Pandemic H1N1 influenza A viruses suppress immunogenic RIPK3-driven dendritic cell death

Boris M. Hartmann, Randy A. Albrecht, Elena Zaslavsky, German Nudelman, Hanna Pincas, Nada Marjanovic, Michael Schotsaert, Carles Martínez-Romero, Rafael Fenutria, Justin P. Ingram, Irene Ramos, Ana Fernandez-Sesma, Siddharth Balachandran, Adolfo García-Sastre and Stuart C. Sealfon ()
Additional contact information
Boris M. Hartmann: Icahn School of Medicine at Mount Sinai
Randy A. Albrecht: Icahn School of Medicine at Mount Sinai
Elena Zaslavsky: Icahn School of Medicine at Mount Sinai
German Nudelman: Icahn School of Medicine at Mount Sinai
Hanna Pincas: Icahn School of Medicine at Mount Sinai
Nada Marjanovic: Icahn School of Medicine at Mount Sinai
Michael Schotsaert: Icahn School of Medicine at Mount Sinai
Carles Martínez-Romero: Icahn School of Medicine at Mount Sinai
Rafael Fenutria: Icahn School of Medicine at Mount Sinai
Justin P. Ingram: Fox Chase Cancer Center
Irene Ramos: Icahn School of Medicine at Mount Sinai
Ana Fernandez-Sesma: Icahn School of Medicine at Mount Sinai
Siddharth Balachandran: Fox Chase Cancer Center
Adolfo García-Sastre: Icahn School of Medicine at Mount Sinai
Stuart C. Sealfon: Icahn School of Medicine at Mount Sinai

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract The risk of emerging pandemic influenza A viruses (IAVs) that approach the devastating 1918 strain motivates finding strain-specific host–pathogen mechanisms. During infection, dendritic cells (DC) mature into antigen-presenting cells that activate T cells, linking innate to adaptive immunity. DC infection with seasonal IAVs, but not with the 1918 and 2009 pandemic strains, induces global RNA degradation. Here, we show that DC infection with seasonal IAV causes immunogenic RIPK3-mediated cell death. Pandemic IAV suppresses this immunogenic DC cell death. Only DC infected with seasonal IAV, but not with pandemic IAV, enhance maturation of uninfected DC and T cell proliferation. In vivo, circulating T cell levels are reduced after pandemic, but not seasonal, IAV infection. Using recombinant viruses, we identify the HA genomic segment as the mediator of cell death inhibition. These results show how pandemic influenza viruses subvert the immune response.

Date: 2017
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-017-02035-9 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:8:y:2017:i:1:d:10.1038_s41467-017-02035-9

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

DOI: 10.1038/s41467-017-02035-9

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 ().