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Molecular Impact of Nicotine on COVID-19

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 15 March 2025 | Viewed by 67

Special Issue Editor


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Guest Editor
1. Department of Human Sciences and Promotion of the Quality of Life, San Raffaele University, Via di Val Cannuta 247, 00166 Rome, Italy
2. Clinical and Molecular Epidemiology, IRCCS San Raffaele Roma, Via di Val Cannuta 247, 00166 Rome, Italy
Interests: DNA damage; nicotine and nicotinic receptor; COVID-19; respiratory disease; toeque teno virus
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Special Issue Information

Dear Colleagues,

Despite the controversial findings of epidemiological studies regarding the impact of cigarette smoking on SARS-CoV-2 infection, a recent thorough review indicates that current and former smokers face a 30–50% higher risk of progressing to severe COVID-19 (encompassing both severity and mortality) compared to those who have never smoked. Consequently, smokers are more susceptible to developing serious illness after contracting SARS-CoV-2 than non-smokers, with a greater chance of hospitalization, ICU admission, and death. Furthermore, there is evidence that other tobacco products, including electronic nicotine delivery systems, might affect the incidence or progression of COVID-19.

The mechanisms linking cigarette smoking, and possibly nicotine, which is the psychoactive component of smoking, to more severe disease may involve (a) the upregulation of ACE2 receptors, (b) immune suppression, (c) oxidative stress, (d) inflammation, and (e) vascular damage. Smoking increases the likelihood of developing chronic lung disease, cardiovascular disease, and diabetes, all of which are associated with worse outcomes in individuals infected with SARS-CoV-2.

Recent amino acid sequence analyses and computational methods have suggested that nicotinic acetylcholine receptors (AChRs) might serve as additional SARS-CoV-2 plasma membrane receptors by allowing the virus’ spike protein to bind at a site overlapping with the orthosteric, ACh-binding sites. However, based on experimental ligand-binding competition assays, it has been concluded that the mutual exclusivity of SARS-CoV-2 and cholinergic ligands binding to the human α7-AChR is unlikely to be a significant factor in this complex disease.

Further research is required to determine the impact of nicotine on the risk of developing severe COVID-19.

The objective of this Special Issue is to clarify the role of nicotine in SARS-CoV-2, with an emphasis on the following:

  • Molecular and cellular mechanisms related to its effects on immune and inflammatory responses to SARS-CoV-2;
  • The role of nAChRs and nAChR variants;
  • Genes and pathways targeted by nicotine within the respiratory tract that may impact SARS-CoV-2 infection and/or resulting COVID-19 severity;
  • The impact of nicotine on long COVID.

Prof. Dr. Patrizia Russo
Guest Editor

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Keywords

  • SARS-CoV-2 infection
  • COVID-19
  • nicotine
  • immune and inflammatory responses
  • nAChRs

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