Smoking and the risk of contracting SARS-CoV-2 and COVID-19 Coronavirus Disease COVID Tobacco Smoking LancetRespirMed UCSF RoswellPark Stanford Yale USC VUMChealth uofl
By Nidhi Saha, BDSAug 21 2022Reviewed by Benedette Cuffari, M.Sc. Smoking increases the risk of respiratory infections, such as colds, flu, pneumonia, and tuberculosis. Smoking may also contribute to coronavirus disease 2019 complications.
More specifically, these substances appear to directly damage the epithelial cells, which subsequently impacts the epithelial barrier and mucociliary clearance. In addition to these direct effects, these damaged cells release modified molecules into the lungs, which stimulate specific receptors that ultimately activate innate and acquired immune responses.
The researchers analyzed the behavioral mechanisms associated with tobacco consumption on COVID-19 and inflammatory immune responses. Furthermore, they also screened risk factors for the development of public health policies and patient care delivery. Study findings Epidemiological studies investigating the impact of cigarette smoking on SARS-CoV-2 infection have rendered mixed results. Thus, further research is needed to ascertain whether smoking or the use of other tobacco products contributes to the susceptibility to COVID-19.
Tobacco products contain a wide range of potentially toxic chemicals, while several harmful chemicals are also formed during the aerosolization process due to the heating or combustion of the product. The use of tobacco products can result in substantial damage; however, it remains unclear how individual chemicals and constituents contribute to these pathophysiological effects.
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Frontiers | Multisystem Inflammatory Syndrome in Children and Long COVID: The SARS-CoV-2 Viral Superantigen HypothesisMultisystem inflammatory syndrome in children (MIS-C) is a febrile pediatric inflammatory disease that may develop weeks after initial SARS-CoV-2 infection or exposure. MIS-C involves systemic hyperinflammation and multiorgan involvement, including severe cardiovascular, gastrointestinal (GI) and neurological symptoms. Some clinical attributes of MIS-C—such as persistent fever, rashes, conjunctivitis and oral mucosa changes (red fissured lips and strawberry tongue)—overlap with features of Kawasaki disease (KD). In addition, MIS-C shares striking clinical similarities with toxic shock syndrome (TSS), which is triggered by bacterial superantigens (SAgs). The remarkable similarities between MIS-C and TSS prompted a search for SAg-like structures in the SARS-CoV-2 virus and the discovery of a unique SAg-like motif highly similar to a Staphylococcal enterotoxin B (SEB) fragment in the SARS-CoV-2 spike 1 (S1) glycoprotein. Computational studies suggest that the SAg-like motif has a high affinity for binding T-cell receptors (TCRs) and MHC Class II proteins. Immunosequencing of peripheral blood samples from MIS-C patients revealed a profound expansion of TCR β variable gene 11-2 (TRBV11-2), which correlates with MIS-C severity and serum cytokine levels, consistent with a SAg-triggered immune response. Computational sequence analysis of SARS-CoV-2 spike further identified conserved neurotoxin-like motifs which may alter neuronal cell function and contribute to neurological symptoms in COVID-19 and MIS-C patients. Additionally, autoantibodies are detected during MIS-C, which may indicate development of post-SARS-CoV-2 autoreactive and autoimmune responses. Finally, prolonged persistence of SARS-CoV-2 RNA in the gut, increased gut permeability and elevated levels circulating of S1 have been observed in children with MIS-C. Accordingly, we hypothesize that continuous and prolonged exposure to the viral SAg-like and neurotoxin-like motifs in SARS-CoV-2 spike may promote autoim
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