Bovine leukemia virus (BLV) infection is characterized by viral latency in a largeIn the course of retrovirus infection, the integration of the viral DNA into the host genome is a crucial step in the virus life cycle. This step is important for the efficient expression of progeny virus and is responsible for the ability of retroviruses to persist and cause disease (72). Once integrated, the proviral DNA is organized into chromatin, as are all cellular genes. At least two different, yet highly conserved, mechanisms are at work to alter chromatin structure: chromatin remodeling activities and/or factors and posttranslational modifications of histone proteins, in particular, histone acetylation (reviewed in references 46 and 63). Acetylation of histones allows DNA to become more accessible to the transcriptional machinery and can lead to nucleosome disruption. In contrast, histone deacetylation allows the histones to bind more tightly to DNA and therefore contributes to a transcriptionally repressed chromatin architecture. The level of histone acetylation is determined by the competition between enzymatic activities of histone acetyltransferases (HATs) and histone deacetylases (HDACs) (18). The activity of a de novo integrated retroviral promoter can be strongly affected by the site of integration and by the histone acetylation status at this site.Previous reports have demonstrated that deacetylases play an important role in transcriptional silencing of several viruses, such as Epstein-Barr virus (EBV) (37, 77), human cytomegalovirus (57), and Kaposi's sarcoma-associated herpesvirus (29). Regarding retroviruses, feline foamy virus was shown to be reactivated following deacetylase inhibitor treatment (32) and histone hyperacetylation induces human immunodeficiency virus type 1 expression by specifically disrupting a single nucleosome positioned immediately downstream of the transcription start site (20,33,83). The presence of HDACs in the human T-cell leukemia virus type 1 (HTLV-1) promoter was recently observed, and treatment of HTLV-1-infected cells with deacetylase inhibitors increases the level of histone H4 acetylation in the HTLV-1 promoter and concomitantly increases viral transcription (48).Bovine leukemia virus (BLV) gene expression is induced at the transcriptional level by the virus-encoded transactivator