COVID-19 Severity Potentially Modulated by Cardiovascular-Disease-Associated Immune Dysregulation.

Patients with underlying cardiovascular conditions are particularly vulnerable to severe COVID-19. In this project, we aimed to characterize similarities in dysregulated immune pathways between COVID-19 patients and patients with cardiomyopathy, venous thromboembolism (VTE), or coronary artery disease (CAD). We hypothesized that these similarly dysregulated pathways may be critical to how cardiovascular diseases (CVDs) exacerbate COVID-19. To evaluate immune dysregulation in different diseases, we used four separate datasets, including RNA-sequencing data from human left ventricular cardiac muscle samples of patients with dilated or ischemic cardiomyopathy and healthy controls; RNA-sequencing data of whole blood samples from patients with single or recurrent event VTE and healthy controls; RNA-sequencing data of human peripheral blood mononuclear cells (PBMCs) from patients with and without obstructive CAD; and RNA-sequencing data of platelets from COVID-19 subjects and healthy controls. We found similar immune dysregulation profiles between patients with CVDs and COVID-19 patients. Interestingly, cardiomyopathy patients display the most similar immune landscape to COVID-19 patients. Additionally, COVID-19 patients experience greater upregulation of cytokine- and inflammasome-related genes than patients with CVDs. In all, patients with CVDs have a significant overlap of cytokine- and inflammasome-related gene expression profiles with that of COVID-19 patients, possibly explaining their greater vulnerability to severe COVID-19.

Using the health belief model to explore nursing students' relationships between COVID-19 knowledge, health beliefs, cues to action, self-efficacy, and behavioral intention: A cross-sectional survey study.

ABSTRACT: Nursing educators should equip nursing students with sufficient knowledge about coronavirus disease 2019 (COVID-19), perceived susceptibility, perceived severity, perceived benefits, perceived barriers, cues to action, self-efficacy, and behavioral intention in order to prevent the spread of COVID-19.The purpose of this study was to use the health belief model to elucidate nursing students' relationships between knowledge about COVID-19, perceived susceptibility, perceived severity, perceived benefits, perceived barriers, cues to action, self-efficacy, and behavioral intention.A cross-sectional survey design was adopted and purposive sampling was utilized. A total of 361 nursing students participated in the study. Quantitative analysis was employed for all data analysis.The findings showed that the nursing students had the following mean scores on knowledge of COVID-19 9.43 [standard deviation (SD)1.19], perceived susceptibility 19.41 (SD2.68), perceived severity 20.31 (SD 4.09), perceived benefits 26.52 (SD 4.08), perceived barriers 15.17 (SD5.88), cues to action 3.30 (SD1.70), self-efficacy 17.68 (SD2.83), and behavioral intention 18.46 (SD2.33). Nursing students' demographic background, knowledge of COVID-19, perceived susceptibility, perceived severity, perceived benefits, perceived barriers, cues to action, and self-efficacy explained 58.1% of the variance in behavioral intention (R2 = 0.581, F = 29.775, P < .001).Nursing educators can increase nursing students' knowledge of COVID-19, perceived susceptibility, perceived severity, perceived benefits, perceived barriers, cues to action, and self-efficacy as effective means of health promotion to improve their behavioral intention to prevent the spread of COVID-19.

Tobacco, but Not Nicotine and Flavor-Less Electronic Cigarettes, Induces ACE2 and Immune Dysregulation.

The COVID-19 pandemic caused by the SARS-CoV-2 virus, overlaps with the ongoing epidemics of cigarette smoking and electronic cigarette (e-cig) vaping. However, there is scarce data relating COVID-19 risks and outcome with cigarette or e-cig use. In this study, we mined three independent RNA expression datasets from smokers and vapers to understand the potential relationship between vaping/smoking and the dysregulation of key genes and pathways related to COVID-19. We found that smoking, but not vaping, upregulates ACE2, the cellular receptor that SARS-CoV-2 requires for infection. Both smoking and use of nicotine and flavor-containing e-cigs led to upregulation of pro-inflammatory cytokines and inflammasome-related genes. Specifically, chemokines including CCL20 and CXCL8 are upregulated in smokers, and CCL5 and CCR1 are upregulated in flavor/nicotine-containing e-cig users. We also found genes implicated in inflammasomes, such as CXCL1, CXCL2, NOD2, and ASC, to be upregulated in smokers and these e-cig users. Vaping flavor and nicotine-less e-cigs, however, did not lead to significant cytokine dysregulation and inflammasome activation. Release of inflammasome products, such as IL-1B, and cytokine storms are hallmarks of COVID-19 infection, especially in severe cases. Therefore, our findings demonstrated that smoking or vaping may critically exacerbate COVID-19-related inflammation or increase susceptibility to COVID-19.