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Virus host evasion genes are ready-made tools for gene manipulation and therapy. In this work we have assessed the impact  in vivo  of the evasion gene A238L of the African Swine Fever Virus, a gene which inhibits transcription mediated by both NF-κB and NFAT. The A238L gene has been selectively expressed in mouse T lymphocytes using tissue specific promoter, enhancer and locus control region sequences for CD2. The resulting two independently derived transgenic mice expressed the transgene and developed a metastasic, angiogenic and transplantable CD4 + CD8 + CD69 –  lymphoma. The CD4 + CD8 + CD69 –  cells also grew vigorously  in vitro . The absence of CD69 from the tumour cells suggests that they were derived from T cells at a stage prior to positive selection. In contrast, transgenic mice similarly expressing a mutant A238L, solely inhibiting transcription mediated by NF-κB, were indistinguishable from wild type mice. Expression of Rag1, Rag2, TCRβ-V8.2, CD25, FoxP3, Bcl3, Bcl2 l14, Myc, IL-2, NFAT1 and Itk, by purified CD4 + CD8 + CD69 –  thymocytes from A238L transgenic mice was consistent with the phenotype. Similarly evaluated expression profiles of CD4 + CD8 +  CD69 –  thymocytes from the mutant A238L transgenic mice were comparable to those of wild type mice. These features, together with the demonstration of (mono-)oligoclonality, suggest a transgene-NFAT-dependent transformation yielding a lymphoma with a phenotype reminiscent of some acute lymphoblastic lymphomas.

Neoplastic Transformation of T Lymphocytes through Transgenic Expression of a Virus Host Modification Protein