Vibrio vulnificus quorum-sensing molecule cyclo(Phe-Pro) inhibits RIG-I-mediated antiviral innate immunity

Wooseong Lee, Seung-Hoon Lee, Minwoo Kim, Jae-Su Moon, Geon-Woo Kim, Hae-Gwang Jung, In Hwang Kim, Ji Eun Oh, Hi Eun Jung, Heung Kyu Lee, Keun Bon Ku, Dae-Gyun Ahn, Seong-Jun Kim, Kun-Soo Kim and Jong-Won Oh ()
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Wooseong Lee: Yonsei University
Seung-Hoon Lee: Yonsei University
Minwoo Kim: Yonsei University
Jae-Su Moon: Yonsei University
Geon-Woo Kim: Yonsei University
Hae-Gwang Jung: Yonsei University
In Hwang Kim: Sogang University
Ji Eun Oh: Korea Advanced Institute of Science and Technology (KAIST)
Hi Eun Jung: Korea Advanced Institute of Science and Technology (KAIST)
Heung Kyu Lee: Korea Advanced Institute of Science and Technology (KAIST)
Keun Bon Ku: Korea Research Institute of Chemical Technology
Dae-Gyun Ahn: Korea Research Institute of Chemical Technology
Seong-Jun Kim: Korea Research Institute of Chemical Technology
Kun-Soo Kim: Sogang University
Jong-Won Oh: Yonsei University

Nature Communications, 2018, vol. 9, issue 1, 1-13

Abstract: Abstract The recognition of pathogen-derived ligands by pattern recognition receptors activates the innate immune response, but the potential interaction of quorum-sensing (QS) signaling molecules with host anti-viral defenses remains largely unknown. Here we show that the Vibrio vulnificus QS molecule cyclo(Phe-Pro) (cFP) inhibits interferon (IFN)-β production by interfering with retinoic-acid-inducible gene-I (RIG-I) activation. Binding of cFP to the RIG-I 2CARD domain induces a conformational change in RIG-I, preventing the TRIM25-mediated ubiquitination to abrogate IFN production. cFP enhances susceptibility to hepatitis C virus (HCV), as well as Sendai and influenza viruses, each known to be sensed by RIG-I but did not affect the melanoma-differentiation-associated gene 5 (MDA5)-recognition of norovirus. Our results reveal an inter-kingdom network between bacteria, viruses and host that dysregulates host innate responses via a microbial quorum-sensing molecule modulating the response to viral infection.

Date: 2018
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DOI: 10.1038/s41467-018-04075-1

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