ArticleProceedings of the National Academy of Sciences of the United States of America2017
Characterization of cytopathic factors through genome-wide analysis of the Zika viral proteins in fission yeast.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 64 citations in OpenAlex.
- Review
- Multi-omics analysis of antiviral interactions of Elizabethkingia anophelis and Zika virus.Scientific reports · 2024Article
- Advanced Protocol for Molecular Characterization of Viral Genome in Fission Yeast (Pathogens (Basel, Switzerland) · 2024Article
- SARS-CoV-2 ORF3a Protein as a Therapeutic Target against COVID-19 and Long-Term Post-Infection Effects.Pathogens (Basel, Switzerland) · 2024Review
- CMPK2 restricts Zika virus replication by inhibiting viral translation.PLoS pathogens · 2023Article
- Redox Regulation and Metabolic Dependency of Zika Virus Replication: Inhibition by Nrf2-Antioxidant Response and NAD(H) Antimetabolites.Journal of virology · 2023Article
- Severe acute respiratory syndrome coronavirus-2 accessory proteins ORF3a and ORF7a modulate autophagic flux and CaFrontiers in microbiology · 2023Article
- Improving Drug Sensitivity of HIV-1 Protease Inhibitors by Restriction of Cellular Efflux System in a Fission Yeast Model.Pathogens (Basel, Switzerland) · 2022Article
- Congenital Zika Syndrome: Genetic Avenues for Diagnosis and Therapy, Possible Management and Long-Term Outcomes.Journal of clinical medicine · 2022Review
- An overview of Zika virus genotypes and their infectivity.Revista da Sociedade Brasileira de Medicina Tropical · 2022Review
- The Intersection of Parkinson's Disease, Viral Infections, and COVID-19.Molecular neurobiology · 2021Review
- Article
- Structure and function of capsid protein in flavivirus infection and its applications in the development of vaccines and therapeutics.Veterinary research · 2021Review
- Contribution of yeast models to virus research.Applied microbiology and biotechnology · 2021Review
- Article
- Zika M Oligopeptide ZAMP Confers Cell Death-Promoting Capability to a Soluble Tumor-Associated Antigen through Caspase-3/7 Activation.International journal of molecular sciences · 2020Article
- Article
- A distinct class of plant and animal viral proteins that disrupt mitosis by directly interrupting the mitotic entry switch Wee1-Cdc25-Cdk1.Science advances · 2020Article
- Zika virus infection leads to mitochondrial failure, oxidative stress and DNA damage in human iPSC-derived astrocytes.Scientific reports · 2020Article
- Zika Virus-Induced Neuronal Apoptosis via Increased Mitochondrial Fragmentation.Frontiers in microbiology · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The Zika virus (ZIKV) causes microcephaly and the Guillain-Barré syndrome. Little is known about how ZIKV causes these conditions or which ZIKV viral protein(s) is responsible for the associated ZIKV-induced cytopathic effects, including cell hypertrophy, growth restriction, cell-cycle dysregulation, and cell death. We used fission yeast for the rapid, global functional analysis of the ZIKV genome. All 14 proteins or small peptides were produced under an inducible promoter, and we measured the intracellular localization and the specific effects on ZIKV-associated cytopathic activities of each protein. The subcellular localization of each ZIKV protein was in overall agreement with its predicted protein structure. Five structural and two nonstructural ZIKV proteins showed various levels of cytopathic effects. The expression of these ZIKV proteins restricted cell proliferation, induced hypertrophy, or triggered cellular oxidative stress leading to cell death. The expression of premembrane protein (prM) resulted in cell-cycle G1 accumulation, whereas membrane-anchored capsid (anaC), membrane protein (M), envelope protein (E), and nonstructural protein 4A (NS4A) caused cell-cycle G2/M accumulation. A mechanistic study revealed that NS4A-induced cellular hypertrophy and growth restriction were mediated specifically through the target of rapamycin (TOR) cellular stress pathway involving Tor1 and type 2A phosphatase activator Tip41. These findings should provide a reference for future research on the prevention and treatment of ZIKV diseases.
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