Influenza A(H7N9) virus gains neuraminidase inhibitor resistance without loss of in vivo virulence or transmissibility

Rong Hai, Mirco Schmolke, Victor H. Leyva-Grado, Rajagowthamee R. Thangavel, Irina Margine, Eric L. Jaffe, Florian Krammer, Alicia Solórzano, Adolfo García-Sastre, Peter Palese and Nicole M. Bouvier ()
Additional contact information
Rong Hai: Icahn School of Medicine at Mount Sinai
Mirco Schmolke: Icahn School of Medicine at Mount Sinai
Victor H. Leyva-Grado: Icahn School of Medicine at Mount Sinai
Rajagowthamee R. Thangavel: Icahn School of Medicine at Mount Sinai
Irina Margine: Icahn School of Medicine at Mount Sinai
Eric L. Jaffe: Icahn School of Medicine at Mount Sinai
Florian Krammer: Icahn School of Medicine at Mount Sinai
Alicia Solórzano: Public Health Research Institute and Regional Biocontainment Laboratory, New Jersey Medical School, RUTGERS, The State University of New Jersey
Adolfo García-Sastre: Icahn School of Medicine at Mount Sinai
Peter Palese: Icahn School of Medicine at Mount Sinai
Nicole M. Bouvier: Icahn School of Medicine at Mount Sinai

Nature Communications, 2013, vol. 4, issue 1, 1-9

Abstract: Abstract Without baseline human immunity to the emergent avian influenza A(H7N9) virus, neuraminidase inhibitors are vital for controlling viral replication in severe infections. An amino acid change in the viral neuraminidase associated with drug resistance, NA-R292K (N2 numbering), has been found in some H7N9 clinical isolates. Here we assess the impact of the NA-R292K substitution on antiviral sensitivity and viral replication, pathogenicity and transmissibility of H7N9 viruses. Our data indicate that an H7N9 isolate encoding the NA-R292K substitution is highly resistant to oseltamivir and peramivir and partially resistant to zanamivir. Furthermore, H7N9 reassortants with and without the resistance mutation demonstrate comparable viral replication in primary human respiratory cells, virulence in mice and transmissibility in guinea pigs. Thus, in stark contrast to oseltamivir-resistant seasonal influenza A(H3N2) viruses, H7N9 virus replication and pathogenicity in these models are not substantially altered by the acquisition of high-level oseltamivir resistance due to the NA-R292K mutation.

Date: 2013
References: Add references at CitEc
Citations: View citations in EconPapers (2)

Downloads: (external link)
https://www.nature.com/articles/ncomms3854 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3854

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms3854

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().