Could aquaporin modulators be employed as prospective drugs for COVID-19 related pulmonary comorbidity?
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ABSTRACT:
SUBMITTER: Mariajoseph-Antony L
PROVIDER: S-EPMC7430244 | biostudies-literature | 2020 Aug
REPOSITORIES: biostudies-literature
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Project description:It is well established that pre-existing comorbid conditions such as hypertension, diabetes, obesity, cardiovascular diseases (CVDs), chronic kidney diseases (CKDs), cancers, and chronic obstructive pulmonary disease (COPD) are associated with increased severity and fatality of COVID-19. The increased death from COVID-19 is due to the unavailability of a gold standard therapeutic and, more importantly, the lack of understanding of how the comorbid conditions and COVID-19 interact at the molecular level, so that personalized management strategies can be adopted. Here, using multi-omics data sets and bioinformatics strategy, we identified the pathway crosstalk between COVID-19 and diabetes, hypertension, CVDs, CKDs, and cancers. Further, shared pathways and hub gene-based targets for COVID-19 and its associated specific and combination of comorbid conditions are also predicted towards developing personalized management strategies. The approved drugs for most of these identified targets are also provided towards drug repurposing. Literature supports the involvement of our identified shared pathways in pathogenesis of COVID-19 and development of the specific comorbid condition of interest. Similarly, shared pathways- and hub gene-based targets are also found to have potential implementations in managing COVID-19 patients. However, the identified targets and drugs need further careful evaluation for their repurposing towards personalized treatment of COVID-19 cases having pre-existing specific comorbid conditions we have considered in this analysis. The method applied here may also be helpful in identifying common pathway components and targets in other disease-disease interactions too.
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Project description:COVID-19 is a highly contagious respiratory disease, which mainly affects the lungs. Critically ill patients are easily complicated by cytokine storms, acute respiratory distress syndrome (ARDS), and respiratory failure, which seriously threaten their lives. Pulmonary fibrosis (PF) is a common interstitial lung disease, and its pathogenesis may involve the participation of a variety of immune cells and inflammatory factors. Current studies have shown that patients with COVID-19 may be complicated by pulmonary fibrosis, and patients with pulmonary fibrosis may also be at higher risk of contracting COVID-19 than healthy people. Pulmonary fibrosis is an important risk factor leading to the aggravation of COVID-19 disease. COVID-19 complicated by cytokine storm and ARDS mechanism pathways are similar to the pathogenesis of pulmonary fibrosis. The potential interaction between pulmonary fibrosis and COVID-19 can cause acute exacerbation of the patient's condition, but the potential mechanism between the two has not been fully elucidated. Most of the drug treatment programs for COVID-19-related pulmonary fibrosis are currently formulated about the relevant guidelines for idiopathic pulmonary fibrosis (IPF), and there is no clear drug treatment program recommendation. This article aims to summarize the relevant mechanism pathways of COVID-19 and pulmonary fibrosis, explore the interrelationships and possible mechanisms, and discuss the value and risks of existing and potential COVID-19-related pulmonary fibrosis treatment drugs, to provide reference for anti-fibrosis treatment for patients.
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Project description:As a primary target of SARS-CoV-2, lung exhibits heterogeneous histopathological changes following infection. However, comprehensive insight into their protein basis with spatial resolution remains deficient, which hinders further understanding of COVID-19-related pulmonary injury. Here, we generated a region-resolved proteomic atlas of hallmark pathological pulmonary structures by integrating histological examination, laser microdissection, and ultrasensitive proteomics. Over 10,000 proteins were quantified across 71 post-mortem specimens. We identified a spectrum of pathway dysregulations in alveolar epithelium, bronchial epithelium, and blood vessels comparing with non-COVID-19 controls, providing evidence for transitional-state pneumocyte hyperplasia. Additionally, our data revealed the region-specific enrichment of functional markers in bronchiole mucus plug, pulmonary fibrosis, airspace inflammation, and alveolar type 2 cells, uncovering their distinctive features. Furthermore, we detected increased protein expression associated with viral entry and inflammatory response across multiple regions, suggesting potential therapeutic targets. Collectively, this study provides a unique perspective for deciphering COVID-19-caused pulmonary dysfunction by spatial proteomics.
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Project description:This study estimates random effects and difference-in-difference-in-differences models to examine the initial impacts of COVID-19 on the employment and hours of unincorporated self-employed workers using monthly panel data from the Current Population Survey. For these workers, effects were visible in March as voluntary social distancing began, largest in April as complete shutdowns occurred, and slightly smaller in May as some restrictions were eased. We find differential effects by gender that favor men, by marital status and gender that favor married men over married women, and by gender, marital, and parental status that favor married fathers over married mothers. The evidence suggests that self-employed married mothers were forced out of the labor force to care for children presumably due to prescribed gender norms and the division and specialization of labor within households. Remote work and working in an essential industry mitigated some of the negative effects on employment and hours. Plain English Summary Among the unincorporated self-employed, married mothers were less likely to be employed and worked fewer hours during the COVID-19 pandemic than married fathers. Effects were visible in March as voluntary social distancing began, largest in April as complete shutdowns occurred, and slightly smaller in May as some restrictions were eased. Our results suggest that COVID-19 forced self-employed women back into the home due to gender norms about who cares for children. However, having a plausibly remote job or being in an essential industry helped mitigate some of the negative effects on employment and hours worked. Besides providing evidence that married mothers’ presence among the self-employed has been diminished by COVID-19, we find that the pandemic hurt the unincorporated self-employed more than other types of workers. This finding provides further evidence that it is important for researchers to distinguish between the incorporated and unincorporated self-employed when analyzing variation in self-employment at different points in the business cycle.
