The Domestic and International Impacts of the 2009-H1N1 Influenza A Pandemic Global Challenges, Global Solutions: Workshop Summary (2010) / Chapter Skim
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A14 Origins and Evolutionary Genomics of the 2009 Swine-Origin H1N1 Influenza A Epidemic
A14 Origins and Evolutionary Genomics of the 2009 Swine-Origin H1N1 Influenza A Epidemic
Pages 342-380
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From page 342... ...
A phylogenetic estimate of the gaps in genetic surveillance indicates a long period of unsampled ancestry before the S-OIV outbreak, suggesting that the reassortment of swine lineages may have occurred years before emergence in humans, and that the multiple genetic ancestry of S-OIV is not indicative of an artificial origin. Furthermore, the unsampled history of the epidemic means that the nature and location of the genetically closest swine viruses reveal little about the immediate origin of the epidemic, despite the fact that we included a panel of closely related and previously unpublished swine influenza isolates.
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. Co-circulation and mixing of the triple-reassortant H3N2 with established swine lineages subsequently generated further H1N1 and H1N2 reassortant swine viruses (CDC, 2009a; Shortridge et al., 1977; Shope and Lewis, 1931)
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. Given that S-OIV contains genes of Eurasian origin, we included in our phylogenetic analyses 15 newly sequenced swine influenza viruses from Hong Kong, sampled in the course of a surveillance program conducted since the early 1990s.
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. Internal nodes are reconstructed common ancestors with 95% credible intervals on their date given by the red bars.
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This data set comprises complete or partial genomes of swine-origin influenza A (H1N1) virus outbreak isolates sampled predominantly in the United States between March and May 2009.
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We did detect a difference in the viral molecular evolution in the outbreak clade when compared to that observed in related swine influenza sequences: all S-OIV genes showed a comparatively higher non-synonymous to synonymous (dN/dS) substitution rate ratio (Supplementary Tables A14-2 and A14-3)
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Movement of live pigs between Eurasia and North America seems to have facilitated the mixing of diverse swine influenza viruses, leading to the multiple reassortment events associated with the genesis of the S-OIV strain. Domestic pigs have been described as a hypothetical ‘mixing-vessel', mediating by reassort ment the emergence of new influenza viruses with avian or avian-like genes into the human population, and triggering a pandemic associated with antigenic shift (Shortridge et al., 1977)
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and the Area of Excellence Scheme of the University Grants Committee (grant AoE/M-12/06) of the Hong Kong SAR Government.
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New Swine Influenza Sequences from Hong Kong To evaluate the evolutionary history of swine/human influenza A H1N1 viruses, 15 viruses isolated from swine in Hong Kong during 1993 to 2009 were sequenced. Viral RNA was directly extracted from infected allantoic fluid or cell culture using QIAamp viral RNA minikit (Qiagen, Inc.)
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Assuming the same rate of synonymous substitution in both the outbreak and reference data sets, the relative rate expected in the outbreak sequences compared to the reference sequences is thus equal to (s+(N/S) (ωoutbreak)
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H The epidemiology and evolution of influenza viruses in pigs.
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H Persistence of Hong Kong influenza virus variants in pigs.
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Human viruses are coloured blue, swine viruses in red and avian viruses in green.
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APPENDIX A 355 SUPPLEMENTARY FIGURE A14-3 Continued
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356 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC SUPPLEMENTARY FIGURE A14-3 Continued
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APPENDIX A 357 SUPPLEMENTARY FIGURE A14-3 Continued
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358 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC SUPPLEMENTARY FIGURE A14-3 Continued
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APPENDIX A 359 SUPPLEMENTARY FIGURE A14-3 Continued
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360 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC SUPPLEMENTARY FIGURE A14-3 Continued
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APPENDIX A 361 SUPPLEMENTARY FIGURE A14-3 Continued
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virus as represented in Figure A14-2 of the main text but with full virus names and GenBank accession numbers. Internal nodes are reconstructed common ancestors with
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Newly described Hong Kong sequences have bold labels.
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364 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC SUPPLEMENTARY FIGURE A14-4 Continued
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APPENDIX A 365 SUPPLEMENTARY FIGURE A14-4 Continued
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366 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC SUPPLEMENTARY FIGURE A14-4 Continued
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APPENDIX A 367 SUPPLEMENTARY FIGURE A14-4 Continued
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368 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC SUPPLEMENTARY FIGURE A14-4 Continued
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APPENDIX A 369 SUPPLEMENTARY FIGURE A14-4 Continued
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For each gene, the degree of scatter about the linear regression reflects evolutionary rate heterogeneity among lineages, such that a "strict clock" corre
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2003. Inference of viral evolutionary rates from molecular sequences.
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372 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC SUPPLEMENTARY FIGURE A14-5 Continued
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APPENDIX A 373 SUPPLEMENTARY FIGURE A14-5 Continued
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Kosakovsky Pond, available at http://datamonkey.org) bSubstitution rate in outbreak clade relative to non-outbreak sequences based on excess nonsynonymous mutations inferred from the higher dN/dS ratio.
