ArticleCommunications biology2026
STING is a key driver of Japanese encephalitis virus induced inflammatory response.
Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- The cGAS-STING/MITA pathway in innate antiviral immunity and beyond.Cell insight · 2026Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interferon (IFN) and inflammation are the key early defence mechanisms that combat pathogen infection. The cytosolic DNA sensor cGAS activates immune signaling via the stimulator of interferon genes (STING) protein. Emerging evidence suggests crosstalk between innate immune DNA and RNA sensing, implicating a role of STING protein in RNA virus infection. This study characterizes STING in the context of Japanese encephalitis virus (JEV), an RNA virus of the flaviviridae family. We observe that activation of type I IFN through MAVS is essential for cGAS and STING activation. Knockdown, null mutant and inhibitor studies confirm that STING restricts JEV replication independently of IFNβ signaling and autophagy. Transcriptomic analysis of STING
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