作者: P Kerkhofs , E Adam , L Droogmans , D Portetelle , M Mammerickx
DOI: 10.1128/JVI.70.4.2170-2177.1996
关键词:
摘要: Bovine leukemia virus (BLV) is the etiologic agent of enzootic bovine leukosis. The adopts a strategy based on lack viral expression in vivo; only very rare BLV-infected B lymphocytes express information. When cells are isolated from animals persistent lymphocytosis and cultivated ex vivo, tremendous increase occurs. To gain insight into this mechanism, we employed general approach using chemicals that interfere specifically with cellular pathways involved signal transduction cell membrane to nucleus. Our data demonstrate BLV not correlated activity protein kinase A (PKA) even inhibited by cyclic AMP (cAMP). cAMP/PKA pathway thus apparently vivo expression. In contrast, PKC appears play key role process. Phorbol myristate acetate can directly activate (in absence T cells). Furthermore, calphostin C, highly specific inhibitor PKC, partly decreases further calmodulin calcineurin, calmodulin-dependent phosphatase, induction involvement could explain cannot be assigned PKC. it activation requires but PKA-dependent pathway. These highlight major differences between transient transfection experiments. Finally, despite their homologies, human T-cell appear use different induce