ArticleNature communications2017
Replication defective viral genomes exploit a cellular pro-survival mechanism to establish paramyxovirus persistence.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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
69 citing papers in PubMed, 103 citations in OpenAlex.
- SARS-CoV-2 defective viral genomes from distinct genomic regions drive divergent interferon responses.PLoS pathogens · 2026Article
- Implications of RNA virus persistence for post-acute sequelae and chronic inflammatory syndromes.Nature immunology · 2026Review
- Ebola virus persistence and the hidden cost of immune privilege.Nature microbiology · 2026Article
- Strain-dependent differences in the capacity of peste des petits ruminants virus to infect antigen-presenting cells.Journal of virology · 2026Article
- A respiratory syncytial virus trailer sequence modulates viral replication and the generation and propagation kinetics of copy-back defective viral genomes.Journal of virology · 2026Article
- Host genotype and sex shape influenza evolution and defective viral genomes.Nature communications · 2026Article
- Detailed single-cell mapping of the transcriptional response to a virus infection driven by copy-back viral genomes.PLoS pathogens · 2026Article
- Article
- Filamentous virions act as non-infectious interfering particles to modulate papillomavirus infection.Journal of virology · 2026Article
- Variable and conserved features of copy-back viral genome populations generatedJournal of virology · 2026Article
- Detailed single-cell mapping of the transcriptional response to a virus infection driven by copy-back viral genomes.bioRxiv : the preprint server for biology · 2026Article
- Classification, functions, evolution, and applications of defective viral genomes.Frontiers in microbiology · 2026Review
- Hidden in Plain Sight: Alphavirus Persistence and Its Potential for Driving Chronic Pathogenesis.Viruses · 2025Review
- Risk factors for emerging, re-emerging, and newly recognized arboviruses and zoonotic viruses in Brazilian amazon.PLoS neglected tropical diseases · 2025Review
- A Respiratory Syncytial Virus trailer sequence modulates viral replication and copy-back defective viral genome generation and propagation kinetics.bioRxiv : the preprint server for biology · 2025Article
- Validation of diverse and previously untraceable Sendai virus copyback viral genomes by direct RNA sequencing.Journal of virology · 2025Article
- Deep Sequencing Reveals Dual Evolution of SARS-CoV-2: Insights Into Defective Genomes From Wuhan-Hu-1 Variants to Omicron Subvariants.Journal of medical virology · 2025Article
- PWWP3A disrupts the assembly of VISA/MAVS signalosome to inhibit innate immune response against RNA viruses.Nature communications · 2025Article
- Cooperative role of PACT and ADAR1 in preventing aberrant PKR activation by self-derived double-stranded RNA.Nature communications · 2025Article
- A region of mumps virus nucleoprotein affects defective interfering particle production.The Journal of general virology · 2025Article
9 more citing papers are in PubMed but not listed here.
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 at 1 institution in 1 country.
Funding
Abstract
Replication defective viral genomes (DVGs) generated during virus replication are the primary triggers of antiviral immunity in many RNA virus infections. However, DVGs can also facilitate viral persistence. Why and how these two opposing functions of DVGs are achieved remain unknown. Here we report that during Sendai and respiratory syncytial virus infections DVGs selectively protect a subpopulation of cells from death, thereby promoting the establishment of persistent infections. We find that during Sendai virus infection this phenotype results from DVGs stimulating a mitochondrial antiviral-signaling (MAVS)-mediated TNF response that drives apoptosis of highly infected cells while extending the survival of cells enriched in DVGs. The pro-survival effect of TNF depends on the activity of the TNFR2/TRAF1 pathway that is regulated by MAVS signaling. These results identify TNF as a pivotal factor in determining cell fate during a viral infection and delineate a MAVS/TNFR2-mediated mechanism that drives the persistence of otherwise acute viruses.Replication defective viral genomes (DVGs) can facilitate persistence of paramyxoviruses, but the underlying mechanisms are unclear. Using FISH, Xu et al. here analyze the cellular response to DVGs on a single cell level and show that a MAVS-mediated TNF response specifically extends survival of cells enriched in DVGs.
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.