ArticleEmerging microbes & infections2024
Novel transcription and replication-competent virus-like particles system modelling the Nipah virus life cycle.
Article in Emerging microbes & infections, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Engineering Nipah virus: Reverse genetics as a gateway to novel drug discovery.New microbes and new infections · 2026Review
- Engineering virus-like particles for safe and versatile modeling of SARS-CoV-2 host interaction and immune escape.Communications biology · 2025Article
- Mechanistic insights into Nipah virus 5' UTR functionality reveal an antiviral target.The Journal of general virology · 2025Article
- Construction of Minigenome Replicon of Nipah Virus and Investigation of Biological Activity.Viruses · 2025Article
- Tetracistronic minigenomes elucidate a functional promoter for Ghana virus and unveils Cedar virus replicase promiscuity for all henipaviruses.Journal of virology · 2024Article
- A Comparative Assessment of the Pathogenic Potential of Newly Discovered Henipaviruses.Pathogens (Basel, Switzerland) · 2024Review
- A Single-Copy Sensitive and Field-Deployable One-Pot RT-RPA CRISPR/Cas12a Assay for the Specific Visual Detection of the Nipah Virus.Transboundary and emerging diseases · 2024Article
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Authors and funding
15 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Nipah virus (NiV), a highly pathogenic Henipavirus in humans, has been responsible for annual outbreaks in recent years. Experiments involving live NiV are highly restricted to biosafety level 4 (BSL-4) laboratories, which impedes NiV research. In this study, we developed transcription and replication-competent NiV-like particles (trVLP-NiV) lacking N, P, and L genes. This trVLP-NiV exhibited the ability to infect and continuously passage in cells ectopically expressing N, P, and L proteins while maintaining stable genetic characteristics. Moreover, the trVLP-NiV displayed a favourable safety profile in hamsters. Using the system, we found the NiV nucleoprotein residues interacting with viral RNA backbone affected viral replication in opposite patterns. This engineered system was sensitive to well-established antiviral drugs, innate host antiviral factors, and neutralizing antibodies. We then established a high-throughput screening platform utilizing the trVLP-NiV, leading to the identification of tunicamycin as a potential anti-NiV compound. Evidence showed that tunicamycin inhibited NiV replication by decreasing the infectivity of progeny virions. In conclusion, this trVLP-NiV system provided a convenient and versatile molecular tool for investigating NiV molecular biology and conducting antiviral drug screening under BSL-2 conditions. Its application will contribute to the development of medical countermeasures against NiV infections.
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