Influenza A Virus Causes Histopathological Changes and Impairment in Functional Activity of Blood Vessels in Different Vascular Beds.

Vladimir Marchenko,Ekaterina Podyacheva,Irina N Zhilinskaya,Yana Toropova,Irina Zelinskaya,Tatyana Shmakova,Dmitry Lioznov

doi:10.3390/v14020396

Abstract

It has been established that blood vessels are a target for influenza virus; however, the mechanism by which virus affects the cardiovascular system remains unknown. The aim of the study is the identification of histological changes and changes in the functional activity of the pulmonary and mesenteric blood vessels of Wistar rats. Wistar rats were intranasally infected with the influenza A(H1N1)pdm09 virus. At 24 and 96 h post infection (hpi), histopathological changes were observed in lung tissues with the absence of histological changes in mesenteric tissues. The functional activity of pulmonary and mesenteric arteries was determined using wire myography. In pulmonary arteries, there was a tendency towards an increase in integral response to the vasodilator and a decrease in the integral response to the vasoconstrictor at 24 hpi (compared with control). At 96 hpi, a tendency towards a decrease in the integral response to the vasoconstrictor persisted, while the response to acetylcholine was slightly increased. The functional activity of the mesenteric blood vessels was inverted: a significant decrease in the integral response to the vasodilator and an increase in the response to the vasoconstrictor at 24 hpi were observed; at 96 hpi, the integral response to the vasoconstrictor persisted, while the response to the vasodilator remained significantly reduced. Obtained data indicate the development of endothelial dysfunction in non-lethal and clinically non-severe experimental influenza virus infection.

Highlights

Influenza virus selectively infects and damages the epithelium of the respiratory tract but can infect other tissues and organs, including the nervous and cardiovascular system [1,2]
It was shown that these disorders are mainly associated with damage to the vascular endothelium in different organs and tissues that have receptors, which are necessary for virus adsorption [15–17]
We developed an experimental model of non-lethal influenza virus infection in mature Wistar rats [21]

Summary

Introduction

Influenza virus selectively infects and damages the epithelium of the respiratory tract but can infect other tissues and organs, including the nervous and cardiovascular system [1,2]. As shown by epidemiological and clinical studies, a high incidence of cardiovascular pathology in influenza is noted, especially in patients with comorbidities, including any chronic respiratory condition and cardiovascular disorders [11,12]. It was shown that these disorders are mainly associated with damage to the vascular endothelium in different organs and tissues that have receptors (sialic acids with an α2, 6 glycosidic bond), which are necessary for virus adsorption [15–17]. It has been established that the vascular endothelium and hemostatic system are targets for the influenza virus [16,18–20]. This aspect of pathogenesis is currently not taken into consideration in the development of treatment approaches for influenza, and the mechanism by which the virus affects the cardiovascular system remains unknown

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