ArticleViruses2025
Role of Defective Interfering Particles in Complement-Mediated Lysis of Parainfluenza Virus-Infected Cells.
Article in Viruses, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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Who cites it
4 citing papers in PubMed.
- Detection, isolation, and co-infection of parainfluenza virus 5 and porcine teschovirus 4 in colostrum-deprived piglets in Russia.Veterinary research communications · 2026Article
- Classification, functions, evolution, and applications of defective viral genomes.Frontiers in microbiology · 2026Review
- Relationship Between Cell Surface Viral Glycoprotein Expression and Resistance of Parainfluenza Virus Persistently Infected Cells to Complement-Mediated Lysis.Pathogens (Basel, Switzerland) · 2025Article
- A Type I IFN-Inducing Oncolytic Virus Improves NK Cell-Mediated Killing of Tumor Cells In Vitro Through Multiple Mechanisms.Viruses · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
RNA viruses pose a significant global public health burden due to their high mutation rates, zoonotic potential, and ability to evade immune responses. A common aspect of their replication is the generation of defective interfering particles (DIPs), which contain truncated defective viral genomes (DVGs) that depend on full-length standard (STD) virus for replication. DVGs have gained recognition as they are increasingly detected in clinical samples from natural infections. While their role in modulating type I interferon (IFN-I) responses is well established, their impact on the complement (C') system is not understood. In this study, we examined how DVGs influence C'-mediated lysis during parainfluenza virus 5 (PIV5) infection using real-time in vitro cell viability assays. Our results demonstrated that C' effectively killed human lung epithelial cells infected with STD PIV5, whereas co-infection with DIP-enriched stocks significantly suppressed C'-mediated killing through mechanisms that were dependent on DVG replication but independent of IFN-I production. The titration of DI units in co-infection with STD PIV5 showed a strong linear relationship between DIP-mediated decreases in surface viral glycoprotein expression and the inhibition of C'-mediated lysis. Our findings reveal a previously unrecognized function of DVGs in modulating C' pathways, shedding light on their potential role in viral persistence and immune evasion.
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