This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Human herpesviruses, such as Epstein Barr virus and Kaposi?s sarcoma-associated herpesvirus, have been associated with the development of lymphomas, as well as other tumors. Since ?-herpesviruses have an extremely limited host range, study of these viruses in vivo has been difficult. Murine gamma-herspesvirus 68 (?HV68) is providing valuable insights into the understanding of the factors involved with the establishment and maintenance of latency by ?-herpesviruses. One of the main factors critical in the establishment of latency is the ability of the virus to silence the promoters of genes necessary for the lytic cycle of the virus. The key mechanism in silencing both cellular and viral promoters is increased methylation of CpG motifs by cellular methyltransferases.
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