Human rhinovirus promotes STING trafficking to replication organelles to promote viral replication

Martha Triantafilou (), Joshi Ramanjulu, Lee M. Booty, Gisela Jimenez-Duran, Hakan Keles, Ken Saunders, Neysa Nevins, Emma Koppe, Louise K. Modis, G. Scott Pesiridis, John Bertin and Kathy Triantafilou
Additional contact information
Martha Triantafilou: GlaxoSmithKline
Joshi Ramanjulu: GlaxoSmithKline
Lee M. Booty: GlaxoSmithKline
Gisela Jimenez-Duran: GlaxoSmithKline
Hakan Keles: GlaxoSmithKline
Ken Saunders: GlaxoSmithKline
Neysa Nevins: GlaxoSmithKline
Emma Koppe: GlaxoSmithKline
Louise K. Modis: GlaxoSmithKline
G. Scott Pesiridis: GlaxoSmithKline
John Bertin: GlaxoSmithKline
Kathy Triantafilou: GlaxoSmithKline

Nature Communications, 2022, vol. 13, issue 1, 1-16

Abstract: Abstract Human rhinovirus (HRV), like coronavirus (HCoV), are positive-strand RNA viruses that cause both upper and lower respiratory tract illness, with their replication facilitated by concentrating RNA-synthesizing machinery in intracellular compartments made of modified host membranes, referred to as replication organelles (ROs). Here we report a non-canonical, essential function for stimulator of interferon genes (STING) during HRV infections. While the canonical function of STING is to detect cytosolic DNA and activate inflammatory responses, HRV infection triggers the release of STIM1-bound STING in the ER by lowering Ca2+, thereby allowing STING to interact with phosphatidylinositol 4-phosphate (PI4P) and traffic to ROs to facilitates viral replication and transmission via autophagy. Our results thus hint a critical function of STING in HRV viral replication and transmission, with possible implications for other RO-mediated RNA viruses.

Date: 2022
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DOI: 10.1038/s41467-022-28745-3

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