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Nat.Microb. Entry of the bat influenza H17N10 virus into mammalian cells is enabled by the MHC class II HLA-DR receptor

tetano

Editor, Senior Moderator
Nat Microbiol. 2019 Jul 29. doi: 10.1038/s41564-019-0517-3. [Epub ahead of print]
[h=1]Entry of the bat influenza H17N10 virus into mammalian cells is enabled by the MHC class II HLA-DR receptor.[/h] Giotis ES[SUP]1[/SUP], Carnell G[SUP]2,[/SUP][SUP]3[/SUP], Young EF[SUP]4,[/SUP][SUP]5[/SUP], Ghanny S[SUP]6[/SUP], Soteropoulos P[SUP]6[/SUP], Wang LF[SUP]7[/SUP], Barclay WS[SUP]8[/SUP], Skinner MA[SUP]8[/SUP], Temperton N[SUP]2[/SUP].
[h=3]Author information[/h]

[h=3]Abstract[/h] Haemagglutinin and neuraminidase surface glycoproteins of the bat influenza H17N10 virus neither bind to nor cleave sialic acid receptors, indicating that this virus employs cell entry mechanisms distinct from those of classical influenza A viruses. We observed that certain human haematopoietic cancer cell lines and canine MDCK II cells are susceptible to H17-pseudotyped viruses. We identified the human HLA-DR receptor as an entry mediator for H17 pseudotypes, suggesting that H17N10 possesses zoonotic potential.


PMID: 31358984 DOI: 10.1038/s41564-019-0517-3
 
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