Literature DB >> 33777332

SARS-CoV-2 infection and smoking: What is the association? A brief review.

Ishita Gupta1,2, Muhammad Umar Sohail3, Khaled E Elzawawi1, Ahmed H Amarah1, Semir Vranic1,2, Maha Al-Asmakh2,4,5, Ala-Eddin Al Moustafa1,2,5.   

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.
© 2021 The Author(s).

Entities:  

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, α7 nicotinic acetylcholine receptor

Year:  2021        PMID: 33777332      PMCID: PMC7985684          DOI: 10.1016/j.csbj.2021.03.023

Source DB:  PubMed          Journal:  Comput Struct Biotechnol J        ISSN: 2001-0370            Impact factor:   7.271


  135 in total

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