Influence of 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin on Bovine Herpesvirus 1 Replication

Abstract Bovine herpesvirus 1 (BHV-1) is a cattle pathogen that can provoke infectoius bovine rhinotracheitis (IBR), conjunctivitis, abortions and shipping fever. 2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persistent environmental contamination, which suppresses immune responses and decreases host resistance to infectious disease. Following BHV-1 infection in bovine kidney (MDBK) cells we showed that TCDD increases BHV-1 replication, accelerates BHV-1-induced apoptosis as well as, significantly decreased telomerase activity when virus-induced apoptosis occurred. It is known that TCDD acts on the cells through aryl hydrocarbon receptor (AhR). In our recent study in MDBK clls we demonstrated a dose-dependent overxpression of AhR in the presence of TCDD. Moreover, in the presence of TCDD, we detected an increase in the levels of both gene and protein expression of the immediate-early BHV-1 infected cell protein 0 (bICP0), which regulates all the three phases of viral replication by acting as a strong activator or as a repressor of specific viral promoters. Since, BHV-1 is a DNA virus which requires an iron-replete host for efficient replication, we investigated the role of TCDD in virus infection and demonstrated that TCDD increases the free intracellular iron availability. This might promote the onset of BHV-1 infection and render bovine cells more vulnerable to the virus. These results suggest that TCDD may act as an additional risk factor for progression of BHV-1 infection in cattle.