scholarly journals Histopathological findings in fatal COVID-19 severe acute respiratory syndrome: preliminary experience from a series of 10 Spanish patients

Thorax ◽  
2020 ◽  
Vol 75 (12) ◽  
pp. 1116-1118
Author(s):  
Borja Recalde-Zamacona ◽  
Laura García-Tobar ◽  
Alan Argueta ◽  
Laura Álvarez ◽  
Carlos Eduardo De Andrea ◽  
...  
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Biochemical Markers ◽  
Inflammatory Infiltrate ◽  
Diffuse Alveolar Damage ◽  
Cardiac Injury ◽  
Medium Size ◽  
Cytokine Storm ◽  
Paraffin Sections ◽  
Histopathological Findings ◽  
Lung Histopathology

In December 2019, an outbreak of severe acute respiratory syndrome associated to SARS-CoV2 was reported in Wuhan, China. To date, little is known on histopathological findings in patients infected with the new SARS-CoV2. Lung histopathology shows features of acute and organising diffuse alveolar damage. Subtle cellular inflammatory infiltrate has been found in line with the cytokine storm theory. Medium-size vessel thrombi were frequent, but capillary thrombi were not present. Despite the elevation of biochemical markers of cardiac injury, little histopathological damage could be confirmed. Viral RNA from paraffin sections was detected at least in one organ in 90% patients.

COVID-19

2022 ◽  
pp. 97-108
Author(s):  
Ahmed Draoui ◽  
Hicham Chatoui ◽  
Soraia El Baz ◽  
Hanane Rais ◽  
Bilal El-Mansoury ◽  
...  
Keyword(s):  
Respiratory Failure ◽  
Inflammatory Infiltrate ◽  
Early Stage ◽  
Diffuse Alveolar Damage ◽  
Advanced Stage ◽  
Cytokine Storm ◽  
Invasive Ventilation ◽  
Hypoxemic Respiratory Failure ◽  
Non Invasive ◽  
Viral Inclusions

SARS-CoV-2 infection is characterized by its high contagiousness and unusual potential lethality. Microscopically, diffuse alveolar damage is the main histologic lung injury dominated by alveolar destruction. At the early stage, the authors note non-specific lesions similar to lesions of diffuse alveolar damage. In particular, the alveoli dilated and filled with exudative fibromyxoid material, the thickening of the interalveolar partitions by edema and an essentially mononuclear inflammatory infiltrate with eosinophilic hyaline membranes covering the alveoli. Viral inclusions are not generally found, and at an advanced stage, the installation of pulmonary fibrosis is noted. The place of non-invasive and/or invasive ventilation is undetermined in hypoxemic respiratory failure secondary to SARS-Cov-2 pneumonia, whereas in the most severe cases of COVID-19, the use of oxygenation by extracorporeal membrane is immediate. The cytokine storm in the lungs prompted clinicians to administer immunomodulators, the results of which was a reduction in hospital mortality.

scholarly journals COVID-19 and the Heart

2020 ◽  
Vol 126 (10) ◽  
pp. 1443-1455 ◽  
Author(s):  
Akbarshakh Akhmerov ◽  
Eduardo Marbán
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Cardiac Injury ◽  
Clinical Syndrome ◽  
Cytokine Storm ◽  
Novel Coronavirus

Infection with the severe acute respiratory syndrome novel coronavirus produces a clinical syndrome known as 2019 novel coronavirus disease (COVID-19). When severe, COVID-19 is a systemic illness characterized by hyperinflammation, cytokine storm, and elevations of cardiac injury biomarkers. Here, we review what is known about the pathophysiology of COVID-19, its cardiovascular manifestations, and emerging therapeutic prospects. In this rapidly moving field, this review was comprehensive as of April 3, 2020.

scholarly journals Laboratory biochemical markers of cardiac injury by COVID-19: an integrative review.

2021 ◽  
Vol 47 (1) ◽  
Author(s):  
Wagner Rodrigues de Assis Soares ◽  
Máyra Beatriz Alves Andrade ◽  
Anne Araújo de Jesus Oliveira ◽  
Pedro Gabriel Santos Brito ◽  
Gabriel Novaes Miranda ◽  
...  
Keyword(s):  
Biochemical Markers ◽  
Cardiac Injury ◽  
Integrative Review

scholarly journals Non-Coding RNAs in COVID-19: Emerging Insights and Current Questions

2021 ◽  
Vol 7 (3) ◽  
pp. 54
Author(s):  
Tobias Plowman ◽  
Dimitris Lagos
Keyword(s):  
Immune Response ◽  
Severe Acute Respiratory Syndrome ◽  
Immune Cell ◽  
Cytokine Storm ◽  
Cell Recruitment ◽  
Vascular Dysregulation ◽  
Virus Rna ◽  
Growing Body ◽  
Non Coding Rnas ◽  
Immune Cell Recruitment

The highly infectious severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged as the causative agent of coronavirus disease 2019 (COVID-19) in late 2019, igniting an unprecedented pandemic. A mechanistic picture characterising the acute immunopathological disease in severe COVID-19 is developing. Non-coding RNAs (ncRNAs) constitute the transcribed but un-translated portion of the genome and, until recent decades, have been undiscovered or overlooked. A growing body of research continues to demonstrate their interconnected involvement in the immune response to SARS-CoV-2 and COVID-19 development by regulating several of its pathological hallmarks: cytokine storm syndrome, haemostatic alterations, immune cell recruitment, and vascular dysregulation. There is also keen interest in exploring the possibility of host–virus RNA–RNA and RNA–RBP interactions. Here, we discuss and evaluate evidence demonstrating the involvement of short and long ncRNAs in COVID-19 and use this information to propose hypotheses for future mechanistic and clinical studies.

