Key result
Influenza A drives severe disease and cardiovascular complications through vascular endothelial activation and dysfunction.
Why the study?
Endothelial dysfunction is an important aspect of the pathogenesis of severe influenza that leads to vascular complications and cardiovascular disease, requiring analysis of its causes and specific mechanisms.
Influenza A virus infection leads to endothelial activation and dysfunction, which is an important mechanism in the pathogenesis of severe influenza and associated cardiovascular complications.
Suggests endothelial-targeted strategies in severe influenza; leaves open clinical translation pending prospective trials.
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.
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Marchenko et al. (2024) conducted a review in Influenza A virus infection. Influenza A viruses infect the vascular endothelium, leading to endothelial activation and dysfunction that contributes to severe influenza pathogenesis and cardiovascular complications.
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