Article

Diversity of influenza viruses in swine and the emergence of a novel human pandemic influenza A (H1N1)

Division of Virology, Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Influenza and Other Respiratory Viruses (Impact Factor: 1.9). 09/2009; 3(5):207-13. DOI: 10.1111/j.1750-2659.2009.00096.x
Source: PubMed

ABSTRACT The novel H1N1 influenza virus that emerged in humans in Mexico in early 2009 and transmitted efficiently in the human population with global spread has been declared a pandemic strain. Here we review influenza infections in swine since 1918 and the introduction of different avian and human influenza virus genes into swine influenza viruses of North America and Eurasia. These introductions often result in viruses of increased fitness for pigs that occasionally transmit to humans. The novel virus affecting humans is derived from a North American swine influenza virus that has acquired two gene segments [Neuraminidase (NA) and Matrix (M)] from the European swine lineages. This reassortant appears to have increased fitness in humans. The potential for increased virulence in humans and of further reassortment between the novel H1N1 influenza virus and oseltamivir resistant seasonal H1N1 or with highly pathogenic H5N1 influenza stresses the need for urgent pandemic planning.

1 Follower
 · 
139 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Since the 2009 pandemic, monoclonal antibodies (mAbs) for rapid influenza diagnostic tests (RIDT) have been developed for specific diagnostics of pandemic viral infection. Most of the mAbs were poorly characterized because of urgency during the pandemic. Further characterization of the mAbs for RIDTs would be beneficial for understanding the immunological properties of the pandemic virus and utilizing the mAbs for other research purposes. In this study, it was confirmed that two mAbs (I38 and D383) in an RIDT for H1N1pdm09 diagnostics were able to detect H1N1pdm09 virus through enzyme-linked immunosorbent assay (ELISA) and immunofluorescence assay (IFA). Also, the two mAbs exhibited reactivity to hemagglutinins (HAs) of both the H1N1pdm09 and 1918 H1N1 viruses; therefore, the RIDT using the mAbs could detect HAs of H1N1pdm09 and also HAs of 1918 H1N1-like strains. In an extension to our previous study, the epitopes (Sa antigenic site and the interface area of F' and vestigial esterase subdomains on the HA1 domain of HA of H1N1pdm09) recognized by the mAbs were corroborated in depth by IFA with escape-mutants from the mAbs and mapping of the epitopes on the crystal structure of human H1N1 viral HAs. Collectively, these results imply that the mAbs for the RIDT may be suitable for use in studying the immunological properties of H1N1pdm09 viruses and that the Sa antigenic site and the interface area between F' and vestigial esterase subdomains on influenza viral HA recognized by the mAbs are immunologically conserved regions between H1N1pdm09 and 1918 H1N1.
  • Emerging infectious diseases 03/2011; DOI:10.3201/eid1703100581 · 7.33 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Swine influenza viruses (SIV) are zoonotic pathogens that pose a potential threat to human health. In this study, we analyzed the differential mitochondrial proteomes of H3N2 SIV-infected human lung A549 cells using two-dimensional gel electrophoresis (2-DE) followed by matrix-assisted laser desorption ionization time-of-flight/time-of-flight (MALDI-TOF/TOF) analysis. In the comparative analysis, 24 altered proteins (13 upregulated and 11 downregulated) were identified in the mitochondria of H3N2 SIV-infected cells; these proteins were involved in cell-to-cell signaling and interaction, cellular movement, and post-translational modification. Moreover, the transcriptional profiles of 16 genes corresponding to the identified proteins were estimated by real time RT-PCR. IPA analysis suggested that the differentially expressed proteins were clustered primarily into the mammalian target of rapamycin (mTOR) and d-glucose signaling pathways. In addition, oxidative phosphorylation and integrin signaling appeared to be major pathways modulated in the mitochondria of infected cells. We further demonstrated that apolipoprotein L2 was upregulated in the cytoplasm and translocated to mitochondria during virus infection. These results were verified by Western blot analysis coupled with confocal microscopy. Collectively, the mitochondrial proteome data provide insights to further understand the underlying mechanisms of H3N2 SIV cross-species infection.
    Journal of Proteomics 10/2013; 91:136-50. DOI:10.1016/j.jprot.2013.06.037 · 3.93 Impact Factor

Preview

Download
2 Downloads
Available from