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Published on: May 16, 2019
Possible Benefits of Zinc supplement in CVD and COVID-19 Comorbidity
Muhammad Manjurul Karim1, Shahnaz Sultana2, Rokaia Sultana2
1Department of Microbiology, University of Dhaka, Dhaka 1000, Bangladesh.
Insights
Cardiovascular diseases (CVD) increase COVID-19 severity. Zinc supplementation may improve outcomes for COVID-19 patients with CVD by supporting ACE2 function and inhibiting viral replication.
Area of Science:
- Cardiology
- Virology
- Immunology
Background:
- Cardiovascular diseases (CVD) are highly prevalent and severe in COVID-19 patients.
- The interaction between CVD and COVID-19 complicates prognosis and treatment.
- ACE2, a SARS-CoV-2 receptor, plays a role in blood pressure regulation and is downregulated by the virus.
Purpose of the Study:
- To explore therapeutic strategies for COVID-19 patients with CVD.
- To identify treatments that balance the renin-angiotensin-aldosterone system (RAAS) arms.
- To investigate the potential role of zinc in managing comorbid CVD and COVID-19.
Main Methods:
- Review of existing literature on CVD, COVID-19, ACE2, RAAS, and zinc.
- Analysis of the molecular mechanisms linking SARS-CoV-2 infection, ACE2, and cardiovascular function.
- Exploration of zinc's biochemical properties relevant to viral replication and immune modulation.
Main Results:
- SARS-CoV-2 infection reduces functional ACE2 expression, potentially worsening CVD.
- A balanced approach to RAAS modulation is crucial for COVID-19 patients with CVD.
- Zinc exhibits immune-modulatory effects and can inhibit viral replication, with ACE2 being a zinc metalloenzyme.
Conclusions:
- Zinc supplementation may offer a beneficial therapeutic adjunct for COVID-19 patients with CVD.
- Targeting ACE2 and balancing RAAS are key considerations in managing these comorbidities.
- Further clinical investigation is warranted to confirm zinc's efficacy in this patient population.
Abstract:
As far as comorbidity is concerned, cardiovascular diseases (CVD) appear to be accounted for the highest prevalence, severity, and fatality among COVID 19 patients. A wide array of causal links connecting CVD and COVID-19 baffle the overall prognosis as well as the efficacy of the given therapeutic interventions. At the centre of this puzzle lies ACE2 that works as a receptor for the SARS-CoV-2, and functional expression of which is also needed to minimize vasoconstriction otherwise would lead to high blood pressure. Furthermore, SARS-CoV-2 infection seems to reduce the functional expression of ACE2. Given these circumstances, it might be advisable to consider a treatment plan for COVID-19 patients with CVD in an approach that would neither aggravate the vasodeleterious arm of the renin-angiotensinogen-aldosterone system (RAAS) nor compromise the vasoprotective arm of RAAS but is effective to minimize or if possible, inhibit the viral replication. Given the immune modulatory role of Zn in both CVD and COVID-19 pathogenesis, zinc supplement to the selective treatment plan for CVD and COVID-19 comorbid conditions, to be decided by the clinicians depending on the cardiovascular conditions of the patients, might greatly improve the therapeutic outcome. Notably, ACE2 is a zinc metalloenzyme and zinc is also known to inhibit viral replication.
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