ReviewViruses2018
Role of Host Cell Secretory Machinery in Zika Virus Life Cycle.
Review in Viruses, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
52 citing papers in PubMed, 91 citations in OpenAlex.
- A pan-viral map of host dependency factors from multi-omics integration and machine learning across influenza A, SARS-CoV-2, Zika, and dengue viruses.Journal of translational medicine · 2026Article
- Optimization of a malachite green-pyrophosphatase assay for the Zika virus RNA-dependent RNA polymerase and preliminary identification of natural product modulators.Frontiers in drug discovery · 2026Article
- Discovery of Inhibitors Targeting the RNA-Dependent RNA Polymerase of the Zika Virus.bioRxiv : the preprint server for biology · 2025Article
- Induction of systemic and mucosal immune response against Zika virus by vaccination with non-infectious chimeric VLPs.Scientific reports · 2025Article
- Review
- The ACBD3 protein coordinates ER-Golgi contacts to enable productive TBEV infection.Journal of virology · 2025Article
- Synchronized Visualization and Analysis of Intracellular Trafficking and Maturation ofBio-protocol · 2025Article
- Erp57 facilitates ZIKV-induced DNA damage via NS2B/NS3 complex formation.Emerging microbes & infections · 2024Article
- Activation of ATF3 via the integrated stress response pathway regulates innate immune response to restrict Zika virus.Journal of virology · 2024Article
- Temperature Interference on ZIKV and CHIKV Cycles in Mosquitoes and Mammalian Cells.Pathogens (Basel, Switzerland) · 2024Article
- Activation of ATF3 via the Integrated Stress Response Pathway Regulates Innate Immune Response to Restrict Zika Virus.bioRxiv : the preprint server for biology · 2024Article
- Article
- N-linked glycosylation of flavivirus E protein contributes to viral particle formation.PLoS pathogens · 2023Article
- Article
- Mechanisms of Zika astrocyte infection and neuronal toxicity.NeuroImmune pharmacology and therapeutics · 2023Article
- Serum proteomics reveals a tolerant immune phenotype across multiple pathogen taxa in wild vampire bats.Frontiers in immunology · 2023Article
- B-cell epitope discovery: The first protein flexibility-based algorithm-Zika virus conserved epitope demonstration.PloS one · 2023Article
- Novel Therapeutic Nutrients Molecules That Protect against Zika Virus Infection with a Special Note on Palmitoleate.Nutrients · 2022Review
- Mechanical regulation of the helicase activity of Zika virus NS3.Biophysical journal · 2022Article
- Development and characterization of an inducible assay system to measure Zika virus capsid interactions.Journal of medical virology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The high human cost of Zika virus infections and the rapid establishment of virus circulation in novel areas, including the United States, present an urgent need for countermeasures against this emerging threat. The development of an effective vaccine against Zika virus may be problematic because of the cross reactivity of the antibodies with other flaviviruses leading to antibody-dependent enhancement of infection. Moreover, rapidly replicating positive strand RNA viruses, including Zika virus, generate large spectrum of mutant genomes (quasi species) every replication round, allowing rapid selection of variants resistant to drugs targeting virus-specific proteins. On the other hand, viruses are ultimate cellular parasites and rely on the host metabolism for every step of their life cycle, thus presenting an opportunity to manipulate host processes as an alternative approach to suppress virus replication and spread. Zika and other flaviviruses critically depend on the cellular secretory pathway, which transfers proteins and membranes from the ER through the Golgi to the plasma membrane, for virion assembly, maturation and release. In this review, we summarize the current knowledge of interactions of Zika and similar arthropod-borne flaviviruses with the cellular secretory machinery with a special emphasis on virus-specific changes of the secretory pathway. Identification of the regulatory networks and effector proteins required to accommodate the trafficking of virions, which represent a highly unusual cargo for the secretory pathway, may open an attractive and virtually untapped reservoir of alternative targets for the development of superior anti-viral drugs.
Indexed as
Identifiers
What OpenQuestion holds
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.