Key result
H1N1 influenza infection causes long-term endothelial dysfunction in rats, reducing eNOS expression by ~39%.
Why the study?
Influenza A(H1N1)pdm09 virus alters blood vessel function in the acute period of infection, but the duration of systemic microvascular endothelial vasomotor alterations remained to be studied.
p-value: p=<0.05
Influenza A(H1N1)pdm09 infection induces prolonged systemic endothelial dysfunction long after viral clearance, highlighting a potential pathogenetic mechanism for post-influenza cardiovascular complications.
May link resolved influenza to lasting endothelial dysfunction; hypothesis-generating for post-influenza CV complications pending human studies.
Introduction. The influenza A virus (IAV) can infect vascular endothelial cells and cause activation and/or dysfunction of the endothelium. Previously, we have shown that the influenza A(H1N1)pdm09 virus leads to alteration in functional activity of blood vessels in different vascular beds, and also causes various histopathological changes in pulmonary blood vessels of Wistar rats in the acute period of infection. Aim – to study the duration of systemic alteration in vasomotor function of microvascular endothelium caused by the influenza A(H1N1)pdm09 virus. Materials and methods. The Wistar rats were intranasally infected with the influenza A/St. Petersburg/48/16 (H1N1)pdm09 virus and at 1, 4, 7, 14, 21, 30, 60 and 90 days post infection (dpi) they were anesthetized and necropsied. The expression level of endothelial nitric oxide synthase (eNOS) was determined in mesenteric vascular endothelium by immunohistochemistry. The vasomotor activity of the mesenteric arteries was studied using wire myography. Results. The influenza A(H1N1)pdm09 virus causes a decrease in eNOS expression by 13–39 % within 60 dpi (p<0.05). In addition, the influenza virus also reduces the maximal response of mesenteric arteries to the vasodilator by 74–108 % within 21 days (p<0.0001) and reduces the response by 16–26 % within 30 and 60 dpi (p<0.0001), respectively, and also increases the maximum response of the arteries to the vasoconstrictor by 26–57 % within 30 dpi (p<0.05). It should be noted that such long-term changes are observed while virus is eliminated by the 7th dpi. Conclusion. The influenza A(H1N1) pdm09 virus causes long-term endothelial dysfunction in the Wistar rats which is characterized by the reduced expression of eNOS in mesenteric microvascular endothelium within 60 dpi, decrease of the maximal response of mesenteric microvessels to vasodilator within 60 dpi and increase of the maximal response to vasoconstrictor within 30 dpi. Alterations of systemic functional activity of mesenteric microvessels in rats infected with influenza A(H1N1)pdm09 virus are registered in absence of the reproduction of virus in mesenteric blood vessels while virus is eliminated from pulmonary tissues by the 7th dpi.
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Marchenko et al. (2023) studied Influenza A(H1N1)pdm09 infection (n=60). Influenza A(H1N1)pdm09 infection vs. Vehicle (0.2 ml alpha-MEM) was evaluated on Endothelial nitric oxide synthase (eNOS) expression in mesenteric vascular endothelium and vasomotor activity (p=<0.05). Influenza A(H1N1)pdm09 reduced eNOS expression by 13-39% (p<0.05) up to 60 days and decreased maximal vasodilator response by 74-108% (p<0.0001) up to 21 days post-infection.
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