ArticleJournal of virology2006
Role for nsP2 proteins in the cessation of alphavirus minus-strand synthesis by host cells.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 65 citations in OpenAlex.
- Emetine dihydrochloride inhibits Chikungunya virus nsP2 helicase and shows robust antiviral activity in cells and mice.Journal of biomedical science · 2026Article
- Unveiling the structural and functional implications of uncharacterized NSPs and variations in the molecular toolkit across arteriviruses.NAR genomics and bioinformatics · 2025Article
- 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
- Semliki Forest Virus Chimeras with Functional Replicase Modules from Related Alphaviruses Survive by Adaptive Mutations in Functionally Important Hot Spots.Journal of virology · 2021Article
- Specificity Studies of the Venezuelan Equine Encephalitis Virus Non-Structural Protein 2 Protease Using Recombinant Fluorescent Substrates.International journal of molecular sciences · 2020Article
- Review
- Pseudo-typed Semliki Forest virus delivers EGFP into neurons.Journal of neurovirology · 2017Article
- The SD1 Subdomain of Venezuelan Equine Encephalitis Virus Capsid Protein Plays a Critical Role in Nucleocapsid and Particle Assembly.Journal of virology · 2016Article
- Viral Polymerase-Helicase Complexes Regulate Replication Fidelity To Overcome Intracellular Nucleotide Depletion.Journal of virology · 2015Article
- Article
- Alphavirus RNA synthesis and non-structural protein functions.The Journal of general virology · 2015Review
- Mutations conferring a noncytotoxic phenotype on chikungunya virus replicons compromise enzymatic properties of nonstructural protein 2.Journal of virology · 2015Article
- Discovery of a novel compound with anti-venezuelan equine encephalitis virus activity that targets the nonstructural protein 2.PLoS pathogens · 2014Article
- Hypervariable domain of nonstructural protein nsP3 of Venezuelan equine encephalitis virus determines cell-specific mode of virus replication.Journal of virology · 2013Article
- Differential unfolded protein response during Chikungunya and Sindbis virus infection: CHIKV nsP4 suppresses eIF2α phosphorylation.Virology journal · 2013Article
- ATM kinase is activated by sindbis viral vector infection.Virus research · 2012Article
- Genome-scale phylogeny of the alphavirus genus suggests a marine origin.Journal of virology · 2012Article
- Macromolecular assembly-driven processing of the 2/3 cleavage site in the alphavirus replicase polyprotein.Journal of virology · 2012Article
- Inhibitors of alphavirus entry and replication identified with a stable Chikungunya replicon cell line and virus-based assays.PloS one · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In order to establish nonlytic persistent infections (PI) of BHK cells, replicons derived from Sindbis (SIN) and Semliki Forest (SFV) viruses have mutations in nsP2. Five different nsP2 PI replicons were compared to wild-type (wt) SIN, SFV, and wt nsPs SIN replicons. Replicon PI BHK21 cells had viral RNA synthesis rates that were less than 5% of those of the wt virus and approximately 10% or less of those of SIN wt replicon-infected cells, and, in contrast to wt virus and replicons containing wt nsP2, all showed a phenotype of continuous minus-strand synthesis and of unstable, mature replication/transcription complexes (RC+) that are active in plus-strand synthesis. Minus-strand synthesis and incorporation of [3H]uridine into replicative intermediates differed among PI replicons, depending on the location of the mutation in nsP2. Minus-strand synthesis by PI cells appeared normal; it was dependent on continuous P123 and P1234 polyprotein synthesis and ceased when protein synthesis was inhibited. The failure by the PI replicons to shut off minus-strand synthesis was not due to some defect in the PI cells but rather was due to the loss of some function in the mutated nsP2. This was demonstrated by showing that superinfection of PI cells with wt SFV triggered the shutdown of minus-strand synthesis, which we believe is a host response to infection with alphaviruses. Together, the results indicate alphavirus nsP2 functions to engage the host response to infection and activate a switch from the early-to-late phase. The loss of this function leads to continuous viral minus-strand synthesis and the production of unstable RC+.
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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.