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Is there a smoker’s paradox in COVID-19?
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  • Published on:
    RE: Is there a smoker’s paradox in COVID-19?

    There is a hypothesis that nicotine may have a protective effect in COVID-19 (1). I present two recent reports on the association between smoking and COVID-19 infection/progression, and then presented reports regarding another mechanism of the association.

    Paleiron et al. conducted a cross-sectional study to investigate the association between smoking and COVID-19 (2). The adjusted odds ratios (ORs) (95% confidence intervals [CIs]) of current smokers and subjects aged over 50 years for the risk of developing Covid-19 were 0.64 (0.49-0.84) and 2.6 (1.2-6.9), respectively. Smoking presented a protective effect on the developing COVID-19.

    Farsalinos et al. conducted a meta-analysis to examine the effects of current smoking on adverse outcomes among hospitalized COVID-19 patients (3). Pooled OR (95% CI) of current smokers against non-current smokers and against former smokers for adverse outcomes was 1.53 (1.06-2.20) and 0.42 (0.27-0.74), respectively. Smoking relates to the progression of clinical outcomes in hospitalized COVID-19 patients, although the reason of poor clinical outcomes in former smokers should be explored by further studies.

    There is another hypothesis that lithium will limit SARS-CoV2 infections. Rudd presented a hypothesis that the repurposing of low-cost inhibitors of glycogen synthase kinase-3 (GSK-3) such as lithium will limit SARS-CoV2 infections by both reducing viral replication and potentiating the immune response against the vi...

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    Conflict of Interest:
    None declared.
  • Published on:
    Correcting the record: all studies of smokers with COVID-19 show a protective effect

    Usman et al (1) write that only one of the 18 studies of COVID-19 patients they included in their review of the Smoker's Paradox reported that "the prevalence of smokers resembles that of the general population."

    But this study--by Richardson et al in New York City (2)--actually only reported the prevalence of "never smokers" at 84.4%. It did not distinguish between current and former smokers among the remaining 15.6%, however, so Usman et al should have marked this combined result with an asterisk in their Table 1. Far from resembling the general population, the 15.6% combined rate is less than half the 34% expected in USA, where approximately 14% are current and 20% former smokers. With this correction, all 18 studies support the Smoker’s Paradox, which belies the authors’ conclusion that a “protective effect should NOT be inferred” [emphasis added].

    The protective effect is clearly real and further supported by the largest study of COVID-19 to date (n=7,162) with data on smoking status (3), which Usman et al did not include in their review. Current smokers in this CDC study comprised just 1.3% of all the COVID-19 patients seeking care from US hospitals in 50 states and Washington DC, 1.2% of those treated as outpatients, and 1.1% of those treated in intensive care units.

    Usman et al also did not mention the compound most likely responsible for the protective effects of smoking against respiratory infections, which...

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    Conflict of Interest:
    The author holds a US patent, US20170072151A1, for a breath testing method that can be used with any CO measuring device to distinguish the levels of free carbon monoxide in the lungs, arteries, veins, and the average of all tissues.
  • Published on:
    SARS-CoV-2 mimicry of an epithelial sodium ion channel (ENaC) linked to increased risk of severe COVID-19 symptoms in cigarette smokers
    • Ashutosh Kumar, Assistant Professor All India Institute of Medical Sciences, Patna
    • Other Contributors:
      • Vikas Pareek, Doctoral student

    Dear Editor,
    Recent literature suggested increased risk of severe COVID-19 in smokers which also got affirmation from World Health Organization (WHO) [1, 2]. However, original peer reviewed research which explained pathophysiological basis of the enhanced COVID-19 severity in smokers is currently scarce. Increased expression of SARS-CoV-2 cell entry receptor ACE2 in respiratory tract and lung tissue of smokers unraveled from analysis of gene expression data was used to predict higher chances of SARS-CoV-2 infection but that failed to explain enhanced COVID-19 severity [3]. Few authors have suggested that increased risk of severe complications and higher mortality rate in infected smokers may be due to host-specific factors like weakening of respiratory health and immunity caused by chronic smoking [4]. However, none of the virus-related factors which can be responsible for the COVID-19 severity in smokers has been reported until date. Based on the recent research updates on SARS-CoV-2 specific virulence in host cells, we propose a plausible mechanism which associates smoking with increased severity of COVID-19.
    Apart from a cell surface entry receptor, coronaviruses require furin (a host protease) mediated cleavage of their spike (S) protein for successful invasion of the host cell. SARS-CoV-2, a member of the genus betacoronaviruses, has evolved a unique furin protease S1/S2 cleavage site, which is absent in other family members, including SARS-CoV-1 [5]. Rec...

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    Conflict of Interest:
    None declared.