ArticleJournal of virology2002
Mutations in the yellow fever virus nonstructural protein NS2A selectively block production of infectious particles.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers.
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Who cites it
170 citing papers in PubMed, 291 citations in OpenAlex.
- Zika virus produces two isoforms of the NS2A protein that play mutually exclusive roles in viral replication and virion assembly.PLoS pathogens · 2026Article
- An orthoflavivirus inhibitor targeting multifunctional NS2A protein, a previously unidentified target.PLoS pathogens · 2026Article
- Cryo-electron tomography reveals coupled flavivirus replication, budding and maturation.Nature communications · 2026Article
- AlphaFold Prediction of Protein-Protein Interactions in theInternational journal of molecular sciences · 2025Article
- Amino acid changes in two viral proteins drive attenuation of the yellow fever 17D vaccine.Nature microbiology · 2025Article
- Functional Roles and Host Interactions ofPathogens (Basel, Switzerland) · 2025Review
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- West Nile virus unmasked: from gene variability to future challenges.Frontiers in cellular and infection microbiology · 2025Review
- Cryo-electron tomography reveals coupled flavivirus replication, budding and maturation.bioRxiv : the preprint server for biology · 2024Article
- Distinct chikungunya virus polymerase palm subdomains contribute to viral protein accumulation and virion production.PLoS pathogens · 2024Article
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- Palmitoylation at Residue C221 of Japanese Encephalitis Virus NS2A Protein Contributes to Viral Replication Efficiency and Virulence.Journal of virology · 2023Article
- Flavivirus nonstructural proteins and replication complexes as antiviral drug targets.Current opinion in virology · 2023Review
- Simultaneous membrane and RNA binding by tick-borne encephalitis virus capsid protein.PLoS pathogens · 2023Article
- Attenuation of SARS-CoV-2 replication and associated inflammation by concomitant targeting of viral and host cap 2'-O-ribose methyltransferases.The EMBO journal · 2022Article
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- High-Throughput Platform for Detection of Neutralizing Antibodies Using Flavivirus Reporter Replicon Particles.Viruses · 2022Article
- Biological Characterization of Yellow Fever Viruses Isolated From Non-human Primates in Brazil With Distinct Genomic Landscapes.Frontiers in microbiology · 2022Article
- Review
110 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Little is known about the function of flavivirus nonstructural protein NS2A. Two forms of NS2A are found in yellow fever virus-infected cells. Full-length NS2A (224 amino acids) is the product of cleavage at the NS1/2A and NS2A/2B sites. NS2Aalpha, a C-terminally truncated form of 190 amino acids, results from partial cleavage by the viral NS2B-3 serine protease at the sequence QK /T within NS2A. Exchange of serine for lysine at this site (QKT-->QST) blocks the production of both NS2Aalpha and infectious virus. The present study reveals that this defect is not at the level of RNA replication. Despite normal structural region processing, infectious particles containing genome RNA and capsid protein were not released from cells transfected with the mutant RNA. Nevertheless, production of subviral prM/M- and E-containing particles was unimpaired. The NS2A defect could be complemented in trans by providing NS1-2A or NS1-2Aalpha. However, trans complementation was not observed when the C-terminal lysine of NS1-2Aalpha was replaced with serine. In addition to true reversions, NS2Aalpha cleavage site mutations could be suppressed by two classes of second-site changes. The first class consisted of insertions at the NS2Aalpha cleavage site that restored its basic character and cleavability. A second class of suppressors occurred in the NS3 helicase domain, in which NS3 aspartate 343 was replaced with an uncharged residue (either valine, alanine, or glycine). These mutations in NS3 restored infectious-virus production in the absence of cleavage at the mutant NS2Aalpha site. Taken together, our results reveal an unexpected role for NS2A and NS3 in the assembly and/or release of infectious flavivirus particles.
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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.