Browsing by Subject "African swine fever"
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- PublicationOpen AccessKupffer cells and PlMs in acute experimental African Swine Fever(Murcia : F. Hernández, 1992) Carrasco, L.; Fernández, A.; Gómez-Villamandos, J. C.; Mozos, E.; Méndez, A.; Jover, A.An ultrastructural study of Kupffer cells and pulmonary intravascular macrophages (PIMs) of healthy and African Swine Fever (ASF)-infected pigs was carried out. A vascular perfusion method was performed in order to obtain an optimal intravascular morphology and tissue fixation. The infection developed acute ASF lesions in both organs. Both Kupffer cells and PIMs were studied at different stages of infection. The differences observed in both macrophagic cells from uninfected and infected tissues are shown and discussed.
- PublicationOpen AccessRole of hepatic macrophages during the viral haemorrhagic fever induced by African Swine Fever Virus(Murcia : F. Hernández, 2008) Sánchez-Cordón, Pedro José; Romero-Trevejo, José Lorenzo; Pedrera, Mirian; Sánchez-Vizcaino, José Manuel; Bautista, María José; Gómez-Villamandos, José CarlosTo ascertain the role played by the various liver monocyte-macrophage populations in the course of a viral hemorrhagic fever, fifteen pigs were inoculated intramuscularly with the highly virulent isolate of African Swine Fever Virus (ASFV) España-70 and slaughtered at 1-7 days post-inoculation (dpi). Samples of liver were fixed in different solutions and routinely processed for morphological, immunohistochemical and ultrastructural studies. Viral antigen (vp73) was detected from 3 dpi onward, mainly in circulating monocytes of sinusoid and Kupffer’s cells (KC), as well as in portal macrophages and hepatocytes from 5 dpi. Anti-SWC3 immunolabelled cells were increased from 1 dpi, peaking between 3 and 5 dpi, thereafter declining until the end of the experiment. The significant increase in the number of sinusoidal circulating monocytes and KC expressing IL-1a, TNFa and IL-6 from 1 dpi, confirmed the secretory activation of these cells. The results show that in the course of an ASFV-induced hemorrhagic syndrome, hepatic macrophage populations undergo major quantitative and biosynthetic changes prior to virus detection, suggesting the existence of a mechanism by which the virus concentrates infectable cells, which subsequently spread the virus around the body.