Molecular characterization and comparative analysis of pandemic H1N1/2009 strains with co-circulating seasonal H1N1/2009 strains from eastern India

During the peak outbreak (July–September 2009), a total 1886 patients were screened in eastern India, of which 139 (7.37%) and 52 (2.76%) were positive for pH1N1 and seasonal H1N1, respectively. Full-length HA1, NA, NS1 and PB1-F2 genes of representative strains were sequenced. Phylogenetic analysis of deduced amino acid sequences of pH1N1 strains revealed HA1 and NS1 to be of North American swine lineage, and the NA gene of Eurasian swine lineage. Consistent with previous reports, the PB1-F2 gene of pH1N1 strains was unique due to a mutation resulting in a truncated protein of 11 aa. The HA, NA and NS1 genes of H1N1/2009 strains clustered with H1N1 strains of 2000–2009, whereas a subset of strains contained a pH1N1-like truncated PB1-F2. The truncated PB1-F2 may confer the advantage of lower pathogenicity but higher replication and infectivity to the human H1N1 strains. This is the first report of seasonal H1N1/2009 strains with a pH1N1/2009-like gene segment.

[1]  Lucy A. Perrone,et al.  A Single Mutation in the PB1-F2 of H5N1 (HK/97) and 1918 Influenza A Viruses Contributes to Increased Virulence , 2007, PLoS pathogens.

[2]  Timothy B. Stockwell,et al.  The early diversification of influenza A/H1N1pdm , 2009, PLoS currents.

[3]  R. Lamb,et al.  A new influenza virus virulence determinant: The NS1 protein four C-terminal residues modulate pathogenicity , 2008, Proceedings of the National Academy of Sciences.

[4]  S. Chakrabarti,et al.  Genetic characterization of circulating seasonal Influenza A viruses (2005-2009) revealed introduction of oseltamivir resistant H1N1 strains during 2009 in eastern India. , 2010, Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases.

[5]  S. Chakrabarti,et al.  Comparative evaluation of real-time PCR and conventional RT-PCR during a 2 year surveillance for influenza and respiratory syncytial virus among children with acute respiratory infections in Kolkata, India, reveals a distinct seasonality of infection. , 2009, Journal of medical microbiology.

[6]  M. Zambon,et al.  The epidemiology of influenza , 2002, Occupational medicine.

[7]  K. Subbarao,et al.  Genetic characterization of H3N2 influenza viruses isolated from pigs in North America, 1977-1999: evidence for wholly human and reassortant virus genotypes. , 2000, Virus research.

[8]  Fernanda L. Sirota,et al.  Mapping the sequence mutations of the 2009 H1N1 influenza A virus neuraminidase relative to drug and antibody binding sites , 2009, Biology Direct.

[9]  M. Beer,et al.  Pathogenesis and transmission of the novel swine-origin influenza virus A/H1N1 after experimental infection of pigs. , 2009, The Journal of general virology.

[10]  R. Shope SWINE INFLUENZA III. FILTRATION EXPERIMENTS AND ETIOLOGY , 1931 .

[11]  J. Lan,et al.  Structure and function of the NS1 protein of influenza A virus. , 2007, Acta biochimica et biophysica Sinica.

[12]  S. I. Golovin,et al.  [Synthesis of a full-length DNA copy of the hemagglutinin gene of the the influenza virus A H1N1 subtype, its cloning and primary structure]. , 1984, Bioorganicheskaia khimiia.

[13]  D. J. Stevens,et al.  The Structure and Receptor Binding Properties of the 1918 Influenza Hemagglutinin , 2004, Science.

[14]  Gavin J. D. Smith,et al.  Origins and evolutionary genomics of the 2009 swine-origin H1N1 influenza A epidemic , 2009, Nature.

[15]  J. R. Coleman The PB1-F2 protein of Influenza A virus: increasing pathogenicity by disrupting alveolar macrophages , 2007, Virology Journal.

[16]  J. P. Davis,et al.  Human Case of Swine Influenza A (H1N1) Triple Reassortant Virus Infection, Wisconsin , 2008, Emerging infectious diseases.

[17]  Rong Wang,et al.  Influenza Virus PB1-F2 Protein Induces Cell Death through Mitochondrial ANT3 and VDAC1 , 2005, PLoS pathogens.

[18]  Ron A M Fouchier,et al.  Antigenic and Genetic Characteristics of Swine-Origin 2009 A(H1N1) Influenza Viruses Circulating in Humans , 2009, Science.

[19]  W. Liu,et al.  Genetic stability and linkage analysis of the 2009 influenza A(H1N1) virus based on sequence homology , 2009, Archives of Virology.

[20]  Jindrich Cinatl,et al.  Novel swine-origin influenza A virus in humans: another pandemic knocking at the door , 2009, Medical Microbiology and Immunology.

[21]  E. Padlan The pandemic 2009 (H1N1) swine influenza virus is mild compared to the pandemic 1918 (H1N1) virus because of a proline-to-serine substitution in the receptor-binding site of its hemagglutinin - a hypothesis. , 2010, Medical hypotheses.

[22]  S. Cherian,et al.  Genetic Characterization of the Influenza A Pandemic (H1N1) 2009 Virus Isolates from India , 2010, PloS one.

[23]  Jonathan W. Yewdell,et al.  The Influenza A Virus PB1-F2 Protein Targets the Inner Mitochondrial Membrane via a Predicted Basic Amphipathic Helix That Disrupts Mitochondrial Function , 2003, Journal of Virology.

[24]  R. Krug,et al.  The 3'-end-processing factor CPSF is required for the splicing of single-intron pre-mRNAs in vivo. , 2001, RNA.

[25]  L. Finelli,et al.  Emergence of a novel swine-origin influenza A (H1N1) virus in humans. , 2009, The New England journal of medicine.

[26]  P. Schnitzler,et al.  An update on swine-origin influenza virus A/H1N1: a review , 2009, Virus Genes.

[27]  N. Cox,et al.  Antigenic and Genetic Variation of Influenza A(H1N1) Viruses , 1990 .

[28]  J. Taubenberger,et al.  Pathogenicity and immunogenicity of influenza viruses with genes from the 1918 pandemic virus. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[29]  Sagar M. Goyal,et al.  Evolution of Swine H3N2 Influenza Viruses in the United States , 2000, Journal of Virology.

[30]  Nevena Veljkovic,et al.  Identification of hemagglutinin structural domain and polymorphisms which may modulate swine H1N1 interactions with human receptor , 2009, BMC Structural Biology.

[31]  P. Colman,et al.  The structure of the complex between influenza virus neuraminidase and sialic acid, the viral receptor , 1992, Proteins.

[32]  Michael Shaw,et al.  Clinical aspects of pandemic 2009 influenza A (H1N1) virus infection. , 2010, The New England journal of medicine.

[33]  N. Khardori,et al.  Triple-Reassortant Swine Influenza A (H1) in Humans in the United States, 2005–2009 , 2009 .

[34]  Stephan Ludwig,et al.  The proapoptotic influenza A virus protein PB1‐F2 regulates viral polymerase activity by interaction with the PB1 protein , 2008, Cellular microbiology.

[35]  R. Dwek,et al.  Structural Characterization of the 1918 Influenza Virus H1N1 Neuraminidase , 2008, Journal of Virology.

[36]  Hideo Goto,et al.  In vitro and in vivo characterization of new swine-origin H1N1 influenza viruses , 2009, Nature.