Persistent Ross River virus infection of murine macrophages: An in vitro model for the study of viral relapse and immune modulation during long-term infection

Samantha Way, Brett Lidbury, Joanne Banyer

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    Abstract

    A clinical feature of Ross River virus disease (RRVD) is the periodic relapse of symptoms months after the initial onset of disease. The underlying mechanisms responsible for this relapse have not been determined. In a long-term (148 days) in vitro study of persistently infected murine macrophages we established that RRV infection periodically fell to undetectable biological levels that required genetic detection. However, the virus concentration spontaneously relapsed to biologically detectable levels that corresponded with enhanced viral mRNA expression, cellular detachment, and cytopathic effect. By altering the cell culture conditions we found that relapse could also be induced. We propose that the periodic relapse of symptoms in RRVD may be associated with spontaneous or stress-induced increases in RRV within persistently infected macrophages. This study also established that RRV enhanced macrophage phagocytic activity and dysregulated the immunoregulatory molecules CD80, IFN-γ, and TNF-α that may facilitate persistence of RRV and avoidance of immune responses.
    Original languageEnglish
    Pages (from-to)281-292
    Number of pages12
    JournalVirology
    Volume301
    Issue number2
    DOIs
    Publication statusPublished - 2002

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    Ross River virus
    Virus Diseases
    Macrophages
    Recurrence
    Infection
    Cell Culture Techniques
    Viruses
    Messenger RNA
    In Vitro Techniques

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    title = "Persistent Ross River virus infection of murine macrophages: An in vitro model for the study of viral relapse and immune modulation during long-term infection",
    abstract = "A clinical feature of Ross River virus disease (RRVD) is the periodic relapse of symptoms months after the initial onset of disease. The underlying mechanisms responsible for this relapse have not been determined. In a long-term (148 days) in vitro study of persistently infected murine macrophages we established that RRV infection periodically fell to undetectable biological levels that required genetic detection. However, the virus concentration spontaneously relapsed to biologically detectable levels that corresponded with enhanced viral mRNA expression, cellular detachment, and cytopathic effect. By altering the cell culture conditions we found that relapse could also be induced. We propose that the periodic relapse of symptoms in RRVD may be associated with spontaneous or stress-induced increases in RRV within persistently infected macrophages. This study also established that RRV enhanced macrophage phagocytic activity and dysregulated the immunoregulatory molecules CD80, IFN-γ, and TNF-α that may facilitate persistence of RRV and avoidance of immune responses.",
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    language = "English",
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    Persistent Ross River virus infection of murine macrophages: An in vitro model for the study of viral relapse and immune modulation during long-term infection. / Way, Samantha ; Lidbury, Brett; Banyer, Joanne.

    In: Virology, Vol. 301, No. 2, 2002, p. 281-292.

    Research output: Contribution to journalArticle

    TY - JOUR

    T1 - Persistent Ross River virus infection of murine macrophages: An in vitro model for the study of viral relapse and immune modulation during long-term infection

    AU - Way, Samantha

    AU - Lidbury, Brett

    AU - Banyer, Joanne

    PY - 2002

    Y1 - 2002

    N2 - A clinical feature of Ross River virus disease (RRVD) is the periodic relapse of symptoms months after the initial onset of disease. The underlying mechanisms responsible for this relapse have not been determined. In a long-term (148 days) in vitro study of persistently infected murine macrophages we established that RRV infection periodically fell to undetectable biological levels that required genetic detection. However, the virus concentration spontaneously relapsed to biologically detectable levels that corresponded with enhanced viral mRNA expression, cellular detachment, and cytopathic effect. By altering the cell culture conditions we found that relapse could also be induced. We propose that the periodic relapse of symptoms in RRVD may be associated with spontaneous or stress-induced increases in RRV within persistently infected macrophages. This study also established that RRV enhanced macrophage phagocytic activity and dysregulated the immunoregulatory molecules CD80, IFN-γ, and TNF-α that may facilitate persistence of RRV and avoidance of immune responses.

    AB - A clinical feature of Ross River virus disease (RRVD) is the periodic relapse of symptoms months after the initial onset of disease. The underlying mechanisms responsible for this relapse have not been determined. In a long-term (148 days) in vitro study of persistently infected murine macrophages we established that RRV infection periodically fell to undetectable biological levels that required genetic detection. However, the virus concentration spontaneously relapsed to biologically detectable levels that corresponded with enhanced viral mRNA expression, cellular detachment, and cytopathic effect. By altering the cell culture conditions we found that relapse could also be induced. We propose that the periodic relapse of symptoms in RRVD may be associated with spontaneous or stress-induced increases in RRV within persistently infected macrophages. This study also established that RRV enhanced macrophage phagocytic activity and dysregulated the immunoregulatory molecules CD80, IFN-γ, and TNF-α that may facilitate persistence of RRV and avoidance of immune responses.

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