tetano
Editor, Senior Moderator
Science
. 2026 Feb 26;391(6788):eads4405.
doi: 10.1126/science.ads4405. Epub 2026 Feb 26.
STING-NF-κB signaling builds an influenza spillover barrier
Runxin Ye[SUP] #[/SUP][SUP] 1 [/SUP], Songdi Wang[SUP] #[/SUP][SUP] 1 [/SUP], Ying Hu[SUP] #[/SUP][SUP] 1 [/SUP], Yiran Pan[SUP] 1 [/SUP], Wenwen Zheng[SUP] 1 [/SUP], Fengyan Xia[SUP] 1 [/SUP], Yanpu Wang[SUP] 1 [/SUP], Haoran Guo[SUP] 2 3 [/SUP], Shu Zheng[SUP] 1 [/SUP], Wei Wei[SUP] 2 3 [/SUP], Xiao-Fang Yu[SUP] 1 4 5 [/SUP]
Affiliations
Influenza pandemics are often traced back to the spillover of avian influenza A viruses (IAVs) to humans. However, barriers against IAV transmission remain elusive. We demonstrated human stimulator of interferon genes (STING) as a transmission barrier against IAVs. STING activated nuclear factor κB (NF-κB) and downstream NF-κB-stimulated genes (NSGs) through a specific domain. Among these NSGs, growth arrest and DNA damage-inducible protein 34 (GADD34) was crucial for IAV restriction. Some IAVs have evolved to evade activating human STING by mutating residue 115 in their matrix protein 1 (M1), which is essential for efficient viral replication in human respiratory cells. This barrier against the zoonotic threat of IAVs provides a tool for future investigations into the biological functions of the cyclic guanosine monophosphate-adenosine monosphosphate (cGMP-AMP) synthase (cGAS)-STING-NF-κB signaling pathway.
. 2026 Feb 26;391(6788):eads4405.
doi: 10.1126/science.ads4405. Epub 2026 Feb 26.
STING-NF-κB signaling builds an influenza spillover barrier
Runxin Ye[SUP] #[/SUP][SUP] 1 [/SUP], Songdi Wang[SUP] #[/SUP][SUP] 1 [/SUP], Ying Hu[SUP] #[/SUP][SUP] 1 [/SUP], Yiran Pan[SUP] 1 [/SUP], Wenwen Zheng[SUP] 1 [/SUP], Fengyan Xia[SUP] 1 [/SUP], Yanpu Wang[SUP] 1 [/SUP], Haoran Guo[SUP] 2 3 [/SUP], Shu Zheng[SUP] 1 [/SUP], Wei Wei[SUP] 2 3 [/SUP], Xiao-Fang Yu[SUP] 1 4 5 [/SUP]
Affiliations
- PMID: 41747053
- DOI: 10.1126/science.ads4405
Influenza pandemics are often traced back to the spillover of avian influenza A viruses (IAVs) to humans. However, barriers against IAV transmission remain elusive. We demonstrated human stimulator of interferon genes (STING) as a transmission barrier against IAVs. STING activated nuclear factor κB (NF-κB) and downstream NF-κB-stimulated genes (NSGs) through a specific domain. Among these NSGs, growth arrest and DNA damage-inducible protein 34 (GADD34) was crucial for IAV restriction. Some IAVs have evolved to evade activating human STING by mutating residue 115 in their matrix protein 1 (M1), which is essential for efficient viral replication in human respiratory cells. This barrier against the zoonotic threat of IAVs provides a tool for future investigations into the biological functions of the cyclic guanosine monophosphate-adenosine monosphosphate (cGMP-AMP) synthase (cGAS)-STING-NF-κB signaling pathway.