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Death Mechanisms of Pulmonary Alveolocytes in Mice Infected with Influenza Viruses A/H1N1/California/04/2009 and A/H5N1/Goose/Krasnoozerskoye/627/05

tetano

Editor, Senior Moderator
Bull Exp Biol Med. 2019 Mar 22. doi: 10.1007/s10517-019-04408-0. [Epub ahead of print]
[h=1]Death Mechanisms of Pulmonary Alveolocytes in Mice Infected with Influenza Viruses A/H1N1/California/04/2009 and A/H5N1/Goose/Krasnoozerskoye/627/05.[/h] Cherdantseva LA[SUP]1[/SUP], Kovner AV[SUP]2[/SUP], Sharkova TV[SUP]3[/SUP], Shkurupy VA[SUP]2,[/SUP][SUP]4[/SUP], Shestopalov AM[SUP]2[/SUP], Potapova OV[SUP]3[/SUP].
[h=3]Author information[/h]

[h=3]Abstract[/h] In CBA mice infected with influenza viruses A/H1N1/California/04/2009 and A/H5N1/Goose/Krasnoozerskoye/627/05 in a dose of 10 MLD[SUB]50[/SUB], the mechanisms of death of pulmonary alveolocytes over 10 postinfection days were studied by light microscopy, immunohistochemistry, and morphometry. In mice infected with A/H1N1, alveolocytes died predominantly via necrosis, while apoptosis mostly employed the mitochondrial pathway. In mice infected with A/H5N1, apoptosis was the dominant mechanism of alveolocyte death proceeded via membrane receptor signaling followed by switching to FAS-mediated pathway via activation of FADD, the apoptotic signal transduction protein.


[h=4]KEYWORDS:[/h] alveolocytes; apoptosis; caspases 9, 3; influenza A viruses; necrosis

PMID: 30903504 DOI: 10.1007/s10517-019-04408-0
 
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