Radiology of Severe Acute Respiratory Syndrome (SARS)

Ketai, Loren H.; Paul, Narinder; Wong, Kin Fai Ellick

doi:10.1097/01.rti.0000213581.14225.f1

Cited by 73 publications

(38 citation statements)

References 23 publications

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“…The main lung pathology in SARS and MERS is DAD in various stages, which is basically the histological prototype of acute lung injury [43,44]. According to the previous pathological mechanism of SARS, the emergence of GGO suggests that SARS-CoV-2 causes airspace exudates, and pauci-inflammatory alveolar and interstitial oedema [45]. Crazy paving appearance consists of GGO with superimposed interlobular and intralobular septal thickening, reflecting interstitial lesions [46].…”

Section: Typical Imaging Features Of Covid-19mentioning

confidence: 99%

Diagnostic value and key features of computed tomography in Coronavirus Disease 2019

Wang

et al. 2020

Emerging Microbes & Infections

122

104

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On 31 December 2019, a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in Wuhan, Hubei province, China, and caused the outbreak of the Coronavirus Disease 2019 . To date, computed tomography (CT) findings have been recommended as major evidence for the clinical diagnosis of COVID-19 in Hubei, China. This review focuses on the imaging characteristics and changes throughout the disease course in patients with COVID-19 in order to provide some help for clinicians. Typical CT findings included bilateral ground-glass opacity, pulmonary consolidation, and prominent distribution in the posterior and peripheral parts of the lungs. This review also provides a comparison between COVID-19 and other diseases that have similar CT findings. Since most patients with COVID-19 infection share typical imaging features, radiological examinations have an irreplaceable role in screening, diagnosis and monitoring treatment effects in clinical practice.

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Section: Typical Imaging Features Of Covid-19mentioning

confidence: 99%

Diagnostic value and key features of computed tomography in Coronavirus Disease 2019

Wang

et al. 2020

Emerging Microbes & Infections

122

104

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“…In view of the apparent lack of success thus far with antiviral therapies and the time needed to develop vaccines, we propose strategies that focus on blunting the pathobiology that we hypothesize results from ACE1 (angiotensin-converting enzyme 1)/ACE2 imbalance and enhanced Ang II signalling that occurs with SARS-CoV-2 infection. Figure 2 shows a schema of the RAS pathway and is based on data for angiotensin signalling from a range of sources (Forrester et al, 2018;Karnik, Singh, Tirupula, & Unal, 2017;Santos et al, 2019;Tikellis & Thomas, 2012), including the Guide to Pharmacology database (GtoPdb; https://www.guidetopharmacology.org/) (Armstrong et al, 2020). In the 'traditional'/canonical RAS pathway, renin is secreted from the kidney, and angiotensinogen (AGT) is produced and secreted by the liver.…”

Section: Sars-cov-2 Infection Typically Begins In the Upper Respiratorymentioning

confidence: 99%

“…ACE2, a carboxypeptidase (zinc metalloprotease), is the primary enzyme responsible for Ang II degradation, thus regulating signal transduction by Ang II. The conversion by ACE2 of Ang II to Ang (1-7) (and its signalling via MAS1) produces effects that oppose those of Ang II (Karnik et al, 2017;Santos et al, 2018;Santos et al, 2019).…”

Section: The Renin-angiotensin Signalling (Ras) Pathwaymentioning

confidence: 99%

A hypothesis for pathobiology and treatment of COVID‐19: The centrality of ACE1/ACE2 imbalance

Sriram

Insel

2020

British J Pharmacology

171

200

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Angiotensin Converting Enzyme2 is the cell surface binding site for the coronavirus SARS-CoV-2, which causes COVID-19. We propose that an imbalance in the action of ACE1-and ACE2-derived peptides, thereby enhancing angiotensin II (Ang II) signalling is primary driver of COVID-19 pathobiology. ACE1/ACE2 imbalance occurs due to the binding of SARS-CoV-2 to ACE2, reducing ACE2-mediated conversion of Ang II to Ang peptides that counteract pathophysiological effects of ACE1-generated ANG II. This hypothesis suggests several approaches to treat COVID-19 by restoring ACE1/ACE2 balance: (a) AT receptor antagonists; (b) ACE1 inhibitors (ACEIs); (iii) agonists of receptors activated by ACE2-derived peptides (e.g. Ang (1-7), which activates MAS1); (d) recombinant human ACE2 or ACE2 peptides as decoys for the virus.Reducing ACE1/ACE2 imbalance is predicted to blunt COVID-19-associated morbidity and mortality, especially in vulnerable patients. Importantly, approved AT antagonists and ACEIs can be rapidly repurposed to test their efficacy in treating COVID-19.

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“…During the next phase of infection (weeks 2e5), the lungs display signs of fibrosis, in which epithelial cells and alveolar spaces show fibrin deposition and infiltration of inflammatory cells and fibroblasts. During the final stage (weeks 6e8), pulmonary tissue becomes fibrotic with collagen deposits, and cellular proliferation is seen in alveoli and interstitial spaces (Cheung et al, 2004;Gu and Korteweg, 2007;Ketai et al, 2006). Radiographic features of patient's lungs varied greatly by individual however characteristic features were present in most patients including progression from unilateral focal air-space opacity to multifocal or bilateral consolidation in the later phases of disease.…”

Section: Sars Pathogenesismentioning

confidence: 99%

The role of epidermal growth factor receptor (EGFR) signaling in SARS coronavirus-induced pulmonary fibrosis

2017

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Many survivors of the 2003 outbreak of severe acute respiratory syndrome (SARS) developed residual pulmonary fibrosis with increased severity seen in older patients. Autopsies of patients that died from SARS also showed fibrosis to varying extents. Pulmonary fibrosis can be occasionally seen as a consequence to several respiratory viral infections but is much more common after a SARS coronavirus (SARS-CoV) infection. Given the threat of future outbreaks of severe coronavirus disease, including Middle East respiratory syndrome (MERS), it is important to understand the mechanisms responsible for pulmonary fibrosis, so as to support the development of therapeutic countermeasures and mitigate sequelae of infection. In this article, we summarize pulmonary fibrotic changes observed after a SARS-CoV infection, discuss the extent to which other respiratory viruses induce fibrosis, describe available animal models to study the development of SARS-CoV induced fibrosis and review evidence that pulmonary fibrosis is caused by a hyperactive host response to lung injury mediated by epidermal growth factor receptor (EGFR) signaling. We summarize work from our group and others indicating that inhibiting EGFR signaling may prevent an excessive fibrotic response to SARS-CoV and other respiratory viral infections and propose directions for future research.

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Radiology of Severe Acute Respiratory Syndrome (SARS)

Cited by 73 publications

References 23 publications

Diagnostic value and key features of computed tomography in Coronavirus Disease 2019

Diagnostic value and key features of computed tomography in Coronavirus Disease 2019

A hypothesis for pathobiology and treatment of COVID‐19: The centrality of ACE1/ACE2 imbalance

The role of epidermal growth factor receptor (EGFR) signaling in SARS coronavirus-induced pulmonary fibrosis

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