Triantafilou, Martha ![]() ![]() ![]() |
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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.
Item Type: | Article |
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Date Type: | Publication |
Status: | Published |
Schools: | Medicine |
Additional Information: | This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. |
Publisher: | Nature Research |
ISSN: | 2041-1723 |
Date of First Compliant Deposit: | 14 April 2022 |
Date of Acceptance: | 18 January 2022 |
Last Modified: | 06 Jan 2024 04:27 |
URI: | https://orca.cardiff.ac.uk/id/eprint/149208 |
Citation Data
Cited 15 times in Scopus. View in Scopus. Powered By Scopus® Data
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