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Japanese Encephalitis virus persistence in porcine tonsils is associated with a weak induction of the innate immune response, an absence of IFN gamma mRNA expression, and a decreased frequency of CD4+CD8+ double-positive T cells
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Pseudorabies virus infection causes downregulation of Ligands for the activating NK cell receptor NKG2D
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Herpesviruses and thetType III interferon system
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β-glucan-induced IL-10 secretion by monocytes triggers porcine NK cell cytotoxicity
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Pseudorabies virus infection triggers NF-κB activation via the DNA damage response but actively inhibits NF-κB-dependent gene expression
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Alphaherpesvirus-induced activation of plasmacytoid dendritic cells depends on the viral glycoprotein gD and is inhibited by non-infectious light particles
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Bridging the gap : virus long-distance spread via tunneling nanotubes
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Pseudorabies virus infection of epithelial cells leads to persistent but aberrant activation of the NF-kappa B pathway, inhibiting hallmark NF-kappa B-induced proinflammatory gene expression
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An unbiased approach to mapping the signaling network of the pseudorabies virus US3 protein
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Efficient control of Japanese encephalitis virus in the central nervous system of infected pigs occurs in the absence of a pronounced inflammatory immune response