ArticleVirus evolution2018
Chikungunya virus evolution following a large 3'UTR deletion results in host-specific molecular changes in protein-coding regions.
Article in Virus evolution, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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28 citing papers in PubMed, 31 citations in OpenAlex.
- Optimized Amplicon Strategy for Long-Read Sequencing of the Chikungunya Virus Genome.Methods in molecular biology (Clifton, N.J.) · 2027Article
- The 3'Untranslated region is a critical determinant of Getah virus replication, pathogenesis, and vector competence.Virulence · 2026Article
- The La Crosse virus M segment determines virus isolate cell-to-cell spread and virulence.bioRxiv : the preprint server for biology · 2026Article
- Chikungunya Virus E2 N218K Enhances Heparan Sulfate-Dependent Attachment and Viral Internalization While Conferring Partial Attenuation in A129 Mice.Pathogens (Basel, Switzerland) · 2026Article
- Ewing sarcoma breakpoint region 1 (EWSR1) protein binds to nonstructural protein 2 and non-coding regions of chikungunya virus genome to inhibit virus replication.Journal of virology · 2026Article
- Alphavirus replicase and regulatory RNA elements in host interactions and viral vector engineering.Journal of virology · 2026Review
- A conserved opal termination codon optimizes a temperature-dependent trade-off between protein production and processing in alphaviruses.Science advances · 2025Article
- Molecular basis of RNA recombination in the 3'UTR of chikungunya virus genome.Nucleic acids research · 2024Article
- A 44-Nucleotide Region in the Chikungunya Virus 3' UTR Dictates Viral Fitness in Disparate Host Cells.Viruses · 2024Article
- Increased interregional virus exchange and nucleotide diversity outline the expansion of chikungunya virus in Brazil.Nature communications · 2023Article
- A conserved Y-shaped RNA structure in the 3'UTR of chikungunya virus genome as a host-specialized element that modulates viral replication and evolution.PLoS pathogens · 2023Article
- Generation of a Live-Attenuated Strain of Chikungunya Virus from an Indian Isolate for Vaccine Development.Vaccines · 2022Article
- Alphavirus Virulence Determinants.Pathogens (Basel, Switzerland) · 2021Review
- De-Coding the Contributions of the Viral RNAs to Alphaviral Pathogenesis.Pathogens (Basel, Switzerland) · 2021Review
- Review
- Article
- Chikungunya Virus Replication Rate Determines the Capacity of Crossing Tissue Barriers in Mosquitoes.Journal of virology · 2021Article
- Using SHAPE-MaP To Model RNA Secondary Structure and Identify 3'UTR Variation in Chikungunya Virus.Journal of virology · 2020Article
- Cross-utilisation of template RNAs by alphavirus replicases.PLoS pathogens · 2020Article
- Review
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
The 3'untranslated region (UTR) in alphavirus genomes functions in virus replication and plays a role in determining virus host range. However, the molecular evolution of virus UTRs is understudied compared to the evolution of protein-coding regions. Chikungunya virus (CHIKV) has the longest 3'UTR among the alphaviruses (500-700 nt), and 3'UTR length and sequence structure vary substantially among different CHIKV lineages. Previous studies showed that genomic deletions and insertions are key drivers of CHIKV 3'UTR evolution. Inspired by hypothesized deletion events in the evolutionary history of CHIKV, we used experimental evolution to examine CHIKV adaptation in response to a large 3'UTR deletion. We engineered a CHIKV mutant with a 258 nt deletion in the 3'UTR (ΔDR1/2). This deletion reduced viral replication on mosquito cells, but did not reduce replication on mammalian cells. To examine how selective pressures from vertebrate and invertebrate hosts shape CHIKV evolution after a deletion in the 3'UTR, we passaged ΔDR1/2 virus populations strictly on primate cells, strictly on mosquito cells, or with alternating primate/mosquito cell passages. We found that virus populations passaged on a single host cell line increased in fitness relative to the ancestral deletion mutant on their selected host, and viruses that were alternately passaged improved on both hosts. Surprisingly, whole genome sequencing revealed few changes in the 3'UTR of passaged populations. Rather, virus populations evolved improved fitness through mutations in protein coding regions that were associated with specific hosts.
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