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  • Identification and Characterization of a Ross River Virus Variant That Grows Persistently in Macrophages, Shows Altered Disease Kinetics in a Mouse Model, and Exhibits Resistance to Type I Interferon

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    Author(s)
    Lidbury, Brett A
    Rulli, Nestor E
    Musso, Cristina M
    Cossetto, Susan B
    Zaid, Ali
    Suhrbier, Andreas
    Rothenfluh, Harald S
    Rolph, Michael S
    Mahalingam, Suresh
    Griffith University Author(s)
    Mahalingam, Suresh
    Year published
    2011
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    Abstract
    Alphaviruses, such as chikungunya virus, o'nyong-nyong virus, and Ross River virus (RRV), cause outbreaks of human rheumatic disease worldwide. RRV is a positive-sense single-stranded RNA virus endemic to Australia and Papua New Guinea. In this study, we sought to establish an in vitro model of RRV evolution in response to cellular antiviral defense mechanisms. RRV was able to establish persistent infection in activated macrophages, and a small-plaque variant (RRVPERS) was isolated after several weeks of culture. Nucleotide sequence analysis of RRVPERS found several nucleotide differences in the nonstructural protein (nsP) ...
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    Alphaviruses, such as chikungunya virus, o'nyong-nyong virus, and Ross River virus (RRV), cause outbreaks of human rheumatic disease worldwide. RRV is a positive-sense single-stranded RNA virus endemic to Australia and Papua New Guinea. In this study, we sought to establish an in vitro model of RRV evolution in response to cellular antiviral defense mechanisms. RRV was able to establish persistent infection in activated macrophages, and a small-plaque variant (RRVPERS) was isolated after several weeks of culture. Nucleotide sequence analysis of RRVPERS found several nucleotide differences in the nonstructural protein (nsP) region of the RRVPERS genome. A point mutation was also detected in the E2 gene. Compared to the parent virus (RRV-T48), RRVPERS showed significantly enhanced resistance to beta interferon (IFN-ߩ-stimulated antiviral activity. RRVPERS infection of RAW 264.7 macrophages induced lower levels of IFN-ߠexpression and production than infection with RRV-T48. RRVPERS was also able to inhibit type I IFN signaling. Mice infected with RRVPERS exhibited significantly enhanced disease severity and mortality compared to mice infected with RRV-T48. These results provide strong evidence that the cellular antiviral response can direct selective pressure for viral sequence evolution that impacts on virus fitness and sensitivity to alpha/beta IFN (IFN-a/ߩ.
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    Journal Title
    Journal of Virology
    Volume
    85
    Issue
    11
    DOI
    https://doi.org/10.1128/JVI.01189-10
    Copyright Statement
    © 2011 American Society for Microbiology. The attached file is reproduced here in accordance with the copyright policy of the publisher. Please refer to the journal's website for access to the definitive, published version.
    Subject
    Biological sciences
    Other biological sciences not elsewhere classified
    Agricultural, veterinary and food sciences
    Biomedical and clinical sciences
    Publication URI
    http://hdl.handle.net/10072/43517
    Collection
    • Journal articles

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