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1.
Front Med (Lausanne) ; 7: 604640, 2020.
Article in English | MEDLINE | ID: covidwho-1156129

ABSTRACT

[This corrects the article DOI: 10.3389/fmed.2020.00539.].

3.
Transl Res ; 232: 37-48, 2021 06.
Article in English | MEDLINE | ID: covidwho-989352

ABSTRACT

Approximately 15%-20% of patients infected with SARS-CoV-2 coronavirus (COVID-19) progress beyond mild and self-limited disease to require supplemental oxygen for severe pneumonia; 5% of COVID-19-infected patients further develop acute respiratory distress syndrome (ARDS) and multiorgan failure. Despite mortality rates surpassing 40%, key insights into COVID-19-induced ARDS pathology have not been fully elucidated and multiple unmet needs remain. This review focuses on the unmet need for effective therapies that target unchecked innate immunity-driven inflammation which drives unchecked vascular permeability, multiorgan dysfunction and ARDS mortality. Additional unmet needs including the lack of insights into factors predicting pathogenic hyperinflammatory viral host responses, limited approaches to address the vast disease heterogeneity in ARDS, and the absence of clinically-useful ARDS biomarkers. We review unmet needs persisting in COVID-19-induced ARDS in the context of the potential role for damage-associated molecular pattern proteins in lung and systemic hyperinflammatory host responses to SARS-CoV-2 infection that ultimately drive multiorgan dysfunction and ARDS mortality. Insights into promising stratification-enhancing, biomarker-based strategies in COVID-19 and non-COVID ARDS may enable the design of successful clinical trials of promising therapies.


Subject(s)
Alarmins/physiology , COVID-19/complications , Inflammation/etiology , Respiratory Distress Syndrome/etiology , SARS-CoV-2 , Vascular System Injuries/etiology , Blood Coagulation Disorders/etiology , Capillary Permeability , Cytokines/physiology , Humans , Nicotinamide Phosphoribosyltransferase/physiology , SARS-CoV-2/pathogenicity
4.
Front Med (Lausanne) ; 7: 539, 2020.
Article in English | MEDLINE | ID: covidwho-843396

ABSTRACT

After decades of research, two therapies for chronic fibrotic lung disease are now approved by the FDA, with dozens more anti-fibrotic therapies in the pipeline. A great deal of enthusiasm has been generated for the use of these drugs, which are by no means curative but clearly have a favorable impact on lung function decline over time. Amidst a flurry of newly developed and repurposed drugs to treat the coronavirus disease 2019 (COVID-19) and its accompanying acute respiratory distress syndrome (ARDS), few have emerged as effective. Historically, survivors of severe viral pneumonia and related acute lung injury with ARDS often have near full recovery of lung function. While the pathological findings of the lungs of patients with COVID-19 can be diverse, current reports have shown significant lung fibrosis predominantly in autopsy studies. There is growing enthusiasm to study anti-fibrotic therapy for inevitable lung fibrosis, and clinical trials are underway using currently FDA-approved anti-fibrotic therapies. Given the relatively favorable outcomes of survivors of virus-mediated ARDS and the low prevalence of clinically meaningful lung fibrosis in survivors, this perspective examines if there is a rationale for testing these repurposed antifibrotic agents in COVID-19-associated lung disease.

5.
Geroscience ; 42(3): 1013, 2020 06.
Article in English | MEDLINE | ID: covidwho-624400

ABSTRACT

The affiliation of the second author (Kenneth S. Knox) should have been Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, University of Arizona College of Medicine-Phoenix, Phoenix, AZ 85004, USA instead of Department of Medicine, University of Arizona-Phoenix, Phoenix, AZ 85004, USA.

6.
Geroscience ; 42(2): 505-514, 2020 04.
Article in English | MEDLINE | ID: covidwho-46463

ABSTRACT

SARS-CoV-2 virus, the causative agent of the coronavirus infectious disease-19 (COVID-19), is taking the globe by storm, approaching 500,000 confirmed cases and over 21,000 deaths as of March 25, 2020. While under control in some affected Asian countries (Taiwan, Singapore, Vietnam), the virus demonstrated an exponential phase of infectivity in several large countries (China in late January and February and many European countries and the USA in March), with cases exploding by 30-50,000/day in the third and fourth weeks of March, 2020. SARS-CoV-2 has proven to be particularly deadly to older adults and those with certain underlying medical conditions, many of whom are of advanced age. Here, we briefly review the virus, its structure and evolution, epidemiology and pathogenesis, immunogenicity and immune, and clinical response in older adults, using available knowledge on SARS-CoV-2 and its highly pathogenic relatives MERS-CoV and SARS-CoV-1. We conclude by discussing clinical and basic science approaches to protect older adults against this disease.


Subject(s)
Coronavirus Infections/immunology , Coronavirus Infections/pathology , Pneumonia, Viral/immunology , Pneumonia, Viral/pathology , Aged , Angiotensin-Converting Enzyme 2 , Animals , Antibodies, Viral/immunology , Betacoronavirus/genetics , Betacoronavirus/pathogenicity , COVID-19 , Chemokines/immunology , Cytokines/immunology , Fever/diagnosis , Fever/virology , Geriatrics , Humans , Immunosenescence , Middle East Respiratory Syndrome Coronavirus , Pandemics , Peptidyl-Dipeptidase A/genetics , SARS Virus , SARS-CoV-2 , Spike Glycoprotein, Coronavirus/genetics
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