Recognition of viral nucleic acids in innate immunity
Article first published online: 29 DEC 2009
Copyright © 2009 John Wiley & Sons, Ltd.
Reviews in Medical Virology
Volume 20, Issue 1, pages 4–22, January 2010
How to Cite
Yoneyama, M. and Fujita, T. (2010), Recognition of viral nucleic acids in innate immunity. Rev. Med. Virol., 20: 4–22. doi: 10.1002/rmv.633
- Issue published online: 29 DEC 2009
- Article first published online: 29 DEC 2009
- Manuscript Revised: 20 AUG 2009
- Manuscript Accepted: 20 AUG 2009
- Manuscript Received: 21 JUL 2009
Viral infections are detected by sensor molecules, which initiate innate antiviral responses, including the activation of type I interferons (IFNs) and proinflammatory cytokines. These cytokines are responsible for not only inhibiting viral replication in infected cells but also regulating the induction of adaptive immunity, leading to the swift eradication of viruses. Recent advances in the identification of pathogen receptors in the innate immune system have revealed that distinct types of sensors play a role in the detection of viral nucleic acids in different ways; Toll-like receptors (TLRs), which detect viral DNA or RNA in endosomal compartments in immune cells, retinoic acid inducible gene-I (RIG-I)-like receptors (RLRs), which recognise viral RNA in the cytoplasm, and DNA sensors, which detect cytoplasmic viral DNA. Since these sensors have to exclusively recognise viral infections, it is intriguing to understand how they distinguish self nucleic acids from foreign viral ones. Here, we review the current knowledge of the recognition of viral nucleic acids by these sensor molecules and the signal transduction machinery. Copyright © 2009 John Wiley & Sons, Ltd.