2013
DOI: 10.1007/s10517-013-1981-z
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Morphofunctional Changes in the Lung Vascular Endotheliocytes in Mice with Influenza A/H5N1 A/Goose/Krasnoozerskoye/627/05

Abstract: The lung vessels of male C57Bl/6 mice were studied by immunohistochemical and stereometric methods on days 1, 3, 6, and 10 after intranasal infection with influenza A/H5N1 A/Goose/Krasnoozerskoye/627/05 virus. Influenza virus replicates in mouse lung vascular endotheliocytes and persists in these cells until the beginning of convalescence (day 10 after infection). This indicates high pathogenic activity of this strain. Active proliferation and apoptosis of endotheliocytes are detected early after infection; th… Show more

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Cited by 3 publications
(4 citation statements)
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“…Of the proteins with reduced expression identified in our study, the five most-reduced DEPs in samples from influenza-infected patients that were also correlated with higher viral loads were CTSD, KLK7, MFGE8, MAPK9 and CD27, respectively. Cathepsin D (CTSD) is a lysosomal aspartic protease that has been shown to be highly expressed in alveolar resident macrophages and Kupffer cells following IAV infections in mice [ 67 , 68 ]. KLK7 is a chymotrypsin-like serine protease that cleaves proteins at tyrosine, phenylalanine or leucine [ 69 ].…”
Section: Discussionmentioning
confidence: 99%
“…Of the proteins with reduced expression identified in our study, the five most-reduced DEPs in samples from influenza-infected patients that were also correlated with higher viral loads were CTSD, KLK7, MFGE8, MAPK9 and CD27, respectively. Cathepsin D (CTSD) is a lysosomal aspartic protease that has been shown to be highly expressed in alveolar resident macrophages and Kupffer cells following IAV infections in mice [ 67 , 68 ]. KLK7 is a chymotrypsin-like serine protease that cleaves proteins at tyrosine, phenylalanine or leucine [ 69 ].…”
Section: Discussionmentioning
confidence: 99%
“…Hence, the necrotic processes in influenza are implemented via cytodestructive effects of the viruses; they are stimulated by hypoxia, ischemia, and thrombosis of the blood vessels resulting from enhanced tropicity of influenza viruses to endotheliocytes [4,9]. Seemingly, the apoptotic death of the cells is induced by hypoxia; its development depends on the number and activation degree of macrophages in the infiltrates and their up-regulated secretion of nitric oxide, proteases [1,2,4], and apoptosis-inducing factors, which is characteristic of mitochondrial pathway; moreover, apoptosis can be triggered from cell membrane via the plasmalemmal receptor pathway. Probably, the functional status and the number of activated macrophages can select the predominant pathways, which trigger apoptosis during viral influenzas.…”
Section: Resultsmentioning
confidence: 99%
“…In infected mice, immunohistochemistry visualized the positive staining of alveolocytes for viral antigen A [3][4][5].…”
Section: Resultsmentioning
confidence: 99%
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