Gamma interferon blocks gammaherpesvirus reactivation from latency
Gamma interferon blocks gammaherpesvirus reactivation from latency
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DOI：
10.1128/jvi.80.1.192-200.2006
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发表时间：
2006-01-01
影响因子：
5.4
通讯作者：
Virgin, HW
中科院分区：
文献类型：
--
作者：
Steed, AL;Barton, ES;Virgin, HW
Establishment of latent infection and reactivation from latency are critical aspects of herpesvirus infection and pathogenesis. Interfering with either of these steps in the herpesvirus life cycle may offer a novel strategy for controlling herpesvirus infection and associated disease pathogenesis. Prior studies show that mice deficient in gamma interferon (IFN-gamma) or the IFN-gamma receptor have elevated numbers of cells reactivating from murine gammaherpesvirus 68 (gamma HV68) latency, produce infectious virus after the establishment of latency, and develop large-vessel vasculitis. Here, we demonstrate that IFN-gamma is a powerful inhibitor of reactivation of gamma HV68 from latency in tissue culture. In vivo, IFN-gamma controls viral gene expression during latency. Importantly, depletion of IFN-gamma in latently infected mice results in an increased frequency of cells reactivating virus. This demonstrates that IFN-gamma is important for immune surveillance that limits reactivation of gamma HV68 from latency.
