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Antiviral backup plan
RNA viruses are sensed by two distinct pattern recognition receptors (PRRs) that bind to RNA. The transmembrane Toll-like receptor TLR7 detects RNA-infected cells and viruses that are phagocytosed, whereas the cytosolic RIG-I–like receptor (RLR) detects viruses replicating within cells. Activation of either PRR leads to the production of type I interferons (IFNs), the main antiviral components of the immune system. Plasmacytoid dendritic cells (pDCs) are the main producers of type I IFN. Although these cells detect RNA viruses and infected cells through the TLR pathway, Bruni et al. found that infected pDCs also detected replicating RNA viruses in the cytosol through RLRs, suggesting that the PRR used to detect RNA viruses depends on their route of entry. RLR-mediated detection of viral RNA was inhibited by kinases that are thought to act solely downstream of TLR7, suggesting feedback between the two pathways. Together, these results may explain why patients with defective TLR7 signaling still exhibit antiviral responses.
