ArticlePLoS pathogens2025
Newcastle disease virus promotes spreading infection through vimentin-dependent tight junction injury mediated by MLC/p-MLC activation.
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 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
Abstract
Newcastle disease virus (NDV), a widespread poultry pathogen, spreads efficiently via the respiratory tract. However, the precise mechanism governing its spreading infection remains unclear. This study reveals that NDV-induced tight junction (TJ) injury is crucial for viral replication and spread. NDV infection significantly reduced TJ proteins OCLN and ZO-1 through multiple degradation pathways involving viral proteins, disrupting TJ integrity and promoting cell migration. Knockdown of OCLN and ZO-1 further enhanced viral replication and spread, underscoring their importance. Concurrently, NDV altered the distribution of OCLN and ZO-1, accompanied by cytoskeletal rearrangements of vimentin and F-actin. Notably, NDV triggered vimentin and F-actin rearrangement to form cage-like structures, benefiting TJ injury and viral replication. Critically, vimentin rearrangement was essential for the redistribution of OCLN, ZO-1, and F-actin, facilitating viral replication, spread, and inflammation. MLC/p-MLC activation was required for vimentin-mediated TJ injury, thereby promoting NDV replication and spread. Unlike avirulent strains, the virulent NDV promoted replication and spread through vimentin-mediated TJ injury, subsequently worsening lung damage in chickens. These findings elucidate how NDV rapidly disseminates and worsens lung damage, providing insights relevant to the pathogenesis and treatment of viral pneumonias, including those caused by coronaviruses and influenza viruses.
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.