Smoking Reduce Signaling Ability of Cytokines That May Lead to Severe COVID-19, Stanford Researchers Found

Smoking could damage lung immune function and cause harm to upper airways that lead to increased risks of contracting severe infectious diseases. The Centers for Disease Control and Prevention (CDC) included people with chronic lung diseases, particularly those caused by smoking, in the list of people who are at risk of developing a severe type of COVID-19.

Previous studies reveal that illnesses related to smoking may impact the same major organs infected by SARS-CoV-2. In the new study, titled "Determinants of SARS-CoV-2 Entry and Replication in Airway Mucosal Tissue and Susceptibility in Smokers" published in Cell Reports Medicine, researchers from Stanford Medicine tracked the COVID-19 infection to understand why smokers tend to have a higher risk of having severe cases of the infection.

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Smoking Reduce Signaling Ability of Cytokines That May Lead to Severe COVID-19, Stanford Researchers Found

Cellular Pathway of COVID-19

Coronavirus derives its name from its electron microscopic image that resembles a crown. The virus is commonly found among animals, such as cats, camels, and bats.

The Pathologist reported that six coronaviruses have infected humans as of today of which four of them are responsible for one-third of common colds. Some known coronaviruses that infected humans are the SARS-CoV in 2003 and the MERS-CoV in 2012.

Then on December 30, 2019, the SARS-CoV-2 started infecting people in China that later on infected more people around the world. It was first identified as a novel coronavirus 2019 (2019-nCoV) by the World Health Organization but was changed into SARS-CoV-2 on February 11, 2020, by the International Committee in Taxonomy of Viruses.

SARS-CoV-2 shared 79% of its genetic sequence with SARS-CoV and 96% similar homology with the RATG13 strain found in bats. The virus has high-affinity binding to human ACE2 receptors as well as a functional polybasic cleavage site at the junction of S1 and S2 of the spike protein that enhances spike proteins and increases viral infectivity.

When SARS-CoV-2 attached itself to ACE2 receptors, the TMPRSS2 protease cleaves the spike protein and exposes the fusion peptide to allow better access for virions and release their RNA into infected cells where it will become new viral proteins and eventually into new virions.

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Uncovering How Smoking Increases Risk of Severe COVID-19

Researchers wrote in Stanford Medicine's press release that SARS-CoV-2 infection typically begins in the lining of the nasal cavity and sinuses before progressing to the truth and lower airways of the trachea and lungs. In addition, they wrote that they found abundant viral materials in the nasal cavity and trachea, indicating that the nose is the major route of transmission.

When they compared the viral level of non-smokers to smokers, they did not find that the virus entry factors were expressed in higher levels in the tissues of smokers. This might explain why smokers are not at a higher risk of initially contracting COVID-19, but are more likely to have the severe disease when infected due to reduced levels of an antiviral molecule known as interferon beta.

This molecule is also called a cytokine, which is a key signaling molecule that regulates how the immune system responds to threats and infection. Previous studies have shown that cigarette smoking reduces cytokine signaling ability.

Furthermore, researchers tested in a laboratory setting how lab-grown human nasal tissues exposed to cigarette smoke would great to SARS-CoV-2 virus. They found that it is more susceptible to infection, but it can be prevented when they added extra interferon beta before exposing the nasal tissues to the smoke.

This highlights the importance of interferon beta in mediating the susceptibility to the SARS-CoV-2 virus in smokers. It also points to the significance of mask-wearing behavior to decrease the chances of inhaling viral particles.