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Review
. 2020 Sep 9;21(18):6581.
doi: 10.3390/ijms21186581.

Smoking and COVID-19: Adding Fuel to the Flame

Vivek K Kashyap  1   2 , Anupam Dhasmana  1   2 , Andrew Massey  1   2 , Sudhir Kotnala  1   2 , Nadeem Zafar  3 , Meena Jaggi  1   2 , Murali M Yallapu  1   2 , Subhash C Chauhan  1   2
Affiliations
Review

Smoking and COVID-19: Adding Fuel to the Flame

Vivek K Kashyap et al. Int J Mol Sci. .

Abstract

The coronavirus disease 2019 (COVID-19) pandemic, an infection caused by the severe acute respiratory syndrome coronavirus (SARS-CoV-2), has led to more than 771,000 deaths worldwide. Tobacco smoking is a major known risk factor for severe illness and even death from many respiratory infections. The effects of smoking on COVID-19 are currently controversial. Here, we provide an overview of the current knowledge on the effects of smoking on the clinical manifestations, disease progression, inflammatory responses, immunopathogenesis, racial ethnic disparities, and incidence of COVID-19. This review also documents future directions of smoking related research in COVID-19. The current epidemiological finding suggests that active smoking is associated with an increased severity of disease and death in hospitalized COVID-19 patients. Smoking can upregulate the angiotensin-converting enzyme-2 (ACE-2) receptor utilized by SARS-CoV-2 to enter the host cell and activate a 'cytokine storm' which can lead to worsen outcomes in COVID-19 patients. This receptor can also act as a potential therapeutic target for COVID-19 and other infectious diseases. The COVID-19 pandemic sheds light on a legacy of inequalities regarding gender, racial, and ethnic health disparities associated with active smoking, thus, smoking cessation may help in improving outcomes. In addition, to flatten the COVID-19 curve, staying indoors, avoiding unnecessary social contact, and bolstering the immune defense system by maintaining a healthy diet/living are highly desirable.

Keywords: ACE-2; COVID-19; SARS-CoV-2; e-cigarettes; hooka and cytokine storm; smoking; vaping; α7-nAChR.

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Figure 1
Figure 1
Reported confirmed COVID-19 cases over time in top ten highly infected countries. Data accessed on 15 August 2020, using Worldometer, https://www.worldometers.info/coronavirus/.
Figure 2
Figure 2
Schematic representation of SARS-CoV-2-driven signaling pathways induced by smoking. Smoking component has tendency to interact with α7-nAChR, this interaction directly stimulates the ACE-2 expression level, which upregulated phospho-S6 ribosomal protein (Ser235/236), phospho-p44/42 MAPK (Thr202/Tyr204) and phospho-Akt (Ser473 and Thr308).
Figure 3
Figure 3
Chronology of events of SARS-CoV-2 infection induced by smoking: When SARS-CoV-2 interacts with TMPRSS2, it activates the S protein by proteolysis. This activated S protein is intended to be attached to and infect cells expressing the surface receptor ACE-2. This activation triggers viral replication and leads to virus release from infected cells. The release virus and their viral proteins also induces molecular events. Once being detected by nearby alveolar macrophages, a cascade is activated leading to the excessive production of pro-inflammatory cytokines and chemokines including IL-2,7, 10, TNF-α, GS-CF, macrophage inflammatory protein 1α (MIP1α), MIP1β and MCP1. These proteins attract other immune cells and promoting further inflammation which establishes a cytokines storm.
Figure 4
Figure 4
Summary of currently tested potential therapeutic agents targeting different steps of SARS-CoV-2 life cycle.
See this image and copyright information in PMC

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