African swine fever is a significant disease of domestic swine, with mortality rates approaching 100%. No vaccine is currently available, making quarantine and slaughter the only effective control strategy (44).African swine fever virus (ASFV), the causative agent of African swine fever, is a unique and complex DNA virus that infects cells of the mononuclear-phagocytic system, including fixed-tissue macrophages and specific lineages of reticular cells. Affected tissues show extensive necrosis following infection with highly virulent viral strains (13,36,38). Moderately virulent ASFV strains also appear to infect these cell types, but the degree of tissue involvement and the resulting tissue damage are much less severe (13,36,38). The abilities of ASFV to replicate and efficiently induce marked cytopathology in monocytes-macrophages in vivo appear to be critical factors for ASFV virulence.ASFV is the sole member of the family Asfarviridae and the only known DNA arbovirus (14,38). ASFV is a large, icosahedral virus that contains a linear double-stranded DNA genome (170 to 190 kbp) encoding approximately 165 genes (50; C. A. Balinsky et al., unpublished data). The availability of complete ASFV genome sequences has revealed that, similar to poxviruses, ASFVs encode proteins with functions essential for viral replication, including those involving structure and assembly of the virion and those responsible for biogenesis of mRNA and DNA. A large number of ASFV genes are of unknown function and may be involved in aspects of viral virulence and host range (46,50; Balinsky et al., unpublished).Pathogenic ASFV genomes contain 11 to 15 multigene family 360 (MGF360) genes and either 9 or 10 multigene family 530 (MGF530) genes (Balinsky et al., unpublished). Recently, we have identified MGF360 and MGF530 genes as novel macrophage host range determinants necessary for efficient growth in macrophages (54). Infection of macrophage cell cultures with MGF360-MGF530 (MGF360/530) gene deletion mutant Pr4⌬35 (six MGF360 and two MGF530 genes deleted) resulted in a 2-to 3-log reduction in virus titers and early cell death, suggesting a direct or indirect role for these genes in some aspect of infected-cell survival (54) (L. Zsak, unpublished data). In addition, a swine virulence determinant (VAD) containing MGF360/530 genes was mapped by using in vivo marker rescue to the left variable region of the ASFV genome (37).The mode of action of the ASFV MGF360/530 genes is unknown. Homology searches reveal no homology to other known genes. MGF360/530 genes have a conserved motif of 100 amino acids (28% amino acid identity) at the amino ter-
A major route of infection of avian influenza virus (AIV) and Newcastle disease virus (NDV) in chickens is through cells of the respiratory epithelium. Here we describe the development of a method for culture of tracheal epithelial cells from chicken embryos as well as their use in studies of infection with avian respiratory viruses such as low-pathogenicity AIV and lentogenic NDV. Positive immunostaining for cytokeratin, the presence of cilia and microvilli, and microarray analysis of transcribed RNA demonstrated that the isolated cells were epithelial in nature. Infection of the epithelial cell cultures with AIV and NDV was demonstrated using immunofluorescence or green fluorescence protein fluorescence microscopy, respectively. Growth curves of AIV and NDV in tracheal epithelial cells revealed that tracheal epithelial cells can fully support AIV and NDV growth and reinfection. This system, which mimics that of the natural infection, will be useful to study the mechanisms of early viral infection and cellular host transcriptional responses.
Classical swine fever virus (CSFV)-macrophage interactions during infection were analysed by examining macrophage transcriptional responses via microarray. Eleven genes had increased mRNA levels (.2.5-fold, P,0.05) in infected cell cultures, including arginase-1, an inhibitor of nitric oxide production, phosphoinositide 3-kinase, chemokine receptor 4 and interleukin-1b. Lower levels of nitric oxide and increased arginase activity were found in CSFV-infected macrophages. These changes in gene expression in macrophages suggest viral modulation of host expression to suppress nitric oxide production.
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