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  • siRNA against the G gene of human metapneumovirus

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    Author(s)
    Preston, Faith Maxine
    Straub, Claire P
    Ramirez, Ruben
    Mahalingam, Suresh
    Spann, Kirsten M
    Griffith University Author(s)
    Mahalingam, Suresh
    Year published
    2012
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    Abstract
    Background Human metapneumovirus (hMPV) is a significant viral respiratory pathogen of infants and children, the elderly and immunocompromised individuals. Disease associated with hMPV infection resembles that of human respiratory syncytial virus (RSV) and includes bronchiolitis and pneumonia. The glycosylated G attachment protein of hMPV is required for viral entry in vivo and has also been identified as an inhibitor of innate immune responses. Findings We designed and validated two siRNA molecules against the G gene using A549 cells and demonstrated consistent 88-92% knock-down for one siRNA molecule, which was used in ...
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    Background Human metapneumovirus (hMPV) is a significant viral respiratory pathogen of infants and children, the elderly and immunocompromised individuals. Disease associated with hMPV infection resembles that of human respiratory syncytial virus (RSV) and includes bronchiolitis and pneumonia. The glycosylated G attachment protein of hMPV is required for viral entry in vivo and has also been identified as an inhibitor of innate immune responses. Findings We designed and validated two siRNA molecules against the G gene using A549 cells and demonstrated consistent 88-92% knock-down for one siRNA molecule, which was used in subsequent experiments. Significant reduction of G mRNA in A549 cells infected with hMPV did not result in a reduction in viral growth, nor did it significantly increase the production of type I interferon (a/ߩ in response to infection. However, there was a moderate increase in IFN-ߠmRNA expression in response to infection in siG-transfected cells compared to untransfected and si-mismatch-transfected cells. Expression of G by recombinant adenovirus did not affect type I IFN expression. Conclusion G has been previously described as a type I interferon antagonist, although our findings suggest it may not be a significant antagonist.
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    Journal Title
    Virology Journal
    Volume
    9
    Issue
    105
    DOI
    https://doi.org/10.1186/1743-422X-9-105
    Copyright Statement
    © 2012 Preston et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
    Note
    Page numbers are not for citation purposes. Instead, this article has the unique article number of 105.
    Subject
    Microbiology
    Virology
    Medical microbiology
    Publication URI
    http://hdl.handle.net/10072/51446
    Collection
    • Journal articles

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