A Descriptive Review of Epidemiology of COVID-19 in Smokers

Background: COVID-19 is an ongoing global pandemic with paucity of the understanding of the natural history of the disease and how it affects smokers. We aim to study the outcomes of COVID-19 in smokers in this descriptive review. Coronavirus disease 2019 caused by severe acute respiratory syndrome Coronavirus 2, gains entry to bronchial epithelial cells by attachment of the viral spike protein to Angiotensin-Converting Enzyme-2 (ACE-2) receptors. Accordingly, this review aims to understand the associated risk and worsen disease in relation to smoking and explore conflicting information regarding nicotine as well as its potential protective role. Methods: We conducted a non-systematic review of databases with search engines such as, PubMed, Google Scholar with keywords like “COVID-19,” “SARS-CoV-2,” “novel coronavirus,” smoking,” “smokers,” “nicotine.” It included English articles related to the epidemiology of COVID-19 in adult smokers, containing systematic reviews, meta-analysis, prospective and retrospective cohort studies, cross-sectional studies, case series, and case reports based on the relevance of titles and abstracts to the topic. Results: A total of 33 articles were reviewed. Smokers were 1.4 times more likely to have severe COVID-19 (RR = 1.4, 95% CI: 0.98 - 2.00), and 2.4 times more likely to require an ICU admission (RR = 2.4, CI: 1.43 - 4.04) when compared to non-smokers (n = 926). Current smokers were less likely to experience an adverse outcome (OR: 0.42, 95% CI: 0.24 - 0.74), compared to former smokers. 22% of current smokers and 46% of former smokers had more severe complications compared to non-smokers with COVID-19 infection. Current smokers had a case fatality rate of 38.5% (n = 1790). They had higher odds of mortality compared to non-smokers (OR = 1.25), especially males > 65 years age (OR = 2.51). Tobacco smoke upregulates inflammatory cytokines like TNF-α, IL-1β, and neutrophils by activating NF-k. Hence, it leads to increased epithelial cell permeability, mucus production, and impaired mucociliary clearance. The pro-inflammatory action of tobacco smoke impairs the basal laminar cells and causes endothelial dysfunction of the BBB and blood vessels, which leads to neurological, cerebrovascular, and thrombotic complications. Conclusion: Smoking is associated with worse outcomes and mortality in COVID-19. Public education about smoking cessation should be implemented along with standard guidelines to prevent disease progression in this susceptible population.

Thymosin alpha 1:A comprehensive review of the literature

Thymosin alpha 1 is a peptide naturally occurring in the thymus that has long been recognized for modifying,enhancing,and restoring immune function.Thymosin alpha 1 has been utilized in the treatment of immunocompromised states and malignancies,as an enhancer of vaccine response,and as a means of curbing morbidity and mortality in sepsis and numerous infections.Studies have postulated that thymosin alpha 1 could help improve the outcome in severely ill corona virus disease 2019 patients by repairing damage caused by overactivation of lymphocytic immunity and how thymosin alpha 1 could prevent the excessive activation of T cells.In this review,we discuss key literature on the background knowledge and current clinical uses of thymosin alpha 1.Considering the known biochemical properties including antibacterial and antiviral properties,timehonored applications,and the new promising findings regarding the use of thymosin,we believe that thymosin alpha 1 deserves further investigation into its antiviral properties and possible repurposing as a treatment against severe acute respiratory syndrome coronavirus-2.