ArticlePloS one2020
Chikungunya virus superinfection exclusion is mediated by a block in viral replication and does not rely on non-structural protein 2.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Double trouble: how co- and superinfections shape viral dynamics and host responses.Journal of virology · 2026Review
- Evaluation of the Impact of Coinfection and Superinfection on Chikungunya and Mayaro Viruses' Replication inMicroorganisms · 2025Article
- SARS-CoV-2 cellular coinfection is limited by superinfection exclusion.Journal of virology · 2025Article
- Venezuelan equine encephalitis virus non-structural protein 3 dictates superinfection exclusion in mammalian cells.Npj viruses · 2024Article
- Safety concern of recombination between self-amplifying mRNA vaccines and viruses is mitigated in vivo.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Eilat virus (EILV) causes superinfection exclusion against West Nile virus (WNV) in a strain-specific manner inThe Journal of general virology · 2024Article
- Multiplexed multicolor antiviral assay amenable for high-throughput research.Nature communications · 2024Article
- 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
- Review
- Article
- Construction of a Chikungunya Virus, Replicon, and Helper Plasmids for Transfection of Mammalian Cells.Viruses · 2022Article
- Incomplete bunyavirus particles can cooperatively support virus infection and spread.PLoS biology · 2022Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Superinfection exclusion (SIE) is a process by which a virally infected cell is protected from subsequent infection by the same or a closely related virus. By preventing cell coinfection, SIE favors preservation of genome integrity of a viral strain and limits its recombination potential with other viral genomes, thereby impacting viral evolution. Although described in virtually all viral families, the precise step(s) impacted by SIE during the viral life cycle have not been systematically explored. Here, we describe for the first time SIE triggered by chikungunya virus (CHIKV), an alphavirus of public health importance. Using single-cell technologies, we demonstrate that CHIKV excludes subsequent infection with: CHIKV; Sindbis virus, a related alphavirus; and influenza A, an unrelated RNA virus. We further demonstrate that SIE does not depend on the action of type I interferon, nor does it rely on host cell transcription. Moreover, exclusion is not mediated by the action of a single CHIKV protein; in particular, we observed no role for non-structural protein 2 (nsP2), making CHIKV unique among characterized alphaviruses. By stepping through the viral life cycle, we show that CHIKV exclusion occurs at the level of replication, but does not directly influence virus binding, nor viral structural protein translation. In sum, we characterized co-infection during CHIKV replication, which likely influences the rate of viral diversification and evolution.
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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.