tetano
Editor, Senior Moderator
Comput Struct Biotechnol J
. 2021 Mar 23.
doi: 10.1016/j.csbj.2021.03.023. Online ahead of print.
SARS-CoV-2 Infection and Smoking: What is the association? A brief review
Ishita Gupta[SUP] 1 2 [/SUP], Muhammad Umar Sohail[SUP] 3 [/SUP], Khaled E Elzawawi[SUP] 1 [/SUP], Ahmed H Amarah[SUP] 1 [/SUP], Semir Vranic[SUP] 1 2 [/SUP], Maha Al-Asmakh[SUP] 2 4 5 [/SUP], Ala-Eddin Al Moustafa[SUP] 1 2 6 [/SUP]
Affiliations
Abstract
Susceptibility to severe illness from COVID-19 is anticipated to be associated with cigarette smoking as it aggravates the risk of cardiovascular and respiratory illness, including infections. This is particularly important with the advent of a new strain of coronaviruses, the severe acute respiratory syndrome coronavirus (SARS-CoV-2) that has led to the present pandemic, coronavirus disease 2019 (COVID-19). Although, the effects of smoking on COVID-19 are less described and controversial, we presume a link between smoking and COVID-19. Smoking has been shown to enhance the expression of the angiotensin-converting enzyme-2 (ACE-2) and transmembrane serine protease 2 (TMPRSS2) key entry genes utilized by SARS-CoV-2 to infect cells and induce a 'cytokine storm', which further increases the severity of COVID-19 clinical course. Nevertheless, the impact of smoking on ACE-2 and TMPRSS2 receptors expression remains paradoxical. Thus, further research is necessary to unravel the association between smoking and COVID-19 and to pursue the development of potential novel therapies that are able to constrain the morbidity and mortality provoked by this infectious disease. Herein we present a brief overview of the current knowledge on the correlation between smoking and the expression of SARS-CoV-2 key entry genes, clinical manifestations, and disease progression.
Keywords: ACE2, Angiotensin-converting enzyme-2; ACEIs, Angiotensin?converting enzyme inhibitors; ADAM17, ADAM metallopeptidase domain 17; ALCAM, Activated leukocyte cell adhesion molecule; ARBs, Angiotensin receptor blockers; ARDS, Acute respiratory distress syndrome; Ang, Angiotensin; BatCoV, Bat coronavirus; CLDN7, Claudin 7; COPD, Chronic obstructive pulmonary disease; COVID-19; COVID-19, Coronavirus disease 2019; CTNNB1, Catenin beta 1; Coronavirus; ERK, Extracellular signal-regulated kinases; HDAC6, Histone deacetylase 6; HIV-1, Human immunodeficiency virus 1; IFN, Interferons; IPF, Idiopathic pulmonary fibrosis; IR, Ionizing radiation; JNK, c-Jun N-terminal kinase; Lung Disease; MCN, Mucin; MERS, Middle-East respiratory syndrome; NO, Nitric oxide; Oral Disease; R0, R-nought; RAS, Renin-angiotensin; RR, Relative risk; SARS-CoV-2; SARS-CoV-2, Severe acute respiratory syndrome coronavirus; Smoking; TJP3, Tight junction protein 3; TMPRSS, Transmembrane serine protease; hrsACE2, human recombinant soluble ACE-2; nAChR, ?7 nicotinic acetylcholine receptor.
. 2021 Mar 23.
doi: 10.1016/j.csbj.2021.03.023. Online ahead of print.
SARS-CoV-2 Infection and Smoking: What is the association? A brief review
Ishita Gupta[SUP] 1 2 [/SUP], Muhammad Umar Sohail[SUP] 3 [/SUP], Khaled E Elzawawi[SUP] 1 [/SUP], Ahmed H Amarah[SUP] 1 [/SUP], Semir Vranic[SUP] 1 2 [/SUP], Maha Al-Asmakh[SUP] 2 4 5 [/SUP], Ala-Eddin Al Moustafa[SUP] 1 2 6 [/SUP]
Affiliations
- PMID: 33777332
- PMCID: PMC7985684
- DOI: 10.1016/j.csbj.2021.03.023
Abstract
Susceptibility to severe illness from COVID-19 is anticipated to be associated with cigarette smoking as it aggravates the risk of cardiovascular and respiratory illness, including infections. This is particularly important with the advent of a new strain of coronaviruses, the severe acute respiratory syndrome coronavirus (SARS-CoV-2) that has led to the present pandemic, coronavirus disease 2019 (COVID-19). Although, the effects of smoking on COVID-19 are less described and controversial, we presume a link between smoking and COVID-19. Smoking has been shown to enhance the expression of the angiotensin-converting enzyme-2 (ACE-2) and transmembrane serine protease 2 (TMPRSS2) key entry genes utilized by SARS-CoV-2 to infect cells and induce a 'cytokine storm', which further increases the severity of COVID-19 clinical course. Nevertheless, the impact of smoking on ACE-2 and TMPRSS2 receptors expression remains paradoxical. Thus, further research is necessary to unravel the association between smoking and COVID-19 and to pursue the development of potential novel therapies that are able to constrain the morbidity and mortality provoked by this infectious disease. Herein we present a brief overview of the current knowledge on the correlation between smoking and the expression of SARS-CoV-2 key entry genes, clinical manifestations, and disease progression.
Keywords: ACE2, Angiotensin-converting enzyme-2; ACEIs, Angiotensin?converting enzyme inhibitors; ADAM17, ADAM metallopeptidase domain 17; ALCAM, Activated leukocyte cell adhesion molecule; ARBs, Angiotensin receptor blockers; ARDS, Acute respiratory distress syndrome; Ang, Angiotensin; BatCoV, Bat coronavirus; CLDN7, Claudin 7; COPD, Chronic obstructive pulmonary disease; COVID-19; COVID-19, Coronavirus disease 2019; CTNNB1, Catenin beta 1; Coronavirus; ERK, Extracellular signal-regulated kinases; HDAC6, Histone deacetylase 6; HIV-1, Human immunodeficiency virus 1; IFN, Interferons; IPF, Idiopathic pulmonary fibrosis; IR, Ionizing radiation; JNK, c-Jun N-terminal kinase; Lung Disease; MCN, Mucin; MERS, Middle-East respiratory syndrome; NO, Nitric oxide; Oral Disease; R0, R-nought; RAS, Renin-angiotensin; RR, Relative risk; SARS-CoV-2; SARS-CoV-2, Severe acute respiratory syndrome coronavirus; Smoking; TJP3, Tight junction protein 3; TMPRSS, Transmembrane serine protease; hrsACE2, human recombinant soluble ACE-2; nAChR, ?7 nicotinic acetylcholine receptor.