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Elife. 2016 Nov 11;5. pii: e18491. doi: 10.7554/eLife.18491.

Viral factors in influenza pandemic risk assessment.

Author information

1
Center for Communicable Disease Dynamics, Harvard T. H Chan School of Public Health, Boston, United States.
2
Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, United States.
3
Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, United States.
4
Division of Infectious Disease, Faculty of Medicine, Imperial College, London, United Kingdom.
5
Department of Biological Engineering, Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, United States.
6
Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, United States.
7
Centers for Disease Control and Prevention, Atlanta, United States.
8
Department of Ecology and Evolutionary Biology, University of Chicago, Chicago, United States.
9
Department of Biomedical Engineering, University of Virginia, Charlottesville, United States.
10
Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, United States.
11
Department of Ecology and Evolutionary Biology, University of California, Los Angeles, Los Angeles, United States.
12
Fogarty International Center, National Institutes of Health, Bethesda, United States.
13
Bioinformatics Institute, Agency for Science Technology and Research, Singapore, Singapore.
14
National Public Health Laboratory, Communicable Diseases Division, Ministry of Health, Singapore, Singapore.
15
School of Biological Sciences, Nanyang Technological University, Singapore, Singapore.
16
MRC Centre for Outbreak Analysis and Modelling, School of Public Health, Imperial College London, London, United Kingdom.
17
Department of Infectious Disease Epidemiology, School of Public Health, Imperial College London, London, United Kingdom.
18
Department of Physics, Ryerson University, Toronto, Canada.
19
Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, United States.
20
Department of Pathobiological Sciences, University of Wisconsin School of Veterinary Medicine, Madison, United States.
21
Department of Epidemiology and Biostatistics, College of Public Health, University of Georgia, Athens, United States.
22
Department of Viroscience, Erasmus Medical Center, Rotterdam, Netherlands.
23
MRC-University of Glasgow Centre For Virus Research, Glasgow, United Kingdom.
24
IRD/UPMC UMMISCO, Montpellier, France.
25
Center for Computational Biology and Bioinformatics, Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, United States.
26
Department of Integrative Biology, The University of Texas at Austin, Austin, United States.
27
Department of Veterinary Medicine, University of Cambridge, Cambridge, United Kingdom.

Abstract

The threat of an influenza A virus pandemic stems from continual virus spillovers from reservoir species, a tiny fraction of which spark sustained transmission in humans. To date, no pandemic emergence of a new influenza strain has been preceded by detection of a closely related precursor in an animal or human. Nonetheless, influenza surveillance efforts are expanding, prompting a need for tools to assess the pandemic risk posed by a detected virus. The goal would be to use genetic sequence and/or biological assays of viral traits to identify those non-human influenza viruses with the greatest risk of evolving into pandemic threats, and/or to understand drivers of such evolution, to prioritize pandemic prevention or response measures. We describe such efforts, identify progress and ongoing challenges, and discuss three specific traits of influenza viruses (hemagglutinin receptor binding specificity, hemagglutinin pH of activation, and polymerase complex efficiency) that contribute to pandemic risk.

KEYWORDS:

epidemiology; global health; human; infectious disease; influenza A; microbiology; pandemic; risk prediction; virus

PMID:
27834632
PMCID:
PMC5156527
DOI:
10.7554/eLife.18491
[Indexed for MEDLINE]
Free PMC Article

Conflict of interest statement

ML: Reports the following financial disclosures for topics unrelated to this manuscript: consulting income from Pfizer and Affinivax (both donated to charity) and research funding from Pfizer and PATH Vaccine Solutions. These entities had no role in the preparation of this work or in the decision to submit the work for publication. Reviewing editor for eLife. CAR: During the prepartion of this manuscript, CAAB received funding through a research contract with AstraZeneca Inc., but for distinct, unrelated research. AstraZeneca Inc. had no role in the preparation of this work or in the decision to submit the work for publication. The other authors declare that no competing interests exist.

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