[Abstract unavailable

Serum samples were collected from wild boars (Sus scrofa) harvested during the 2005-2006 hunting season in Campania, southern Italy. Samples were tested for antibodies to Leptospira interrogan, Brucella spp., Salmonella spp., Aujeszky disease virus (ADV), porcine reproductive and respiratory stress syndrome virus (PRRSV), porcine parvovirus (PPV), classical swine fever virus (CSFV), and swine vesicular disease virus (SVDV). Of the 342 serum samples tested, 15 (4.4%) were seropositive to Brucella spp., nine (2.6%) were seropositive to L. interrogans, 66 (19.3%) were seropositive for Salmonella spp., 105 (30.7%) were seropositive for ADV, 27 (7.9%) were seropositive for PPV, and 129 (37.7%) were seropositive for PRRSV. All sera tested seronegative for SVDV and CSFV antibodies. These results, recorded for the first time in Campania, support the hypothesis that wild boar are reservoirs of certain infectious agents, but some infections in wild boars originate from their domestic counterparts.

No abstract

Exposure to environmental contaminants, like 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), leads to an increased susceptibility to infectious agents. Infection of bovine cells (MDBK) with Bovine Herpesvirus 1 (BHV-1) anticipates virus-induced apoptosis, suggesting an involvement of TCDD in virus infection. Herein we analyzed the effects of TCDD on apoptotic pathway in MDBK cells infected with BHV-1. After 12 h of infection, TCDD induced a significant increase in apoptotic cells. TCDD caused a dose-dependent up-regulation and anticipated activation of caspases 3, 8 and 9, with respect to unexposed groups. TCDD anticipated cleavage of PARP, compared to controls. Furthermore TCDD increased Bax and Bid levels, and decreased Bcl-2 and Bcl-XL levels. Such events took place earlier in exposed than unexposed cells. These results showed that TCDD influences BHV-1 induced apoptosis through members of Bcl-2 family and up-regulating activation of caspases.

A previous study demonstrated that infection of a canine fibrosarcoma cell line (A-72 cells) by canine coronavirus (CCoV) resulted in apoptosis (Ruggieri et al., 2007). In this study, we investigated the cell death processes during infection and the underlying mechanisms. We found that CCoV-II triggers apoptosis in A-72 cells by activating initiator (caspase-8 and -9) and executioner (caspase-3 and -6) caspases. The proteolytic cleavage of poly(ADP-ribose) polymerases (PARPs) confirmed the activation of executioner caspases. Furthermore, CCoV-II infection resulted in truncated bid (tbid) translocation from the cytosolic to the mitochondrial fraction, the cytochrome c release from mitochondria, and alterations in the pro- and anti-apoptotic proteins of bcl-2 family. Our data indicated that, in this experimental model, both intrinsic and extrinsic pathways are involved. In addition, we demonstrated that the inhibition of apoptosis by caspase inhibitors did not affect CCoV replication, suggesting that apoptosis does not play a role in facilitating viral release.