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• W2012620089 abstract "Leukemogenic viruses like human T-lymphotropic virus and bovine leukemia virus (BLV) presumably persist in the host partly by latent integration of the provirus in a fraction of infected cells, leading to accumulative increase in the outgrowth of transformed cells. Furthermore, viral infection also correlates with a blockade of the apoptotic mechanisms concomitant with an apparent latency of the host cell. Conceptually, induction of viral or cellular gene expression could thus also be used as a therapeutic strategy against retroviral-associated leukemia. Here, we provide evidence that valproate, an inhibitor of deacetylases, activates BLV gene expression in transient transfection experiments and in short-term cultures of primary B-lymphocytes. In vivo , valproate injection into newly BLV-inoculated sheep did not abrogate primary infection. However, valproate treatment, in the absence of any other cytotoxic drug, was efficient for leukemia/lymphoma therapy in the sheep model leading to decreased lymphocyte numbers (respectively from 25.6, 35.7, and 46.5 × 10 3 cells per mm 3 to 1.0, 10.6, and 24.3 × 10 3 cells per mm 3 in three leukemic sheep) and tumor regression (from >700 cm 3 to undetectable). The concept of a therapy that targets the expression of viral and cellular genes might be a promising treatment of adult T cell leukemia or tropical spastic paraparesis/human T-lymphotropic virus-associated myelopathy, diseases for which no satisfactory treatment exists so far." @default.
• W2012620089 created "2016-06-24" @default.
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• W2012620089 date "2005-07-08" @default.
• W2012620089 modified "2023-10-06" @default.
• W2012620089 title "Valproate activates bovine leukemia virus gene expression, triggers apoptosis, and induces leukemia/lymphoma regression <i>in vivo</i>" @default.
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• W2012620089 doi "https://doi.org/10.1073/pnas.0504248102" @default.
• W2012620089 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1177395" @default.
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• W2012620089 hasPublicationYear "2005" @default.
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