Degradation of viral RNA
Activation of RNAase
FIGURE 4-15 Biologic actions of type I interferons. Type I interferons (IFN-a, IFN-P) are produced by virus-infected cells in response to intracellular TLR signaling and other sensors of viral RNA. Type I interferons bind to receptors on neighboring uninfected cells and activate JAKSTAT signaling pathways, which induce expression of genes whose products interfere with viral replication. Type I interferons also bind to receptors on infected cells and induce expression of genes whose products enhance the cell's susceptibility to CTL-mediated killing.
and enhanced sensitivity to extrinsic inducers of apopto-sis. For example, virally infected cells can sense abnormal DNA replication and abnormal glycoprotein synthesis, leading to initiation of p53-dependent or endoplasmic reticulum-dependent apoptotic pathways, respectively. In addition, virally infected cells are sensitized to TNF-induced apoptosis. Abundant TNF is made by plasmacy-toid dendritic cells and macrophages in response to viral infections, in addition to type I interferons. The type I TNF receptor engages both proinflammatory and pro-apoptosis death pathways (see Chapter 7). The dominant pathway that is activated upon TNF binding depends on the state of protein synthesis in the responding cells, and viral infection can shift this balance toward apoptosis.
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