[Molecular recognition of viral infections - immune response stimulation]

The mammalian immune system has evolved several mechanisms that allow bacterial and viral infections to be successfully fought. Animal cells are able to recognize viral infection and this recognition is dependent on the presence of intracellular sensors that instantly identify danger signals and initiate signal cascades leading to an effective antiviral response. Several host proteins have been identified as intracellular sensors, namely: Toll-like receptors, RIG-I-like receptors, AIM2-like receptors and DAI, DNA-dependent activator of IFN regulatory factor. They recognize and bind viral genomic nucleic acids and all their replicative intermediates. Receptor-ligand interaction leads to activation of specific metabolic pathways that include synthesis and release of type I interferons and proinflammatory cytokines. These mediators are in turn responsible for synchronizing mechanisms of innate and adaptive antiviral immunity. They are crucial for blocking viral replication, preventing the spread of infection and eventually eliminating the virus from the host. Signaling pathways dependent on RIG-I, independent of TLR and other viral ligand(s) identification mechanisms leading to antiviral immune response stimulation, are discussed in this review.