Entry of the bat influenza H17N10 virus into mammalian cells is enabled by the MHC class II HLA-DR receptor.
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Accepted version
Author(s)
Type
Journal Article
Abstract
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.
Date Issued
2019-12
Date Acceptance
2019-06-20
Citation
Nature Microbiology, 2019, 4, pp.2035-2038
ISSN
2058-5276
Publisher
Nature Research
Start Page
2035
End Page
2038
Journal / Book Title
Nature Microbiology
Volume
4
Copyright Statement
© 2019 Springer-Verlag. The final publication is available at Springer via https://doi.org/10.1038/s41564-019-0517-3
Identifier
https://www.ncbi.nlm.nih.gov/pubmed/31358984
PII: 10.1038/s41564-019-0517-3
Subjects
Science & Technology
Life Sciences & Biomedicine
Microbiology
A VIRUS
TOPOLOGY
REVEAL
Animals
Chiroptera
Dogs
HEK293 Cells
HLA-DR Antigens
Humans
Madin Darby Canine Kidney Cells
Microarray Analysis
Orthomyxoviridae
Receptors, Virus
Viral Tropism
Virus Internalization
Zoonoses
Animals
Dogs
Chiroptera
Humans
Orthomyxoviridae
Zoonoses
Receptors, Virus
HLA-DR Antigens
Microarray Analysis
Virus Internalization
Viral Tropism
HEK293 Cells
Madin Darby Canine Kidney Cells
0605 Microbiology
1108 Medical Microbiology
Publication Status
Published
Coverage Spatial
England
Date Publish Online
2019-07-29