ReviewPLoS neglected tropical diseases2021
The clinical spectrum and immunopathological mechanisms underlying ZIKV-induced neurological manifestations.
Review in PLoS neglected tropical diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Development of a Reverse Transcription Recombinase Polymerase Amplification CRISPR/Cas12a Assay for Visual and Highly Specific Identification of Zika Virus.Journal of medical virology · 2026Article
- Expression of Purinergic and Endothelial Activation Markers in Brain Tissue From Fatal Microcephaly Associated With ZIKV.Immunity, inflammation and disease · 2026Article
- Zika virus infection induces ultrastructural alterations, mitochondrial dysfunction and oxidative stress in human trophoblast HTR-8/SVneo.Frontiers in cellular and infection microbiology · 2026Article
- Unveiling the cardiovascular impact of Zika Virus: Myocardial injury, prothrombotic state, and oxidative stress in immunocompetent mice.PLoS neglected tropical diseases · 2025Article
- Review
- Neurological Manifestations of Zika Virus Infection: An Updated Review of the Existing Literature.Cureus · 2025Review
- Article
- Role of extracellular vesicles in the pathogenesis of mosquito-borne flaviviruses that impact public health.Journal of biomedical science · 2025Review
- Insect-specific virus platforms for arbovirus vaccine development.Frontiers in immunology · 2025Review
- Epidemic Zika virus strains from the Asian lineage induce an attenuated fetal brain pathogenicity.Nature communications · 2024Article
- Comparison of Three Chimeric Zika Vaccine Prototypes Developed on the Genetic Background of the Clinically Proven Live-Attenuated Japanese Encephalitis Vaccine SAInternational journal of molecular sciences · 2024Article
- Mechanistic insights into bone remodelling dysregulation by human viral pathogens.Nature microbiology · 2024Review
- Hsa_circ_0007321 regulates Zika virus replication through miR-492/NFKBID/NF-κB signaling pathway.Journal of virology · 2023Article
- Low CCL2 and CXCL8 Production and High Prevalence of Allergies in Children with Microcephaly Due to Congenital Zika Syndrome.Viruses · 2023Article
- The Aedes aegypti RNA interference response against Zika virus in the context of co-infection with dengue and chikungunya viruses.PLoS neglected tropical diseases · 2023Article
- Biosafety and mental health: Virus induced cognitive decline.Biosafety and health · 2023Review
- Immunopathogenesis of viral infections in neurological autoimmune disease.BMC neurology · 2023Review
- Zika virus induced microcephaly and aberrant hematopoietic cell differentiation modeled in novel neonatal humanized mice.Frontiers in immunology · 2023Article
- The Innate Defense in the Zika-Infected Placenta.Pathogens (Basel, Switzerland) · 2022Review
- MiR-103a-3p Promotes Zika Virus Replication by Targeting OTU Deubiquitinase 4 to Activate p38 Mitogen-Activated Protein Kinase Signaling Pathway.Frontiers in microbiology · 2022Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Since the 2015 to 2016 outbreak in America, Zika virus (ZIKV) infected almost 900,000 patients. This international public health emergency was mainly associated with a significant increase in the number of newborns with congenital microcephaly and abnormal neurologic development, known as congenital Zika syndrome (CZS). Furthermore, Guillain-Barré syndrome (GBS), a neuroimmune disorder of adults, has also been associated with ZIKV infection. Currently, the number of ZIKV-infected patients has decreased, and most of the cases recently reported present as a mild and self-limiting febrile illness. However, based on its natural history of a typical example of reemerging pathogen and the lack of specific therapeutic options against ZIKV infection, new outbreaks can occur worldwide, demanding the attention of researchers and government authorities. Here, we discuss the clinical spectrum and immunopathological mechanisms underlying ZIKV-induced neurological manifestations. Several studies have confirmed the tropism of ZIKV for neural progenitor stem cells by demonstrating the presence of ZIKV in the central nervous system (CNS) during fetal development, eliciting a deleterious inflammatory response that compromises neurogenesis and brain formation. Of note, while the neuropathology of CZS can be due to a direct viral neuropathic effect, adults may develop neuroimmune manifestations such as GBS due to poorly understood mechanisms. Antiganglioside autoantibodies have been detected in multiple patients with ZIKV infection-associated GBS, suggesting a molecular mimicry. However, further additional immunopathological mechanisms remain to be uncovered, paving the way for new therapeutic strategies.
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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.