ArticlePLoS pathogens2025
SLC35A2 gene product modulates paramyxovirus fusion events during infection.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Insights into the multifunctionality of viral glycoproteins F and HN in the lifecycle and pathogenesis of Newcastle disease virus: a systematic review.Veterinary research · 2025Pooled it
- Genome-wide CRISPR/Cas9 knockout screen identifies host factors essential for bovine parainfluenza virus type 3 replication.Science China. Life sciences · 2026Article
- Variable and conserved features of copy-back viral genome populations generatedJournal of virology · 2026Article
- Genome-scale CRISPR screen identifies host factors associated with bovine parainfluenza virus 3 infection.Virulence · 2025Article
- Identification of β4GALNT2 as an anti-hPIV3 factor through genome-wide CRISPR/Cas9 library screening.Emerging microbes & infections · 2025Article
- Validation of diverse and previously untraceable Sendai virus copyback viral genomes by direct RNA sequencing.Journal of virology · 2025Article
- Newcastle disease virus promotes spreading infection through vimentin-dependent tight junction injury mediated by MLC/p-MLC activation.PLoS pathogens · 2025Article
- Validation of diverse and previously untraceable Sendai virus copyback viral genomes by Direct RNA Sequencing.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
- Update of
Authors and funding
8 authors.
Funding
Abstract
Paramyxoviruses are significant human and animal pathogens that include mumps virus (MuV), Newcastle disease virus (NDV) and the murine parainfluenza virus Sendai (SeV). Despite their importance, few host factors implicated in paramyxovirus infection are known. Using a recombinant SeV expressing destabilized eGFP (rSeVCdseGFP) in a loss-of-function CRISPR screen, we identified the CMP-sialic acid transporter (CST) gene SLC35A1 and the UDP-galactose transporter (UGT) gene SLC35A2 as essential for paramyxovirus infection. As expected, SLC35A1 knockout (KO) cells showed drastic reduction in infections with SeV, NDV and MuV due to the lack of cell surface sialic acids receptors. However, SLC35A2 KO cells revealed unknown critical roles for this factor in virus-cell and cell-to-cell fusion events for the different paramyxoviruses. While UGT was essential for virus-cell fusion during SeV entry to the cell, it was not required for NDV or MuV entry. Importantly, UGT promoted the formation of syncytia during MuV infection, suggesting a role in cell-to-cell virus spread. Our findings demonstrate that paramyxoviruses can bind to or enter A549 cells in the absence of canonical galactose-bound sialic-acid decorations and show that UGT facilitates paramyxovirus fusion processes involved in entry and spread.
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.