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  • Future Medicine Ltd  (3)
  • Auewarakul, Prasert  (3)
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  • Future Medicine Ltd  (3)
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  • 1
    Online Resource
    Online Resource
    Future Medicine Ltd ; 2007
    In:  Future Microbiology Vol. 2, No. 3 ( 2007-06), p. 345-349
    In: Future Microbiology, Future Medicine Ltd, Vol. 2, No. 3 ( 2007-06), p. 345-349
    Abstract: Adequate and timely supply of effective vaccine for pandemic influenza is an urgent issue for the pandemic preparedness. In order to attain this preparedness, concerted efforts from public health, commercial and scientific sectors are needed. Here we discuss obstacles and progress in the development of candidate vaccines for H5N1 avian influenza, currently the most threatening virus.
    Type of Medium: Online Resource
    ISSN: 1746-0913 , 1746-0921
    Language: English
    Publisher: Future Medicine Ltd
    Publication Date: 2007
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Future Medicine Ltd ; 2012
    In:  Future Virology Vol. 7, No. 4 ( 2012-04), p. 345-347
    In: Future Virology, Future Medicine Ltd, Vol. 7, No. 4 ( 2012-04), p. 345-347
    Abstract: Evaluation of: Zeng H, Pappas C, Belser JA et al. Human pulmonary microvascular endothelial cells support productive replication of highly pathogenic avian influenza viruses: possible involvement in the pathogenesis of human H5N1 virus infection. J. Virol. 86(2), 667–678 (2012). The H5N1 highly pathogenic avian influenza (HPAI) virus is still a major threat for pandemic influenza. The severity of the infection, with mortality reaching up to 60%, is of particular concern, and the detailed mechanism of this high pathogenicity is not fully understood. While alveolar epithelial cells are considered to be the main target cells in humans, Zeng et al. reported that human pulmonary vascular endothelial cells were more susceptible to the H5N1 HPAI virus than to seasonal, pandemic or low pathogenic avian influenza viruses. Infection induced the endothelial cells to produce a number of proinflammatory cytokines, which raised the possibility of a new virulence mechanism that may link to the systemic dissemination of the infection in humans. However, there are still many unanswered questions regarding the determinants of the higher infectivity of H5N1 HPAI in this cell type and the role of the infection of this cell type in the pathogenesis of H5N1 HPAI.
    Type of Medium: Online Resource
    ISSN: 1746-0794 , 1746-0808
    Language: English
    Publisher: Future Medicine Ltd
    Publication Date: 2012
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  • 3
    Online Resource
    Online Resource
    Future Medicine Ltd ; 2009
    In:  Future Virology Vol. 4, No. 2 ( 2009-03), p. 177-184
    In: Future Virology, Future Medicine Ltd, Vol. 4, No. 2 ( 2009-03), p. 177-184
    Abstract: H5N1 avian influenza virus is a highly virulent virus. In many avian as well as mammalian species, the virus causes severe disseminated diseases with an almost 100% fatality rate. The reason for this extremely high virulence is not yet well understood. Highly cleavable hamagglutinin allowing the virus to disseminate outside respiratory and digestive tracts is believed to be a major virulence factor. Apoptosis induction by viral protein PB1-F2 and hyperinduction of proinflammatory cytokines may also contribute to virulence. In humans, although viral RNA could be detected in a number of organs, severe inflammation and tissue damage were only observed in the human lungs, and viral antigen was only observed in the type II alveolar epithelial cells. Apoptosis of these cells may play a critical role in respiratory failure, which is the major cause of death. Although high mortality has been shown to be associated with a high viral load, mortality remains high even in the presence of antiviral therapy. This suggests that some damage may not be caused directly by viral replication. A better understanding of viral pathogenesis may lead to a better treatment of this deadly infection.
    Type of Medium: Online Resource
    ISSN: 1746-0794 , 1746-0808
    Language: English
    Publisher: Future Medicine Ltd
    Publication Date: 2009
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