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J Theor Biol. 2014 Jun 21;351:47-57. doi: 10.1016/j.jtbi.2014.02.029. Epub 2014 Mar 2.

Model of influenza A virus infection: dynamics of viral antagonism and innate immune response.

Author information

1
Department of Neurology and Center for Translational Systems Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States.
2
Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States; Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States.
3
Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States; Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States; Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States.
4
Department of Physics, Ohio State University, Columbus, OH 43210, United States.
5
Department of Neurology and Center for Translational Systems Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States. Electronic address: fernand.hayot@mssm.edu.

Abstract

Viral antagonism of host responses is an essential component of virus pathogenicity. The study of the interplay between immune response and viral antagonism is challenging due to the involvement of many processes acting at multiple time scales. Here we develop an ordinary differential equation model to investigate the early, experimentally measured, responses of human monocyte-derived dendritic cells to infection by two H1N1 influenza A viruses of different clinical outcomes: pandemic A/California/4/2009 and seasonal A/New Caledonia/20/1999. Our results reveal how the strength of virus antagonism, and the time scale over which it acts to thwart the innate immune response, differs significantly between the two viruses, as is made clear by their impact on the temporal behavior of a number of measured genes. The model thus sheds light on the mechanisms that underlie the variability of innate immune responses to different H1N1 viruses.

KEYWORDS:

Immunology; Interferon; NS1; ODE model

PMID:
24594370
PMCID:
PMC4012420
DOI:
10.1016/j.jtbi.2014.02.029
[Indexed for MEDLINE]
Free PMC Article
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