Knockdown of fibrillarin reveals cell- and virus- dependent restriction of henipavirus replication and enhanced antiviral immune signalling

Depleting fibrillarin (FBL) with siRNAs impairs Hendra virus (HeV-g1, HeV-g2) and Nipah virus (NiV-B) replication in small airway epithelial cells (HSAEC1-KT), but not NiV-M or Cedar virus.

• Why it matters: Henipaviruses are highly pathogenic zoonotic viruses lacking medical countermeasures, and FBL is a proposed pro-viral host factor whose effects in disease-relevant cell types were unclear.
• What they did: The study used siRNA knockdown of cellular FBL across HSAEC1-KT, NuLi-1, Telo HAEC, and BE(2)-M17 cells, then assessed viral gene transcription/replication and performed transcriptomic analyses.
• The result: In FBL knockdown cells where replication was impaired, innate immune pathways were more strongly activated with robust interferon stimulated gene (ISG) upregulation, supporting a virus- and cell-type dependent role for FBL in antiviral signaling.

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