Increased SARS-CoV-2 Infection, Protease, and Inflammatory Responses in Chronic Obstructive Pulmonary Disease Primary Bronchial Epithelial Cells Defined with Single-Cell RNA Sequencing DOI Creative Commons
Matt D. Johansen, Rashad Mohammad Mahbub,

Sobia Idrees

et al.

American Journal of Respiratory and Critical Care Medicine, Journal Year: 2022, Volume and Issue: 206(6), P. 712 - 729

Published: May 12, 2022

Patients with chronic obstructive pulmonary disease (COPD) develop more severe coronavirus (COVID-19); however, it is unclear whether they are susceptible to acute respiratory syndrome 2 (SARS-CoV-2) infection and what mechanisms responsible for disease.

Language: Английский

A Mouse-Adapted SARS-CoV-2 Induces Acute Lung Injury and Mortality in Standard Laboratory Mice DOI Creative Commons
Sarah R. Leist, Kenneth H. Dinnon,

Alexandra Schäfer

et al.

Cell, Journal Year: 2020, Volume and Issue: 183(4), P. 1070 - 1085.e12

Published: Sept. 23, 2020

Language: Английский

Citations

597

Association of COVID-19 inflammation with activation of the C5a–C5aR1 axis DOI Creative Commons
Julien Carvelli, Olivier Demaria, Fréderic Vely

et al.

Nature, Journal Year: 2020, Volume and Issue: 588(7836), P. 146 - 150

Published: July 29, 2020

Coronavirus disease 2019 (COVID-19) is a caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has resulted in pandemic1. The C5a complement factor its receptor C5aR1 (also known as CD88) have key role the initiation maintenance of several inflammatory responses recruiting activating neutrophils monocytes1. Here we provide longitudinal analysis immune responses, including phenotypic analyses cells assessments soluble factors that are present blood bronchoalveolar lavage fluid patients at various stages COVID-19 severity, those who were paucisymptomatic or had pneumonia distress syndrome. levels increased proportion to severity high expression receptors found pulmonary myeloid cells, which supports for C5a-C5aR1 axis pathophysiology Anti-C5aR1 therapeutic monoclonal antibodies prevented C5a-mediated recruitment activation human inhibited lung injury knock-in mice. These results suggest blockade could be used limit infiltration damaged organs prevent excessive inflammation endothelialitis associated COVID-19.

Language: Английский

Citations

475

COVID-19 and COPD DOI Creative Commons
Janice M. Leung, Masahiro Niikura, Cheng Wei Tony Yang

et al.

European Respiratory Journal, Journal Year: 2020, Volume and Issue: 56(2), P. 2002108 - 2002108

Published: Aug. 1, 2020

COPD patients have increased risk of severe pneumonia and poor outcomes when they develop COVID-19. This may be related to underlying lung reserves or expression ACE-2 receptor in small airways.https://bit.ly/37dSB8l

Language: Английский

Citations

279

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2): a Systemic Infection DOI
Aleksandra Synowiec, Artur Szczepański, Emilia Barreto-Durán

et al.

Clinical Microbiology Reviews, Journal Year: 2021, Volume and Issue: 34(2)

Published: Jan. 12, 2021

To date, seven identified coronaviruses (CoVs) have been found to infect humans; of these, three highly pathogenic variants emerged in the 21st century. The newest member this group, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was first detected at end 2019 Hubei province, China. Since then, novel has spread worldwide, causing a pandemic; disease caused by virus is called (COVID-19). clinical presentation ranges from asymptomatic mild tract infections and influenza-like illness with accompanying lung injury, multiorgan failure, death. Although lungs are believed be site which SARS-CoV-2 replicates, infected patients often report other symptoms, suggesting involvement gastrointestinal tract, heart, cardiovascular system, kidneys, organs; therefore, following question arises: COVID-19 or systemic disease? This review aims summarize existing data on replication different tissues both ex vivo models.

Language: Английский

Citations

184

The glycosylation in SARS-CoV-2 and its receptor ACE2 DOI Creative Commons
Yanqiu Gong,

Suideng Qin,

Lunzhi Dai

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2021, Volume and Issue: 6(1)

Published: Nov. 15, 2021

Coronavirus disease 2019 (COVID-19), a highly infectious caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has infected more than 235 million individuals and led to 4.8 deaths worldwide as of October 5 2021. Cryo-electron microscopy topology show that the SARS-CoV-2 genome encodes lots glycosylated proteins, such spike (S), envelope (E), membrane (M), ORF3a which are responsible for host recognition, penetration, binding, recycling pathogenesis. Here we reviewed detections, substrates, biological functions glycosylation in proteins well human receptor ACE2, also summarized approved undergoing therapeutics associated with glycosylation. This review may not only broad understanding viral glycobiology, but provide key clues development new preventive therapeutic methodologies against its variants.

Language: Английский

Citations

172

Smoking increases the risk of infectious diseases: A narrative review DOI Creative Commons
Chen Jiang, Qiong Chen, Mingxuan Xie

et al.

