ArticleThe Journal of general virology2008
Mutations in the nuclear localization signal of nsP2 influencing RNA synthesis, protein expression and cytotoxicity of Semliki Forest virus.
Article in The Journal of general virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 59 citations in OpenAlex.
- Article
- Alphavirus nsP2: A Multifunctional Regulator of Viral Replication and Promising Target for Anti-Alphavirus Therapies.Reviews in medical virology · 2025Review
- Article
- Mayaro Virus: An Emerging Alphavirus in the Americas.Viruses · 2024Review
- GETV nsP2 plays a critical role in the interferon antagonism and viral pathogenesis.Cell communication and signaling : CCS · 2023Article
- Mimicking superinfection exclusion disrupts alphavirus infection and transmission in the yellow fever mosquitoProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Article
- Small Molecule Inhibitors Targeting Chikungunya Virus.Current topics in microbiology and immunology · 2022Review
- nsP4 Is a Major Determinant of Alphavirus Replicase Activity and Template Selectivity.Journal of virology · 2021Article
- Article
- Cross-utilisation of template RNAs by alphavirus replicases.PLoS pathogens · 2020Article
- Viral replicons as valuable tools for drug discovery.Drug discovery today · 2020Review
- Identification of Natural Molecular Determinants of Ross River Virus Type I Interferon Modulation.Journal of virology · 2020Article
- A Trans-amplifying RNA Vaccine Strategy for Induction of Potent Protective Immunity.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- The Host DHX9 DExH-Box Helicase Is Recruited to Chikungunya Virus Replication Complexes for Optimal Genomic RNA Translation.Journal of virology · 2019Article
- Sindbis Virus Infection Causes Cell Death by nsP2-Induced Transcriptional Shutoff or by nsP3-Dependent Translational Shutoff.Journal of virology · 2018Article
- The Methyltransferase-Like Domain of Chikungunya Virus nsP2 Inhibits the Interferon Response by Promoting the Nuclear Export of STAT1.Journal of virology · 2018Article
- Timeliness of Proteolytic Events Is Prerequisite for Efficient Functioning of the Alphaviral Replicase.Journal of virology · 2018Article
- Review
- Pseudo-typed Semliki Forest virus delivers EGFP into neurons.Journal of neurovirology · 2017Article
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 at 2 institutions in 1 country.
Funding
Abstract
The cytotoxicity of Semliki Forest virus (SFV) infection is caused partly by the non-structural protein nsP2, an essential component of the SFV replicase complex. Due to the presence of a nuclear localization signal (NLS), nsP2 also localizes in the nucleus of infected cells. The present study analysed recombinant SFV replicons and genomes with various deletions or substitutions in the NLS, or with a proline-to-glycine mutation at position 718 of nsP2 (P718G). Deletion of one or two arginine residues from the NLS or substitution of two of the arginines with aspartic acid resulted in a virus with a temperature-sensitive phenotype, and substitution of all three arginines was lethal. Thus, most of the introduced mutations severely affected nsP2 functioning in viral replication; in addition, they inhibited the ability of SFV to induce translational shut-off and kill infected cells. SFV replicons with a P718G mutation or replacement of the NLS residues (648)RRR(650) with RDD were found to be the least cytotoxic. Corresponding replicons expressed non-structural proteins at normal levels, but had severely reduced genomic RNA synthesis and were virtually unable to replicate and transcribe co-electroporated helper RNA. The non-cytotoxic phenotype was maintained in SFV full-length genomes harbouring the corresponding mutations; however, during a single cycle of cell culture, these were converted to a cytotoxic phenotype, probably due to the accumulation of compensatory mutations.
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.