Cell-cell fusion limits activation of the unfolded protein response induced by the Nipah virus glycoproteins.

ABSTRACT: The productive replication of highly pathogenic Nipah virus (NiV) relies on the host cell for the synthesis and correct folding of the viral glycoproteins, which can cause ER stress and activation of the unfolded protein response (UPR). While the UPR can exert proviral functions by restoring ER homeostasis, it can also have antiviral effects. Here, we show that irreversible ER stress induced by thapsigargin resulted in broad expression of UPR target genes and potently inhibited NiV infection. The finding that UPR target gene upregulation was not detectable in NiV-infected cells at 18 h p.i., raised the question of how NiV regulates UPR activation to prevent thapsigargin-like antiviral effects. To address this, we analyzed the effects of NiV glycoprotein expression on UPR activation and fou

SUBMITTER: Jordan P 

PROVIDER: S-EPMC12817901 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature