Gamma Interferon Blocks Gammaherpesvirus Reactivation from Latency Export

@article{citeulike:3054920, abstract = {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. 10.1128/JVI.80.1.192-200.2006}, author = {Steed, Ashley L. and Barton, Erik S. and Tibbetts, Scott A. and Popkin, Daniel L. and Lutzke, Mary L. and Rochford, Rosemary and Virgin, Herbert W.}, citeulike-article-id = {3054920}, citeulike-linkout-0 = {http://dx.doi.org/10.1128/JVI.80.1.192-200.2006}, citeulike-linkout-1 = {http://jvi.asm.org/cgi/content/abstract/80/1/192}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/16352543}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=16352543}, day = {1}, doi = {10.1128/JVI.80.1.192-200.2006}, journal = {J. Virol.}, keywords = {gammaifn, latency, mhv68}, month = {January}, number = {1}, pages = {192--200}, posted-at = {2008-07-29 00:25:56}, priority = {0}, title = {Gamma Interferon Blocks Gammaherpesvirus Reactivation from Latency}, url = {http://dx.doi.org/10.1128/JVI.80.1.192-200.2006}, volume = {80}, year = {2006} }

TY - JOUR ID - citeulike:3054920 L3 - citeulike-article-id:3054920 N2 - 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. 10.1128/JVI.80.1.192-200.2006 IS - 1 JF - J. Virol. EP - 200 TI - Gamma Interferon Blocks Gammaherpesvirus Reactivation from Latency VL - 80 SP - 192 KW - gammaifn KW - latency KW - mhv68 AU - Steed, Ashley AU - Barton, Erik AU - Tibbetts, Scott AU - Popkin, Daniel AU - Lutzke, Mary AU - Rochford, Rosemary AU - Virgin, Herbert PY - 2006/01/01/ UR - http://dx.doi.org/10.1128/JVI.80.1.192-200.2006 ER -