ArticleViruses2018
Zika Virus Fatally Infects Wild Type Neonatal Mice and Replicates in Central Nervous System.
Article in Viruses, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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.
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Who cites it
30 citing papers in PubMed, 74 citations in OpenAlex.
- Zika virus infection in neonatal mice disrupts connexin 43 and induces cardiac inflammation, implicating viral myocarditis in neonatal pathogenesis.Journal of virology · 2025Article
- Zika virus non-structural protein NS2A mediated endoplasmic reticulum stress through interacting with Sarco/endoplasmic reticulum CaJournal of virology · 2025Article
- Development and characterization of a pseudovirus system for human Aichi virus: in vitro and in vivo analysis.Virology journal · 2025Article
- Identification of antiviral RNAi regulators, ILF3/DHX9, recruit at ZIKV stem loop B to protect against ZIKV induced microcephaly.Nature communications · 2025Article
- Emerging and reemerging infectious diseases: global trends and new strategies for their prevention and control.Signal transduction and targeted therapy · 2024Review
- The Susceptibility of Chickens to Zika Virus: A Comprehensive Study on Age-Dependent Infection Dynamics and Host Responses.Viruses · 2024Article
- Postnatal Zika virus infection leads to morphological and cellular alterations within the neurogenic niche.Disease models & mechanisms · 2024Article
- Cytomegalovirus-vectored COVID-19 vaccines elicit neutralizing antibodies against the SARS-CoV-2 Omicron variant (BA.2) in mice.Microbiology spectrum · 2023Article
- Zika virus infection histories in brain development.Disease models & mechanisms · 2023Review
- Zika Virus Infection Downregulates Connexin 43, Disrupts the Cardiomyocyte Gap Junctions and Induces Heart Diseases in A129 Mice.Journal of virology · 2022Article
- A single nonsynonymous mutation on ZIKV E protein-coding sequences leads to markedly increased neurovirulence in vivo.Virologica Sinica · 2022Article
- From Mosquito Bites to Sexual Transmission: Evaluating Mouse Models of Zika Virus Infection.Viruses · 2021Review
- Zika Virus Overview: Transmission, Origin, Pathogenesis, Animal Model and Diagnosis.Zoonoses (Shannon, Ireland) · 2021Article
- Inositol-Requiring Enzyme 1α Promotes Zika Virus Infection through Regulation of Stearoyl Coenzyme A Desaturase 1-Mediated Lipid Metabolism.Journal of virology · 2020Article
- Japanese encephalitis virus-primed CD8+ T cells prevent antibody-dependent enhancement of Zika virus pathogenesis.The Journal of experimental medicine · 2020Article
- Zika virus infection in chemosensory cells.Journal of neurovirology · 2020Article
- Genetic Diversity of Collaborative Cross Mice Controls Viral Replication, Clinical Severity, and Brain Pathology Induced by Zika Virus Infection, Independently ofJournal of virology · 2020Article
- Erythromycin Estolate Inhibits Zika Virus Infection by Blocking Viral Entry as a Viral Inactivator.Viruses · 2019Article
- Article
- Inactivation of Zika Virus by Photoactive Iodonaphthyl Azide Preserves Immunogenic Potential of the Virus.Pathogens (Basel, Switzerland) · 2019Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Zika virus (ZIKV) has been defined as a teratogenic pathogen behind the increased number of cases of microcephaly in French Polynesia, Brazil, Puerto Rico, and other South American countries. Experimental studies using animal models have achieved tremendous insight into understanding the viral pathogenesis, transmission, teratogenic mechanisms, and virus-host interactions. However, the animals used in published investigations are mostly interferon (IFN)-compromised, either genetically or via antibody treatment. Herein, we studied ZIKV infection in IFN-competent mice using African (MR766) and Asian strains (PRVABC59 and SZ-WIV01). After testing four different species of mice, we found that BALB/c neonatal mice were resistant to ZIKV infection, that Kunming, ICR and C57BL/6 neonatal mice were fatally susceptible to ZIKV infection, and that the fatality of C57BL/6 neonates from 1 to 3 days old were in a viral dose-dependent manner. The size and weight of the brain were significantly reduced, and the ZIKV-infected mice showed neuronal symptoms such as hind-limb paralysis, tremor, and poor balance during walking. Pathologic and immunofluorescent experiments revealed that ZIKV infected different areas of the central nervous system (CNS) including gray matter, hippocampus, cerebral cortex, and spinal cord, but not olfactory bulb. Interestingly, ZIKV replicated in multiple organs and resulted in pathogenesis in liver and testis, implying that ZIKV infection may engender a high health risk in neonates by postnatal infection. In summary, we investigated ZIKV pathogenesis using an animal model that is not IFN-compromised.
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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.