ArticleJournal of virology2025
SARS-CoV-2 Nsp15 endoribonuclease subverts host defenses to enhance viral fitness in lung cells.
Article in Journal of virology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed.
- Coronavirus Nsp15 endoribonuclease: linking viral RNA regulation to immune evasion and viral fitness.Journal of virology · 2026Review
- Identification of Nsp15 inhibitors restoring interferon-dependent antiviral activity against SARS-CoV-2.Antiviral research · 2026Article
- Altered infectivity, cell-cell fusion, and immune evasion of SARS-CoV-2 BA.3.2 and LP.8.1 variants.Journal of virology · 2026Article
- Antagonism of stress granules key for SARS-CoV-2 infection and pathogenesis.bioRxiv : the preprint server for biology · 2026Article
- SARS-CoV-2 Nsp15 facilitates immune evasion and viral replication by limiting multiple host innate immune pathways, including cGAS-STING.The Journal of general virology · 2026Article
- Advances in human respiratory organoid models for studying the pathogenesis and intervention strategies of COVID-19.Virologica Sinica · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Coronaviruses encode nonstructural protein 15 (Nsp15), a conserved endoribonuclease (EndoU) known to suppress host antiviral responses. It is imperative to understand the role of Nsp15/EndoU during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in its primary target respiratory epithelial cells. Using a recombinant wild-type SARS-CoV-2 (rWT) and a mutant with catalytically inactive EndoU (rH234A), we show that the EndoU activity is dispensable for viral replication in Vero cells but critically facilitates immune suppression and infection in physiologically relevant human lung cells, including human lung-derived epithelial cell lines, primary bronchial air-liquid interface cultures, and alveolar type 2 organoids derived from induced pluripotent stem cells. Compared to rWT, rH234A infection elicited augmented type I and III interferon (IFN) responses and stronger RNase L activation, suggesting that Nsp15 suppresses these antiviral pathways during SARS-CoV-2 infection. Although rH234A infection increased PKR phosphorylation, downstream eIF2α phosphorylation and stress granule formation remained limited, implying incomplete PKR/eIF2α pathway activation. Furthermore, Nsp15 mutants lacking key residues required for hexamerization or double-stranded RNA binding also showed impaired replication and heightened IFN responses, highlighting the importance of these structural features for EndoU function.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.