Cigarette smoke, the saviour of generation

“We must stress about the strong evidence showing that smoking Cigarette increases the severity of covid-19. But then we discovered recently a mechanism which is worth further investigation as a potential tool to fight SARS-CoV-2 infections,” said Keiji Tanimoto of Hiroshima University’s Research Institute for Radiation Biology and Medicine.

Previous Discovery

A few months before, scientists confirmed that Covid-19 would be heinous specifically for daily smokers. They said that tobacco uses to disable our lungs, and if a person is a smoker, that means his lungs are already damaged. So, when SARS-CoV-2 infects these damaged lungs, the effects of the virus could become worse than an average person. 

Tobacco affects the immune system, reducing the capabilities, which means a smoker is less active in fighting against the “Corona Virus”.

Chemicals in Cigarette, Recent Discovery

The recent discovery revealed that the same cigarette that badly affects the lungs and damages the human body’s immune system can be as effective as medicine to the SARS-CoV-2. 

Is that mean the coronavirus won’t be able to affect smokers? No, it doesn’t mean that the active smokers would get rid off of the previous discovery. 

The smoke of the cigarette contains “Polycyclic Aromatic Hydrocarbons” [PAHs] that can bind to “Aryl Hydrocarbon Receptors” [AHRs]. 

A receptor is a structure on the surface of a cell or inside of the cell. This receptor is shaped in a way so it can receive and bind to a particular substance. 

AHRS receptors are the inside mammalian that can induce a wide range of cellular activities through their ability to decrease or increase the expression of specific genes.

The researchers found that the effect of chemicals that activate AHR on the genes that control the production of ACE2. 

ACE2 is the receptor protein on the surface of some cells that the SARS-CoV-2 virus can hook onto. The virus that causes Covid-19 binds with ACE2 protein to enter and infect the human cell. 

Scientists say that the cells in the oral cavity, lungs and liver had the highest ACE2 expression. These cells of the lungs, liver and oral cavity were later put onto various doses of cigarette smoke which were continuously being extracted for 24 hours.

They said the more the cigarette smoke pulled on the cells, the more impacted the CYP1A1 gene expressions. The activities of the gene led to less production of the ACE2 proteins that the SARS-CoV-2 uses to enter the human cells. However, they didn’t confirm this effectiveness in the oral cavity cells.

They didn’t get why this whole procedure was happening for the first time, so researchers used RNA sequencing analysis to know the exact gene expression of CYP1A1. 

After the experiment of RNA sequencing, they found that the smoke of the cigarette that they extracted increased the expressions of the genes related to key processes within the cell that AHR regulates. 

Two Drugs

Further studies revealed that the impact of two drugs do could activate the AHR in the liver cells.The first drug is the derivative of the Amino Acid Tryptophan, and the second drug is Omeprazole.Doctors use the drug Omeprazole to cure acid reflux and peptic ulcers. 

According to the RNA sequencing data, the CYP1A1 gene strongly induced the AHR activators in the liver cells and strongly inhibited the production of ACE2 protein.

The scientists concluded with the most impressive fact that the two drugs that act as the activators of AHR can suppress the massive production of ACE2 protein in the mammalian cell. 

So, surprisingly these two drugs can reduce the ability of the SARS-CoV-2 virus to infect the liver cells.

Researchers said, “We are now examining and re-examining the drugs in pre-clinical and clinical trials for the treatment of Covid-19.