Why smokers have a lower risk of COVID-19

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In a new study from Hiroshima University, researchers found a potential reason why lower numbers of COVID cases have appeared amongst smokers compared to non-smokers, even as other reports suggest smoking increases the severity of the disease.

They also found two drugs that mimic the effect of chemicals in cigarette smoke that inhibits the production of ACE2 proteins.

Something of a paradox exists with respect to smoking cigarettes and COVID-19.

Active smoking is linked to increased severity of disease, but at the same time, many reports have suggested lower numbers of COVID cases amongst smokers than amongst non-smokers.

It is known that cigarette smoke contains polycyclic aromatic hydrocarbons (PAHs). These can bind to and activate aryl hydrocarbon receptors (AHRs).

A receptor is any structure of the surface or inside of a cell that is shaped to receive and bind to a particular substance.

Knowing this about the relationship between PAHs and AHRs, the researchers wanted to know the effect of drugs that activate AHR on the expression of the genes that control the production of the ACE2 protein.

It is the infamous receptor protein on the surface of many cells types that works like a lock that the SARS-CoV-2 virus is able to pick. After binding the virus to the ACE2 protein, it can then enter and infect the cell.

First, the scientists examined various cell lines to examine their gene expression levels of ACE2. They found that those cells originating in the oral cavity, lungs and liver had the highest ACE2 expression.

They found that cigarette smoking increased the expressions of genes related to a number of key signaling processes within the cell that are regulated by AHR.

The team then tested the effects of two drugs that can activate AHR on the liver cells.

The first, 6‑formylindolo(3,2‑b)carbazole (FICZ) is derivative of the amino acid tryptophan, and the second, omeprazole (OMP), is a medication already widely used in the treatment of acid reflux and peptic ulcers.

They found the cigarette smoke extract and these two drugs—all of which act as activators of AHR—are able to suppress the expression of ACE2 in mammalian cells, and by doing so, reduce the ability of the SARS-CoV-2 virus to enter the cell.

Based on these findings, the team is now doing pre-clinical and clinical trials on the drugs as a novel anti-COVID-19 therapy.

If you care about COVID, please read studies about vitamin D and COVID-19: What you need to know and findings of this cholesterol-lowering drug could reduce COVID-19 infection by up to 70%.

For more information about COVID and your health, please see recent studies about these existing drugs may help treat COVID-19 and results showing that green tea may offer new hope to beat COVID-19.

The study is published in Scientific Reports. One author of the study is Keiji Tanimoto.

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