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Genomics. 2013 Feb;101(2):101-12. doi: 10.1016/j.ygeno.2012.11.008. Epub 2012 Nov 27.

Neutrophils infected with highly virulent influenza H3N2 virus exhibit augmented early cell death and rapid induction of type I interferon signaling pathways.

Author information

1
Computation and Systems Biology Program, Singapore-MIT Alliance, Singapore.
2
Infectious Diseases Program, Department of Microbiology, Yong Loo Lin School of Medicine, National University Health System, National University of Singapore, Kent Ridge, Singapore.
3
Massachusetts Institute of Technology, Cambridge, MA, USA.
4
BioInformatics Research Centre, Nanyang Technological University, Singapore.
5
Infectious Diseases Program, Department of Microbiology, Yong Loo Lin School of Medicine, National University Health System, National University of Singapore, Kent Ridge, Singapore. Electronic address: micctk@nus.edu.sg.

Abstract

We developed a model of influenza virus infection of neutrophils by inducing differentiation of the MPRO promyelocytic cell line. After 5 days of differentiation, about 20-30% of mature neutrophils could be detected. Only a fraction of neutrophils were infected by highly virulent influenza (HVI) virus, but were unable to support active viral replication compared with MDCK cells. HVI infection of neutrophils augmented early and late apoptosis as indicated by annexin V and TUNEL assays. Comparison between the global transcriptomic responses of neutrophils to HVI and low virulent influenza (LVI) revealed that the IFN regulatory factor and IFN signaling pathways were the most significantly overrepresented pathways, with activation of related genes in HVI as early as 3 h. Relatively consistent results were obtained by real-time RT-PCR of selected genes associated with the type I IFN pathway. Early after HVI infection, comparatively enhanced expression of apoptosis-related genes was also elicited.

PMID:
23195410
DOI:
10.1016/j.ygeno.2012.11.008
[Indexed for MEDLINE]
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