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Published on: September 27, 2024
Possible Role of Adenosine in COVID-19 Pathogenesis and Therapeutic Opportunities
Jonathan D Geiger1, Nabab Khan1, Madhuvika Murugan2
1Department of Biomedical Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND, United States.
Abstract:
The outbreak of the novel coronavirus disease 2019 (COVID-19) caused by Severe Acute Respiratory Syndrome CoronaVirus-2 (SARS-CoV-2) requires urgent clinical interventions. Crucial clinical needs are: 1) prevention of infection and spread of the virus within lung epithelia and between people, 2) attenuation of excessive lung injury in Advanced Respiratory Distress Syndrome, which develops during the end stage of the disease, and 3) prevention of thrombosis associated with SARS-CoV-2 infection. Adenosine and the key adenosine regulators adenosine deaminase (ADA), adenosine kinase (ADK), and equilibrative nucleoside transporter 1 may play a role in COVID-19 pathogenesis. Here, we highlight 1) the non-enzymatic role of ADA by which it might out-compete the virus (SARS-CoV-2) for binding to the CD26 receptor, 2) the enzymatic roles of ADK and ADA to increase adenosine levels and ameliorate Advanced Respiratory Distress Syndrome, and 3) inhibition of adenosine transporters to reduce platelet activation, thrombosis and improve COVID-19 outcomes. Depending on the stage of exposure to and infection by SARS-CoV-2, enhancing adenosine levels by targeting key adenosine regulators such as ADA, ADK and equilibrative nucleoside transporter 1 might find therapeutic use against COVID-19 and warrants further investigation.
Insights
Adenosine regulators like ADA and ADK may offer new COVID-19 therapies. Targeting these, along with adenosine transporters, could prevent infection, reduce lung injury, and combat thrombosis in Severe Acute Respiratory Syndrome CoronaVirus-2 patients.
Area of Science:
- Immunology
- Virology
- Pharmacology
Background:
- The COVID-19 pandemic caused by SARS-CoV-2 presents significant clinical challenges, including viral spread, severe lung injury (ARDS), and thrombosis.
- Adenosine and its regulators (ADA, ADK, ENT1) are implicated in COVID-19 pathogenesis.
Purpose of the Study:
- To explore the therapeutic potential of adenosine and its regulators in managing COVID-19.
- To investigate the roles of ADA, ADK, and ENT1 in SARS-CoV-2 infection and associated complications.
Main Methods:
- Review of existing literature on adenosine metabolism and its interaction with SARS-CoV-2.
- Analysis of the non-enzymatic and enzymatic functions of ADA and ADK in the context of COVID-19.
- Evaluation of the potential of targeting adenosine transporters (ENT1) for therapeutic benefit.
Main Results:
- Adenosine deaminase (ADA) may inhibit SARS-CoV-2 entry by competing for CD26 receptor binding.
- Adenosine kinase (ADK) and ADA can increase adenosine levels, potentially ameliorating Advanced Respiratory Distress Syndrome (ARDS).
- Inhibiting adenosine transporters may reduce platelet activation and thrombosis, improving COVID-19 outcomes.
Conclusions:
- Modulating adenosine levels through regulators like ADA, ADK, and ENT1 shows promise as a therapeutic strategy for COVID-19.
- Targeting adenosine pathways could address multiple facets of SARS-CoV-2 infection, including viral spread, lung injury, and thrombosis.
- Further research into adenosine-based therapies for COVID-19 is warranted.
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