2, 3, 7, 8-tetrachlorodibenzo-p-dioxin modulates Bovine Herpesvirus 1 Infection through Akt-mTOR and ERK Patways. [Impact Factor 1.67]

Introduction: 2,3,7,8-tetrachlorodibenzo-pdioxin (TCDD) influences infection of bovine cells (MDBK) with Bovine Herpesvirus 1 (BHV- 1) by increasing virus replication (Fiorito et al., 2008a) and anticipating BHV-1-induced apoptosis (Fiorito et al., 2008b). Moreover, TCDD accelerates the down-regulation of telomerase activity when virus-induced apoptosis occurred (Fiorito et al., 2014), anticipates the presence of bICP0 in the cytoplasm (Fiorito et al., 2010), and enhances the free intracellular iron availability (Fiorito et al., 2013). Several viruses control key cellular signaling pathways to facilitate the infection. For example, BHV-1 increases p53 levels during infection (Devireddy and Jones, 1999), and activates both phosphatidylinositol 3-kinase (PI3K)/Akt and mitogen activated protein kinases/extracellular signalregulated kinase 1/2 (MAPK/Erk1/2) signaling pathways (Zhu et al., 2011). Here to elucidate the influence of TCDD on BHV-1-infection we examined Akt/mTOR, ERK pathways and their downstream effectors including FOXO3, a transcription factor involved in promoting virus-induced apoptosis, as in canine coronavirus type II infection (Marfè et al., 2011).