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Project description:Recent reports have suggested an increased risk of pulmonary embolism (PE) related to COVID-19. The aim of this cohort study is to compare the incidence of PE during a 3-year period and to assess the characteristics of PE in COVID-19. We studied consecutive patients presenting with PE (January 2017–April 2020). Clinical presentation, computed tomography (CT) and biological markers were systematically assessed. We recorded the global number of hospitalizations during the COVID-19 pandemic and during the same period in 2018-2019. We included 347 patients: 326 without COVID-19 and 21 with COVID-19. Patients with COVID-19 experienced more likely dyspnea (p=0.04), had lower arterial oxygen saturation (p<0.001), higher C-reactive protein and white blood cell (WBC) count (p<0.0001 and p=0.001, respectively), and a significantly higher in-hospital mortality (14% versus 3.4%, p=0.04). Among COVID-19 patients, diagnosis of PE was performed at admission in 38% (n=8). COVID-19 patients with diagnosis of PE during hospitalization (n=13) had significantly more dyspnea (p=0.04), lower arterial oxygen saturation (p=0.01), less proximal PE (p=0.02), and higher heart rate (p=0.009), CT severity score (p=0.001), C-reactive protein (p=0.006) and WBC count (p=0.04). During the COVID-19 outbreak, a 97.4% increase of PE incidence was observed as compared to 2017–2019 and the proportion of hospitalizations related to PE was 3.7% versus 1.3% in 2018–2019 (p<0.0001). In conclusion, the COVID-19 pandemic leads to a dramatic increased incidence of PE. Physicians should be aware that PE may be diagnosed at admission, but also after several days of hospitalization, with a different clinical, CT and biological features of thrombotic disease. Electronic supplementary material The online version of this article (10.1007/s11239-020-02292-4) contains supplementary material, which is available to authorized users.
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Project description:Since December 2019, a novel Coronavirus (SARS-CoV-2) was confirmed as the etiologic agent of a worldwide outbreak of a pneumonia that can result in severe respiratory failure. This clinical entity seems to be associated with a marked hypercoagulable state that causes both arterial and venous thromboembolic complications. Therefore, an adequate anti-thrombotic prophylaxis is recommended in hospitalized COVID-19 patients. Although rapidly worsening respiratory symptoms in a patient with SARS-CoV-2 respiratory infection may correlate with worsening pneumonia itself, it may also mask a pulmonary embolism. We report the case of a 50-year-old man affected by SARS-CoV-2 pneumonia, who developed acute pulmonary embolism.
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Project description:Le SARS-CoV-2, responsable de la COVID-19, est un nouveau bêta-coronavirus. Il engendre une réaction inflammatoire intense pouvant aller jusqu’à l’« orage cytokinique », avec des atteintes pulmonaires épithéliales sévères et un tableau de coagulopathie intravasculaire pulmonaire. Le tableau clinique est polymorphe, avec possible survenue d’un syndrome de détresse respiratoire aigu (SDRA). La ventilation non invasive et l’oxygénothérapie à haut débit permettent de traiter efficacement plus de la moitié des patients graves sans recours à l’intubation et sans risque pour le personnel soignant. Le seul traitement actuellement validé est la dexaméthasone à dose modérée (6 mg/j pendant 10 jours). Le haut risque thrombotique justifie en fonction des cas une anticoagulation préventive voire curative.
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Project description:Genomic epidemiology of COVID-19-associated pulmonary aspergillosis from four European countries confirms isolates are drawn from the wider Aspergillus fumigatus population
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Project description:Coronaviruses disease 2019 (COVID-19) is the most crucial threat, the world has ever witnessed. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of this disease pandemic. The World Health Organization has confirmed the continuing epidemic as a worldwide public health crisis. Presently, the research on COVID-19 is even in the primitive stage. Studies on unveiling the natural route of COVID-19 infection and related pathophysiology, the biology of pulmonary airways pose a more rational restorative approach in the management of COVID-19. Thus, based on the existing facts, we methodically reviewed the efforts put forth by various research institutes, pharmaceutical companies and biotechnology firms in pulmonary delivery to prevent and control the COVID-19. This article would be valuable for the healthcare community, which is efficiently dealing with the SARS-CoV-2 crisis.
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Project description:BackgroundLung function impairment persists in some patients for months after acute coronavirus disease 2019 (COVID-19). Long-term lung function, radiological features, and their association remain to be clarified.ObjectivesWe aimed to prospectively investigate lung function and radiological abnormalities over 12 months after severe and non-severe COVID-19.Methods584 patients were included in the Swiss COVID-19 lung study. We assessed lung function at 3, 6, and 12 months after acute COVID-19 and compared chest computed tomography (CT) imaging to lung functional abnormalities.ResultsAt 12 months, diffusion capacity for carbon monoxide (DLCOcorr) was lower after severe COVID-19 compared to non-severe COVID-19 (74.9% vs. 85.2% predicted, p < 0.001). Similarly, minimal oxygen saturation on 6-min walk test and total lung capacity were lower after severe COVID-19 (89.6% vs. 92.2%, p = 0.004, respectively, 88.2% vs. 95.1% predicted, p = 0.011). The difference for forced vital capacity (91.6% vs. 96.3% predicted, p = 0.082) was not statistically significant. Between 3 and 12 months, lung function improved in both groups and differences in DLCO between non-severe and severe COVID-19 patients decreased. In patients with chest CT scans at 12 months, we observed a correlation between radiological abnormalities and reduced lung function. While the overall extent of radiological abnormalities diminished over time, the frequency of mosaic attenuation and curvilinear patterns increased.ConclusionsIn this prospective cohort study, patients who had severe COVID-19 had diminished lung function over the first year compared to those after non-severe COVID-19, albeit with a greater extent of recovery in the severe disease group.
| S-EPMC9932828 | biostudies-literature