In order to survive, all organisms must guard against viral infections. Recognition of viruses is accomplished via multiple sensors. Many mammalian proteins can recognize viral products, such as double-stranded RNA （...In order to survive, all organisms must guard against viral infections. Recognition of viruses is accomplished via multiple sensors. Many mammalian proteins can recognize viral products, such as double-stranded RNA （dsRNA）, yet few of them are known to induce interferon, the central antiviral messenger. Since interferon is indispensable for successful antiviral defense [1], the interferon-inducing sensors have been of particular interest. However, a clear understanding of such sensors has been elusive, and the first well-established sensor family, the toll-like receptors （TLRs）, was described relatively recently [2]. Antiviral TLRs are positioned in the endosomes, where they report the appearance of viral genetic material （DNA, single-and double-stranded RNA）. However, the question of potential virus sensors in the cytoplasm was left open. Given the particular effectiveness ofintracellular dsRNA at inducing interferon, it was suspected that dsRNA-binding sensor molecules would be found in the cytoplasm.展开更多
文摘In order to survive, all organisms must guard against viral infections. Recognition of viruses is accomplished via multiple sensors. Many mammalian proteins can recognize viral products, such as double-stranded RNA （dsRNA）, yet few of them are known to induce interferon, the central antiviral messenger. Since interferon is indispensable for successful antiviral defense [1], the interferon-inducing sensors have been of particular interest. However, a clear understanding of such sensors has been elusive, and the first well-established sensor family, the toll-like receptors （TLRs）, was described relatively recently [2]. Antiviral TLRs are positioned in the endosomes, where they report the appearance of viral genetic material （DNA, single-and double-stranded RNA）. However, the question of potential virus sensors in the cytoplasm was left open. Given the particular effectiveness ofintracellular dsRNA at inducing interferon, it was suspected that dsRNA-binding sensor molecules would be found in the cytoplasm.
