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1.
Front Immunol ; 11: 1312, 2020.
Article in English | MEDLINE | ID: covidwho-615475

ABSTRACT

Respiratory, circulatory, and renal failure are among the gravest features of COVID-19 and are associated with a very high mortality rate. A common denominator of all affected organs is the expression of angiotensin-converting enzyme 2 (ACE2), a protease responsible for the conversion of Angiotensin 1-8 (Ang II) to Angiotensin 1-7 (Ang 1-7). Ang 1-7 acts on these tissues and in other target organs via Mas receptor (MasR), where it exerts beneficial effects, including vasodilation and suppression of inflammation and fibrosis, along an attenuation of cardiac and vascular remodeling. Unfortunately, ACE2 also serves as the binding receptor of SARS viral spike glycoprotein, enabling its attachment to host cells, with subsequent viral internalization and replication. Although numerous reports have linked the devastating organ injuries to viral homing and attachment to organ-specific cells widely expressing ACE2, little attention has been given to ACE-2 expressed by the immune system. Herein we outline potential adverse effects of SARS-CoV2 on macrophages and dendritic cells, key cells of the immune system expressing ACE2. Specifically, we propose a new hypothesis that, while macrophages play an important role in antiviral defense mechanisms, in the case of SARS-CoV, they may also serve as a Trojan horse, enabling viral anchoring specifically within the pulmonary parenchyma. It is tempting to assume that diverse expression of ACE2 in macrophages among individuals might govern the severity of SARS-CoV-2 infection. Moreover, reallocation of viral-containing macrophages migrating out of the lung to other tissues is theoretically plausible in the context of viral spread with the involvement of other organs.


Subject(s)
Betacoronavirus/metabolism , Dendritic Cells/metabolism , Lung/pathology , Macrophages, Alveolar/metabolism , Peptidyl-Dipeptidase A/metabolism , Angiotensin-Converting Enzyme 2 , Betacoronavirus/immunology , COVID-19 , Coronavirus Infections/immunology , Coronavirus Infections/pathology , Dendritic Cells/immunology , Dendritic Cells/virology , Humans , Lung/virology , Macrophages, Alveolar/immunology , Macrophages, Alveolar/virology , Pandemics , Parenchymal Tissue/pathology , Parenchymal Tissue/virology , Pneumonia, Viral/immunology , Pneumonia, Viral/pathology , Receptors, Virus/metabolism , SARS-CoV-2 , Spike Glycoprotein, Coronavirus/metabolism
2.
Thromb Res ; 193: 86-89, 2020 09.
Article in English | MEDLINE | ID: covidwho-548092

ABSTRACT

INTRODUCTION: COVID-19 infections are associated with a high prevalence of venous thromboembolism, particularly pulmonary embolism (PE). It is suggested that COVID-19 associated PE represents in situ immunothrombosis rather than venous thromboembolism, although the origin of thrombotic lesions in COVID-19 patients remains largely unknown. METHODS: In this study, we assessed the clinical and computed tomography (CT) characteristics of PE in 23 consecutive patients with COVID-19 pneumonia and compared these to those of 100 consecutive control patients diagnosed with acute PE before the COVID-19 outbreak. Specifically, RV/LV diameter ratio, pulmonary artery trunk diameter and total thrombus load (according to Qanadli score) were measured and compared. RESULTS: We observed that all thrombotic lesions in COVID-19 patients were found to be in lung parenchyma affected by COVID-19. Also, the thrombus load was lower in COVID-19 patients (Qanadli score -8%, 95% confidence interval [95%CI] -16 to -0.36%) as was the prevalence of the most proximal PE in the main/lobar pulmonary artery (17% versus 47%; -30%, 95%CI -44% to -8.2). Moreover, the mean RV/LV ratio (mean difference -0.23, 95%CI -0.39 to -0.07) and the prevalence of RV/LV ratio >1.0 (prevalence difference -23%, 95%CI -41 to -0.86%) were lower in the COVID-19 patients. CONCLUSION: Our findings therefore suggest that the phenotype of COVID-19 associated PE indeed differs from PE in patients without COVID-19, fuelling the discussion on its pathophysiology.


Subject(s)
Coronavirus Infections/complications , Lung/diagnostic imaging , Pneumonia, Viral/complications , Pulmonary Embolism/diagnostic imaging , Pulmonary Embolism/etiology , Aged , Betacoronavirus/isolation & purification , COVID-19 , Coronavirus Infections/virology , Female , Humans , Lung/virology , Male , Middle Aged , Pandemics , Parenchymal Tissue/diagnostic imaging , Parenchymal Tissue/virology , Pneumonia, Viral/virology , Pulmonary Embolism/virology , SARS-CoV-2 , Tomography, X-Ray Computed
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