scholarly journals Misfortune never comes singly - the first case of COVID-19 with rupture of thoracic aortic aneurysm

2020 ◽  
Author(s):  
Kun Zhao ◽  
Zhang Cao ◽  
Changju Zhu ◽  
Yi Zhang ◽  
Feifan Chen
Keyword(s):  
Aortic Aneurysm ◽  
Severe Acute Respiratory Syndrome ◽  
Hospital Admission ◽  
Thoracic Aortic Aneurysm ◽  
Warning Signs ◽  
Cytokine Storm ◽  
Case Presentation ◽  
First Case

Abstract Background: SARS-CoV-2 is a newly discovered virus, leading COVID-19 a global threaten nowadays. Case Presentation: The first case of a patient with a thoracic aortic aneurysm (TAA) that became infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was reported here. The patient died suddenly from a ruptured aorta 19 h after hospital admission. Conclusion: COVID-19 patients with TAA should attract the highest vigilance as COVID-19 might expedite the process of TAA rupture through cytokine storm syndrome, leading to rapid death with little or no warning signs.

Cytokine storm syndrome in SARS-CoV-2: a review

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Braira Wahid ◽  
Noshaba Rani ◽  
Muhammad Idrees
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Failure ◽  
Severe Acute Respiratory Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Cytokine Storm ◽  
Global Level ◽  
Management Option ◽  
Human Contact

Abstract After wreaking havoc on a global level with a total of 5,488,825 confirmed cases and 349,095 deaths as of May 2020, severe acute respiratory syndrome coronavirus 2 is truly living up to the expectations of a 21st-century pandemic. Since the major cause of mortality is a respiratory failure from acute respiratory distress syndrome, the only present-day management option is supportive as the transmission relies solely on human-to-human contact. Patients suffering from coronavirus disease 2019 (COVID-19) should be tested for hyper inflammation to screen those for whom immunosuppression can increases chances of survival. As more and more clinical data surfaces, it suggests patients with mild or severe cytokine storms are at greater risk of failing fatally and hence these cytokine storms should be targets for treatment in salvaging COVID-19 patients.

scholarly journals SARS Unique Domain (SUD) of Severe Acute Respiratory Syndrome Coronavirus Induces NLRP3 Inflammasome-Dependent CXCL10-Mediated Pulmonary Inflammation

2020 ◽  
Vol 21 (9) ◽  
pp. 3179 ◽  
Author(s):  
Young-Sheng Chang ◽  
Bo-Han Ko ◽  
Jyh-Cherng Ju ◽  
Hsin-Hou Chang ◽  
Su-Hua Huang ◽  
...  
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Nlrp3 Inflammasome ◽  
Inflammatory Responses ◽  
Profile Analysis ◽  
Diffuse Alveolar Damage ◽  
Pulmonary Inflammation ◽  
Antiviral Agents ◽  
Lung Epithelial Cells ◽  
Unique Domain

Severe acute respiratory syndrome–associated coronavirus (SARS-CoV) initiates the cytokine/chemokine storm-mediated lung injury. The SARS-CoV unique domain (SUD) with three macrodomains (N, M, and C), showing the G-quadruplex binding activity, was examined the possible role in SARS pathogenesis in this study. The chemokine profile analysis indicated that SARS-CoV SUD significantly up-regulated the expression of CXCL10, CCL5 and interleukin (IL)-1β in human lung epithelial cells and in the lung tissues of the mice intratracheally instilled with the recombinant plasmids. Among the SUD subdomains, SUD-MC substantially activated AP-1-mediated CXCL10 expression in vitro. In the wild type mice, SARS-CoV SUD-MC triggered the pulmonary infiltration of macrophages and monocytes, inducing CXCL10-mediated inflammatory responses and severe diffuse alveolar damage symptoms. Moreover, SUD-MC actuated NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome-dependent pulmonary inflammation, as confirmed by the NLRP3 inflammasome inhibitor and the NLRP3−/− mouse model. This study demonstrated that SARS-CoV SUD modulated NLRP3 inflammasome-dependent CXCL10-mediated pulmonary inflammation, providing the potential therapeutic targets for developing the antiviral agents.

scholarly journals Platelet Function in Viral Immunity and SARS-CoV-2 Infection

2021 ◽  
Author(s):  
Afaf Allaoui ◽  
Akif A. Khawaja ◽  
Oussama Badad ◽  
Mariam Naciri ◽  
Marie Lordkipanidzé ◽  
...  
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Infectious Diseases ◽  
Immune Responses ◽  
Cytokine Storm ◽  
Blood Components ◽  
Viral Immunity ◽  
Cytokines And Chemokines ◽  
Activated Platelets ◽  
Viral Receptors

AbstractPlatelets, as nonnucleated blood components, are classically recognized for their pivotal role in hemostasis. In recent years, however, accumulating evidence points to a nonhemostatic role for platelets, as active participants in the inflammatory and immune responses to microbial organisms in infectious diseases. This stems from the ability of activated platelets to secrete a plethora of immunomodulatory cytokines and chemokines, as well as directly interplaying with viral receptors. While much attention has been given to the role of the cytokine storm in the severity of the coronavirus disease 2019 (COVID-19), less is known about the contribution of platelets to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Here, we give a brief overview on the platelet contribution to antiviral immunity and response during SARS-CoV-2 infection.

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