ArticleNpj viruses2024
Venezuelan equine encephalitis virus non-structural protein 3 dictates superinfection exclusion in mammalian cells.
Article in Npj viruses, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 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
3 citing papers in PubMed.
- Alphavirus replicase and regulatory RNA elements in host interactions and viral vector engineering.Journal of virology · 2026Review
- The Interplay Between Therapeutic Self-Amplifying RNA and the Innate Immune System: Balancing Efficiency and Reactogenicity.International journal of molecular sciences · 2025Review
- Safety concern of recombination between self-amplifying mRNA vaccines and viruses is mitigated in vivo.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
Abstract
Superinfection exclusion (SIE) prevents secondary infections of already infected cells. Arthritogenic alphaviruses induce SIE via early proteolytical cleavage of replicase precursor by non-structural protein 2 (nsP2). Here, we explore the SIE mechanism of the encephalitic Venezuelan equine encephalitis virus (VEEV). Using single-cell imaging techniques and VEEV replicons encoding green or red fluorescent proteins, we observed full SIE capacity in three hours. Transient expression of VEEV nsP3, but not nsP2, reduced alphavirus replication, suggesting a key role for VEEV nsP3 in the SIE mechanism. In particular, the VEEV nsP3 C-terminal hypervariable domain (HVD) was found to be required and sufficient for the SIE of VEEV and the more distantly related Sindbis virus. As the nsP3 HVD is known to bind multiple host proteins to form RNA replication complexes and modulate the cellular stress response, we propose that sequestering essential host protein(s) by VEEV nsP3 interferes with RNA replication of the superinfecting alphavirus.
Identifiers
What Socratic 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 Socratic graph.