Tobacco Induced Diseases, Journal Year: 2020, Volume and Issue: 18(July)

Published: July 14, 2020

1. Chinese Center for Disease Control and Prevention. [2018 Adult Tobacco Survey Report]. http://www.chinacdc.cn/jkzt/st.... Published 2019. Accessed December 24, Google Scholar

Language: Английский

Citations

164

First contact: the role of respiratory cilia in host-pathogen interactions in the airways DOI Open Access

Li Eon Kuek,

Robert J. Lee

AJP Lung Cellular and Molecular Physiology, Journal Year: 2020, Volume and Issue: 319(4), P. L603 - L619

Published: Aug. 12, 2020

Respiratory cilia are the driving force of mucociliary escalator, working in conjunction with secreted airway mucus to clear inhaled debris and pathogens from conducting airways. also one first contact points between host pathogens. Impaired ciliary function is a common pathological feature patients chronic diseases, increasing susceptibility respiratory infections. Common pathogens, including viruses, bacteria, fungi, have been shown target and/or ciliated epithelial cells, resulting disruption clearance that may facilitate infection. Despite being an integral component innate immunity, role their clinical significance during infections still poorly understood. This review examines expression, structure, pathogenic infection discusses specific known interaction viruses function. The emerging biological functions motile relating intracellular signaling potential immunoregulatory roles will be discussed.

Language: Английский

Citations

140

Sex‐based differences in severity and mortality in COVID‐19 DOI Creative Commons
Mustafa Alwani, Aksam Yassin, Raed M. Al‐Zoubi

et al.

Reviews in Medical Virology, Journal Year: 2021, Volume and Issue: 31(6)

Published: March 1, 2021

Summary The current coronavirus disease (COVID‐19) pandemic caused by novel severe acute respiratory syndrome 2 (SARS‐CoV‐2) has a male bias in severity and mortality. This is consistent with previous pandemics such as SARS‐CoV MERS‐CoV, viral infections general. Here, we discuss the sex‐disaggregated epidemiological data for COVID‐19 highlight underlying differences that may explain sexual dimorphism to help inform risk stratification strategies therapeutic options.

Language: Английский

Citations

113

Sex Disparities in COVID-19 Severity and Outcome: Are Men Weaker or Women Stronger? DOI Creative Commons
Rosario Pivonello,

Renata S. Auriemma,

Claudia Pivonello

et al.

Neuroendocrinology, Journal Year: 2020, Volume and Issue: 111(11), P. 1066 - 1085

Published: Nov. 26, 2020

The coronavirus disease 2019 (COVID-19) outbreak, caused by severe acute respiratory syndrome 2 (SARS-CoV-2), is a global public health issue which has profound effects on most aspects of societal well-being, including physical and mental health. A plethora studies globally have suggested the existence sex disparity in severity outcome COVID-19 patients, mainly due to mechanisms virus infection, immune response virus, development systemic inflammation, consequent complications, particularly thromboembolism. Epidemiological data report difference COVID-19, with more favorable course women compared men regardless age, although rate SARS-CoV-2 infection seems be similar both sexes. Sex hormones, androgens estrogens, may not only impact entry load, but also shape clinical manifestations, ultimately disease. current review comprehensively summarizes literature disparities susceptibility as well underpinning pathophysiological molecular mechanisms, provide rationale disparity. These include hormone influence factors that facilitate priming, inflammatory response, coagulation thrombosis diathesis. Based present evidence, appear relatively protected from because effective less pronounced moderate manifestations disease, together lesser predisposition Conversely, susceptible greater In elderly, generally characterized phenomenon inflammaging, overall mortality following are even palpable elderly prone infections, weaker defense, an enhanced thrombotic state women. information revealed highlights potential novel therapeutic approaches employing administration hormonal or antihormonal therapy combination antiviral drugs patients.

Language: Английский

Citations

124

Smoking and COVID-19: Adding Fuel to the Flame DOI Open Access
Vivek K. Kashyap, Anupam Dhasmana, Andrew E. Massey

et al.

International Journal of Molecular Sciences, Journal Year: 2020, Volume and Issue: 21(18), P. 6581 - 6581

Published: Sept. 9, 2020

The coronavirus disease 2019 (COVID-19) pandemic, an infection caused by the severe acute respiratory syndrome (SARS-CoV-2), has led to more than 771,000 deaths worldwide. Tobacco smoking is a major known risk factor for illness and even death from many infections. effects of on COVID-19 are currently controversial. Here, we provide overview current knowledge clinical manifestations, progression, inflammatory responses, immunopathogenesis, racial ethnic disparities, incidence COVID-19. This review also documents future directions related research in epidemiological finding suggests that active associated with increased severity hospitalized patients. Smoking can upregulate angiotensin-converting enzyme-2 (ACE-2) receptor utilized SARS-CoV-2 enter host cell activate ‘cytokine storm’ which lead worsen outcomes act as potential therapeutic target other infectious diseases. pandemic sheds light legacy inequalities regarding gender, racial, health disparities smoking, thus, cessation may help improving outcomes. In addition, flatten curve, staying indoors, avoiding unnecessary social contact, bolstering immune defense system maintaining healthy diet/living highly desirable.

Language: Английский

Citations

101