Key result
Classical swine fever virus (CSFV) infection protects endothelial cells from apoptosis induced by the dsRNA mimic pIpC by inhibiting caspase activation and mitochondrial membrane potential loss.
CSFV infection inhibits apoptotic signaling at multiple levels in endothelial cells, potentially promoting viral pathogenesis.
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Hypothesis-generating for CSFV endothelial evasion; leaves open relevance to natural swine infection and pathogenesis.
Classical swine fever virus (CSFV) causes severe disease in pigs associated with leukopenia, haemorrhage and fever. We show that CSFV infection protects endothelial cells from apoptosis induced by the dsRNA mimic, pIpC, but not from other apoptotic stimuli, FasL or staurosporine. CSFV infection inhibits pIpC-induced caspase activation, mitochondrial membrane potential loss and cytochrome c release as well as the pro-apoptotic effects of truncated Bid (tBid) overexpression. The CSFV proteins N(pro) and E(rns) both contribute to CSFV inhibition of apoptosis. We conclude that CSFV infection can inhibit apoptotic signalling at multiple levels, including at the caspase-8 and the mitochondrial checkpoints. By supporting viral replication, endothelial cells may promote CSFV pathogenesis.
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Johns et al. (2009) studied Classical swine fever virus infection. Classical swine fever virus (CSFV) infection vs. Uninfected cells was evaluated on Apoptosis induced by pIpC. Classical swine fever virus (CSFV) infection protects endothelial cells from apoptosis induced by the dsRNA mimic pIpC by inhibiting caspase activation and mitochondrial membrane potential loss.
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