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The main cellular target for African swine fever virus (ASFV) is the porcine macrophage. However, existing data about the early phases of infection were previously characterized in non-leukocyte cells such as Vero cells. Here, we report that ASFV enters the natural host cell using dynamin-dependent and clathrin-mediated endocytosis. This pathway is strongly pH-dependent during the first steps of infection in porcine macrophages. We investigated the effect of drugs inhibiting several endocytic pathways in macrophages and compared ASFV with vaccinia virus (VV), which apparently involves different entry pathways. The presence of cholesterol in cellular membranes was found to be essential for a productive ASFV infection while actin-dependent endocytosis and the participation of phosphoinositide-3-kinase (PI3K) activity were other cellular factors required in the process of viral entry. These findings improved our understanding of the ASFV interactions with macrophages that allow for successful viral replication., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Background Patients in fulminant hepatic failure currently do not have a temporary means of support while awaiting liver transplantation. A potential therapeutic approach for such patients is the use of extracorporeal perfusion with porcine livers as a form of 'liver dialysis'. During a 72-h extracorporeal perfusion of porcine livers with human blood, porcine Kupffer cells bind to and phagocytose human red blood cells (h RBC) causing the hematocrit to decrease to 2.5% of the original value. Our laboratory has identified porcine sialoadhesin expressed on Kupffer cells as the lectin responsible for binding N-acetylneuraminic acid on the surface of the h RBC. We evaluated whether blocking porcine sialoadhesin prevents the recognition and subsequent destruction of h RBCs seen during extracorporeal porcine liver xenoperfusion. Methods Ex vivo studies were performed using wild type pig livers perfused with isolated h RBCs for 72-h in the presence of an anti-porcine sialoadhesin antibody or isotype control. Results The addition of an anti-porcine sialoadhesin antibody to an extracorporeal porcine liver xenoperfusion model reduces the loss of h RBC over a 72-h period. Sustained liver function was demonstrated throughout the perfusion. Conclusions This study illustrates the role of sialoadhesin in mediating the destruction of h RBCs in an extracorporeal porcine liver xenoperfusion model. [ABSTRACT FROM AUTHOR]

The present study describes the distinct bone marrow (BM) and peripheral blood (PB) monocyte subpopulations detected by seven-colour flow cytometry. Mononuclear phagocytes were identified as viable CD172a+ SWC8- CD203a- mononuclear leukocytes. After that, monocyte subpopulations were differentiated by using CD14, CD163 and SLA-DR markers. Four distinct monocyte subpopulations were found in the BM and PB. Based on the discovered populations two possible maturation pathways have been proposed. The first pathway was characterised by release of CD14hi CD163- SLA-DR- BM monocytes into the PB where they matured into CD14low CD163+ SLA-DR+ monocytes. In the alternative pathway the monocytes finalised their phenotypical maturation in the BM and then they were released into the PB as CD14low CD163+ SLA-DR+ cells. In Salmonella-infected piglets, the population of CD14low CD163+ SLA-DR+ monocytes was elevated in the BM and mesenteric lymph nodes (MLN), suggesting the role of this population in pathogenesis of Salmonella infection in pigs. [ABSTRACT FROM AUTHOR]