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NP NA M NS Swine/HK/103/93 C C C C C N1 C C Sw/HK/NS1659/01 C C C C C N1 C C Sw/HK/8512/01 C E E E E N1 E E Sw/HK/NS837/01 E E E E C N1 E E Sw/HK/9656/01 E E E E C N1 E E Sw/HK/NS1179/07 E E E E E N1 E E Sw/HK/NS29/09 E E E E E N1 E E Sw/HK/554/03 C C C C C N2 C C Sw/HK/NS857/01 E E E E C N2 E E Sw/HK/NS623/02 T T T T T N2 T T Sw/HK/78/03 T H T T T N2 E T Sw/HK/1110/06 T T T T T N2 T T Sw/HK/915/04 T T T T T N2 E T Sw/HK/1562/05 T T T T T N2 T T Sw/HK/294/09 T T T C T N2 T T A/California/04/2009 T T T T T N1 E T Classical Swine C Eurasian Swine E Triple Reassortant T Human H
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SUPPLEMENTARY TABLE A14-5 S-OIV Sequences Available on NCBI Influenza Virus Database at the Time of Analysis 376 Days1 PB22 PB1 PA HA NP NA MP NS A/Arizona/01/2009 112 GQ117067 GQ117063 GQ117064 GQ117066 GQ117065 A/Arizona/02/2009 116 GQ117076 GQ117075 GQ117079 GQ117074 GQ117077 GQ117078 A/Auckland/3/2009 115 FJ973552 FJ973553 A/California/04/2009 91 FJ966079 FJ966080 FJ966081 FJ966082 FJ966083 FJ966084 FJ966085 FJ966086 A/California/05/2009 89 FJ966955 FJ966952 FJ966957 FJ966952 FJ966953 FJ966956 FJ966954 A/California/06/2009 106 FJ966963 FJ966950 FJ966964 FJ966950 FJ966961 FJ971075 FJ966962 FJ971074 A/California/07/2009 99 FJ984387 FJ969531 FJ969529 FJ981613 FJ984386 FJ966975 A/California/14/2009 115 GQ117035 GQ117037 GQ117037 GQ117040 GQ117033 GQ117036 GQ117039 GQ117038 A/Colorado/03/2009 117 GQ117119 GQ117117 GQ117118 A/Indiana/09/2009 112 GQ117093 GQ117095 GQ117097 GQ117092 GQ117094 GQ117096 A/Kamsas/02/2009 114 GQ117059 GQ117057 Gq117058 A/Korea/01/2009 122 GQ131023 GQ131024 GQ132185 GQ131025 GQ131026 A/Massachusetts/06/2009 116 GQ117043 GQ117041 GQ117042 A/Michigan/02/2009 116 GQ117109 GQ117112 GQ117107 GQ117108 GQ117111 GQ117110 A/Minnesota/02/2009 117 GQ117070 GQ117069 GQ117068 GQ117071 GQ117073 GQ117072 A/Netherlands/602/2009 119 CY039527 CY039528 A/New York/1669/2009 116 CY039900 CY039899 CY039898 CY039893 CY039896 CY039895 CY039894 CY039897 A/New York/1682/2009 117 CY039908 CY039907 CY039906 CY039901 CY039904 CY039903 CY039902 CY039905 A/New York/12/2009 115 FJ984337 FJ984336 FJ984335 FJ984334 A/New York/18/2009 115 FJ984351 FJ984353 FJ984354 FJ984355 FJ984352 FJ984350 FJ984348 FJ984349 A/New York/19/2009 115 FJ984392 FJ984393 FJ984394 FJ984391 FJ984390 FJ984388 FJ984389 A/New York/23/2009 114 FJ984364 FJ984363 FJ984362 FJ984361 A/Ohio/07/2009 114 FJ984401 GQ117100 GQ117098 GQ117099 A/Paos Vasc0/GP20/2009 116 FJ985763 FJ985761 FJ985764 FJ985760 FJ985762
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A/South Carolina/09/2009 116 GQ117056 GQ117052 GQ117052 GQ117055 GQ117054 A/Texas/04/2009 104 FJ969525 FJ981615 FJ981618 FJ981614 FJ981617 FJ981620 FJ966980 A/Texas/07/2009 115 GQ117089 GQ117088 GQ117091 GQ117087 GQ117090 A/Texas/09/2009 115 GQ117027 GQ117026 GQ117029 GQ117032 GQ117025 GQ117028 GQ117031 GQ117030 A/Texas/15/2009 105 GQ122094 GQ122097 GQ122092 GQ122096 GQ122095 GQ122093 A/Valencia/GP4/2009 116 FJ985758 FJ985756 FJ985759 FJ985755 FJ985757 1.The sampling date as number of days since 1-Jan-2009. 2.Accession numbers for each available genomic segment.
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. Amino acid residues relevant to receptor binding were identical to those of classical swine H1N1 and North American H1N1 and recent H1N1 viruses in both the 130-loop and 190-helix.
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. cDNA were synthesized by reverse transcription reaction and gene amplification by PCR were performed using specific primers for each gene segments.
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J Structural identification of the antibody-binding sites of Hong Kong influenza haemagglutinin and their involvement in antigenic variation.
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