Table 1.

Pros and cons for use of statins in people with COVID-19.

PROS
Area of interest (REF)	Action of statins	Clinical effect in people with SARS-CoV2 infection
Immunomodulation [10]	Stabilization of MyD88 levels during hypoxia and stress, mitigating the action of NF-kB	Potential to reduce the severity of SARS-CoV2 infection
Inflammation [13,14]	1.Reduction of LDL cholesterol levels, thereby reducing direct LDL cholesterol mediated inflammation 2)Inhibition of prenylation of G proteins, leading to downregulation of NF-kB, suppression of pro-inflammatory cytokines (TNF α, IL-6) and chemokines (IL-8)	Potential role in reduction of SARS-CoV2 induced lung injury and protection from cytokine storm
Oxidative Stress [18]	Reduction of oxidative injury/maintenance of the redox balance of the endothelium by: 1)Upregulation of nitric oxide synthase 2)Suppression of pro-oxidant enzymes (NADPH oxidase)	Potential role in reduction of SARS-CoV2 induced lung injury
Thrombosis [21,22]	1.Anti-platelet effect (Lipid dependent and lipid independent mechanisms) 2.Weak anti-thrombotic effect 1)Prevents the conversion of factor X to Xa by downregulating tissue factor 2)Upregulation of thrombomodulin to bind thrombin	Potential to reduce/prevent venous and arterial thrombus formation
Membrane (lipid) rafts [23]	Disruption of lipid rafts by depletion of cholesterol from the plasma membrane, which might alter the assembly of angiotensin converting enzyme 2 receptors (act as co-receptors for SARS-CoV2 entry into the cell)	Theoretical possibility of reducing viral entry, leading to low viral titres and infectivity
Angiotensin converting enzyme 2 (ACE2) [4,24]	Upregulation of expression of ACE2	Potential to reduce SARS-CoV2 induced lung injury mediated by excess Angiotensin-II
SARS-CoV2 main protease [26]	Efficient inhibitors of SARS-CoV2 main protease (Computational molecular docking method)	Potential to directly inhibit the virus, reducing viral load
CONS
Total and LDL cholesterol levels [7]	Reduction of serum total and LDL cholesterol	Speculated that this might increase morbidity/mortality from SARS-CoV2 infection, as elevated LDL cholesterol is protective since LDL particles adhere to and inactivate microorganisms and their toxins
Immunomodulation [10]	Inhibition of MyD88 expression	Speculated to reduce innate immunity response, thereby worsening SARS-CoV2 infection
Angiotensin converting enzyme 2 (ACE2) [24]	Upregulation of expression of ACE2	Potential to increase SARS-CoV2 entry into cells
Myositis and liver dysfunction [[31], [32], [33], [34]]	1.Mild elevation of liver enzymes in 10%, and elevation >3 times upper limit of normal in 1%–3% 2.Myalgia in 2%–7%	Detrimental effect in people with COVID-19 with skeletal muscle symptoms or liver dysfunction
Drug interactions [35,37]	Inhibition of cytochrome P-450 group of enzymes by protease inhibitors used in COVID-19 may significantly increase statin levels	Increased risk of toxicity: myopathy and rhabdomyolysis