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10.1038/nrmicro.2016.45

http://scihub22266oqcxt.onion/10.1038/nrmicro.2016.45
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C5072394!5072394!27174148
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suck abstract from ncbi


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pmid27174148      Nat+Rev+Microbiol 2016 ; 14 (6): 360-73
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  • Viral evasion of intracellular DNA and RNA sensing #MMPMID27174148
  • Chan YK; Gack MU
  • Nat Rev Microbiol 2016[]; 14 (6): 360-73 PMID27174148show ga
  • Germline-encoded pattern recognition receptors (PRRs) mediate an early innate immune response against viral pathogens.Retinoic acid-inducible gene I protein (RIG-I) and melanoma differentiation-associated protein 5 (MDA5) are cytoplasmic sensors that detect viral RNA species and signal through the mitochondrial antiviral-signalling protein (MAVS) to induce the production of type I interferons (IFNs) and other cytokines.Intracellular DNA sensors, such as cyclic GMP?AMP synthase (cGAS) and IFN?-inducible protein 16 (IFI16), detect viral DNA in the cytoplasm and/or nucleus and signal through the stimulator of IFN genes (STING) to trigger an immune response.Viruses antagonize PRRs through the sequestration or modification of their viral genomes and through the manipulation of post-translational modifications of PRRs or their adaptor proteins. Some viruses cleave or degrade PRRs or their adaptors, or sequester and relocalize PRRs to escape immunity.A better understanding of the cellular immune-surveillance machinery and viral immune evasion strategies may guide the development of antiviral therapeutics and vaccines.Supplementary information: The online version of this article (doi:10.1038/nrmicro.2016.45) contains supplementary material, which is available to authorized users.
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