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Published on: January 19, 2024
Conflicts over calcium and the treatment of COVID-19
1Department of Biological Sciences, Simon Fraser University, Burnaby, BC, Canada.
Insights
Calcium channel blockers may reduce COVID-19 mortality. Hypocalcemia, low serum calcium, is linked to severe COVID-19, potentially acting as a host defense mechanism against viruses, including SARS-CoV-2.
Area of Science:
- Virology
- Immunology
- Pharmacology
Background:
- Recent studies suggest calcium channel blockers (CCBs) like amlodipine and nifedipine may reduce COVID-19 mortality.
- Hypocalcemia (low serum ionized calcium) is strongly associated with increased COVID-19 severity.
- Similar associations between CCBs, hypocalcemia, and viral outcomes exist for other viruses.
Purpose of the Study:
- To evaluate the role of CCBs and hypocalcemia in the context of virus-host evolutionary conflicts over calcium metabolism.
- To explore hypocalcemia as a potential antiviral mechanism, considering it as pathology, viral manipulation, or host defense.
Main Methods:
- Review and synthesis of existing evidence on CCBs, hypocalcemia, and viral infections, particularly COVID-19.
- Evolutionary analysis of calcium metabolism in virus-host interactions.
Main Results:
- Evidence supports the hypothesis that hypocalcemia functions as a host defense mechanism against viral infections.
- CCBs may exert antiviral effects by interfering with calcium metabolism in infected cells, mirroring hypocalcemia's potential effects.
Conclusions:
- Hypocalcemia may represent a host defense strategy with antiviral properties, potentially modulated by CCBs.
- Further prospective clinical studies are needed to confirm the efficacy of CCBs and understand the role of hypocalcemia in treating COVID-19 and other viral diseases.
Abstract:
Several recent studies have provided evidence that use of calcium channel blockers (CCBs), especially amlodipine and nifedipine, can reduce mortality from coronavirus disease 2019 (COVID-19). Moreover, hypocalcemia (a reduced level of serum ionized calcium) has been shown to be strongly positively associated with COVID-19 severity. Both effectiveness of CCBs as antiviral therapy, and positive associations of hypocalcemia with mortality, have been demonstrated for many other viruses as well. We evaluate these findings in the contexts of virus-host evolutionary conflicts over calcium metabolism, and hypocalcemia as either pathology, viral manipulation or host defence against pathogens. Considerable evidence supports the hypothesis that hypocalcemia represents a host defence. Indeed, hypocalcemia may exert antiviral effects in a similar manner as do CCBs, through interference with calcium metabolism in virus-infected cells. Prospective clinical studies that address the efficacy of CCBs and hypocalcemia should provide novel insights into the pathogenicity and treatment of COVID-19 and other viruses.
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