Unraveling immunity to [gamma]-herpesviruses: a new model for understanding the role of immunity in chronic virus infection Export

@article{citeulike:3054831, abstract = {Murine [gamma]-herpesvirus 68 ([gamma]HV68) infection is a new model for understanding how immunity and chronic [gamma]-herpesvirus infection inter-relate. [gamma]HV68 is closely related to the human Epstein-Barr virus and Kaposi's sarcoma herpesvirus and is associated with tumors, vasculitis of the great elastic arteries and splenic fibrosis. Advances in the past year have provided an even stronger foundation for believing that [gamma]HV68 infection of normal and mutant mice will become the pre-eminent animal model for understanding [gamma]-herpesvirus pathogenesis and immunity. [gamma]HV68 latency has been characterized employing new assays for quantitating cells carrying the [gamma]HV68 genome and cells that reactivate [gamma]HV68 and for detecting the presence of preformed infectious virus in tissues. These advances have fostered the first steps towards a molecular definition of [gamma]HV68 latency. It appears that [gamma]HV68 shares latency programs with human [gamma]-herpesviruses -- including the loci for gene 73, v-bcl-2 and the viral homolog of the G-protein coupled receptor. This provides candidate antigens for analysis of the role of T and B cells in regulating latency. Multiple cellular reservoirs for [gamma]HV68 latency were uncovered with the demonstration that [gamma]HV68 latently infects macrophages in addition to B cells. A critical role for B cells in regulating the nature of [gamma]HV68 latency was discovered and the mechanism was shown to be via alteration of the efficiency of reactivation. Studies of the response of CD4+ and CD8+ cells during acute and chronic [gamma]HV68 were performed. These new studies provide key building blocks for further development of this novel and interesting model system.}, author = {Virgin and Speckt, Samuel H.}, citeulike-article-id = {3054831}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/S0952-7915(99)80063-6}, citeulike-linkout-1 = {http://www.sciencedirect.com/science/article/B6VS1-3XG1YST-5/1/5a7096f348dbf018b3e39baf7d7e57f5}, doi = {10.1016/S0952-7915(99)80063-6}, journal = {Current Opinion in Immunology}, keywords = {b\_cells, cd4\_t\_cells, cd8\_t\_cells, chronic, gammaifn, latency, mhv68, review}, month = {August}, number = {4}, pages = {371--379}, posted-at = {2008-07-28 23:11:16}, priority = {2}, title = {Unraveling immunity to [gamma]-herpesviruses: a new model for understanding the role of immunity in chronic virus infection}, url = {http://dx.doi.org/10.1016/S0952-7915(99)80063-6}, volume = {11}, year = {1999} }

TY - JOUR ID - citeulike:3054831 L3 - citeulike-article-id:3054831 N2 - Murine [gamma]-herpesvirus 68 ([gamma]HV68) infection is a new model for understanding how immunity and chronic [gamma]-herpesvirus infection inter-relate. [gamma]HV68 is closely related to the human Epstein-Barr virus and Kaposi's sarcoma herpesvirus and is associated with tumors, vasculitis of the great elastic arteries and splenic fibrosis. Advances in the past year have provided an even stronger foundation for believing that [gamma]HV68 infection of normal and mutant mice will become the pre-eminent animal model for understanding [gamma]-herpesvirus pathogenesis and immunity. [gamma]HV68 latency has been characterized employing new assays for quantitating cells carrying the [gamma]HV68 genome and cells that reactivate [gamma]HV68 and for detecting the presence of preformed infectious virus in tissues. These advances have fostered the first steps towards a molecular definition of [gamma]HV68 latency. It appears that [gamma]HV68 shares latency programs with human [gamma]-herpesviruses -- including the loci for gene 73, v-bcl-2 and the viral homolog of the G-protein coupled receptor. This provides candidate antigens for analysis of the role of T and B cells in regulating latency. Multiple cellular reservoirs for [gamma]HV68 latency were uncovered with the demonstration that [gamma]HV68 latently infects macrophages in addition to B cells. A critical role for B cells in regulating the nature of [gamma]HV68 latency was discovered and the mechanism was shown to be via alteration of the efficiency of reactivation. Studies of the response of CD4+ and CD8+ cells during acute and chronic [gamma]HV68 were performed. These new studies provide key building blocks for further development of this novel and interesting model system. IS - 4 JF - Current Opinion in Immunology EP - 379 TI - Unraveling immunity to [gamma]-herpesviruses: a new model for understanding the role of immunity in chronic virus infection VL - 11 SP - 371 KW - b_cells KW - cd4_t_cells KW - cd8_t_cells KW - chronic KW - gammaifn KW - latency KW - mhv68 KW - review AU - Virgin AU - Speckt, Samuel PY - 1999/08// UR - http://dx.doi.org/10.1016/S0952-7915(99)80063-6 ER -