ArticleBiosemiotics2015
Virus is a Signal for the Host Cell.
Article in Biosemiotics, 2015. 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
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
4 citing papers in PubMed.
- Adapting the rhizome concept to an extended definition of viral quasispecies and the implications for molecular evolution.Scientific reports · 2024Article
- Social Networking of Quasi-Species Consortia drive Virolution via Persistence.AIMS microbiology · 2021Review
- Two genetic codes: Repetitive syntax for active non-coding RNAs; non-repetitive syntax for the DNA archives.Communicative & integrative biology · 2017Article
- Viral tRNA Mimicry from a Biocommunicative Perspective.Frontiers in microbiology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Currently, the concept of the cell as a society or an ecosystem of molecular elements is gaining increasing acceptance. The basic idea arose in the 19th century, from the surmise that there is not just a single unit underlying an individual's appearance, but a plurality of entities with both collaborative and conflicting relationships. The following hypothesis is based around this model. The incompatible activities taking place between different original elements, which were subsumed into the first cell and could not be eliminated, had to be controlled very closely. Similarly, a strong level of control had to be developed over many cellular elements after the cell changed its genome to DNA. We assume that at least some of those original RNA agents and other biomolecules which carry incompatibilities and risks, are retained within current cells, although they are now under strict control. A virus functions as a signal informing these repressed cellular RNAs and other elements of ancient origin how to restore suppressed degrees of molecular freedom, favoring pre-existing molecular affinities and activities, re-establishing ancient molecular webs of interactions, and giving fragments of ancient coded information (mostly in the form of RNA structural motifs) the opportunity to be re-expressed. Collectively, these newly activated mechanisms lead to different possibilities for pathological cell states. All these processes are opposed by cell-control mechanisms. Thus, in this new scenario, the battle is considered intracellular rather than between the virus and the cell. And so the virus is treated as the signal that precipitates the cell's change from a latent to an active pathological state.
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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.