Endothelial activation and dysfunction caused by influenza A virus (Alphainfluenzavirus influenzae)

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Annual epidemics of influenza result in 3–5 million cases of severe illness and more than 600 000 deaths. Severe forms of influenza are usually characterized by vascular endothelial cells damage. Thus, influenza A viruses, including subtypes A(H1N1)pdm09, A(H3N2), as well as highly pathogenic avian influenza viruses, can infect the vascular endothelium, leading to activation and subsequent dysfunction of these cells. In turn, endothelial dysfunction resulting in systemic morphofunctional changes of endothelial cells, which leads to impaired vascular tone, thrombosis and other complications, and is also a risk factor and profoundly implicated in the pathogenesis of many cardiovascular diseases. Thus, endothelial dysfunction is an important aspect of the pathogenesis of severe influenza, which must be considered in the pathogenetic therapy of this infectious disease.

The aim of the review is to analyze the causes and specify mechanisms of development of endothelial activation and dysfunction caused by influenza A virus.

作者简介

Vladimir Marchenko

North-Western State Medical University Named after I.I. Mechnikov

编辑信件的主要联系方式.
Email: vmarcenco@mail.ru
ORCID iD: 0000-0001-6870-3157

Ph. D. in medicine, Associate Professor of Medical Microbiology Department

俄罗斯联邦, 191015, St. Petersburg

Irina Zhilinskaya

North-Western State Medical University Named after I.I. Mechnikov

Email: vmarcenco@mail.ru
ORCID iD: 0000-0002-0084-1323

D. Sc. in Biology, Professor of Medical Microbiology Department

俄罗斯联邦, 191015, St. Petersburg

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2. Fig. 1. Vascular endothelium functions.

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3. Fig. 2. The coagulation cascades. 1 ‒ intact endothelial cells express antiplatelet and anticoagulant agents (thrombomodulin, antithrombin, tissue factor pathway inhibitor and ADPase) that prevent aggregation of platelet and fibrin formation; 2 ‒ coagulation is usually initiated by an injury to the endothelium, with the exposure of tissue factor and collagen from the subendothelium to the blood factors and the release of von Willebrand factor (vWF); 3 ‒ activation of platelets is initiated by exposure to tissue factor, collagen and vWF. Activated platelets release several mediators (including ADP and vWF), leading to further platelet recruitment, activation, aggregation and plug formation (primary hemostasis); 4 ‒ the extrinsic pathway is initiated by the interaction between tissue factor and Factor VII; 5 ‒ the intrinsic pathway is initiated by the exposure of collagen to Factor XII; 6 ‒ the extrinsic and intrinsic coagulation pathways lead into the final common pathway, which contains cascades involved in the production of thrombin, activated Factor X and the formation of fibrin strands; 7 ‒ fibrin strands increase stability of the platelet plug and lead to the formation of platelet-fibrin clot (secondary hemostasis); 8 ‒ kallikrein, tissue plasminogen activator (tPA) or urokinase plasminogen activator (uPA) convert plasminogen to plasmin, which then degrades and reabsorbs the fibrin strands in process called fibrinolysis. Endothelial factors whose concentration in influenza A virus infection is reliably changed are underlined (see Table).

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