The suppression of innate immune response by human rhinovirus C

Biochem Biophys Res Commun. 2017 Aug 12;490(1):22-28. doi: 10.1016/j.bbrc.2017.05.169. Epub 2017 May 31.

Abstract

Rhinovirus C (RV-C), a newly identified group of human rhinoviruses (RVs), is associated with exacerbation of severe asthma. The type I interferon (IFN) response induced by this virus and the mechanisms of evasion of IFN-mediated innate immunity for RV-C remain unclear. In this study, we constructed a full-length cDNA clone of RV-C (LZ651) from a clinical sample. IFN-β mRNA and protein levels were not elevated in differentiated Human bronchial epithelial (HBE) cells at the air-liquid interface infected with RV-C, except in the early stage of infection. The ability to attenuate IFN-β activation was ascribed to 3Cpro of RV-C, and the 40-His site of 3Cpro played an important role. Furthermore, RIG-I was degraded by 3Cpro in a caspase-dependent manner and 3Cpro cleaved MAVS at 148 Q/A, which inhibited IFN signaling. Taken together, our results demonstrate the mechanism by which RV-C circumvents the production of type I IFN in infected cells.

Keywords: 3C protein; Interferon response; MAVS; RIG-I signaling pathway; Rhinovirus C.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • HEK293 Cells
  • HeLa Cells
  • Humans
  • Immune Tolerance*
  • Immunity, Innate / immunology*
  • Interferon Type I / immunology
  • Rhinovirus / immunology*

Substances

  • Interferon Type I