement, coagulation, and KKS pathways offers potential for adjunctive treatments in COVID-19.
- Further research into these physiological networks is crucial for identifying effective therapies and patient subgroups who may benefit most.
- Understanding these interactions is vital in the absence of universally effective antiviral treatments.
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