ArticleCell death & disease2016
ZIKA virus elicits P53 activation and genotoxic stress in human neural progenitors similar to mutations involved in severe forms of genetic microcephaly.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 127 citations in OpenAlex.
- The oxidative stress paradigm in arbovirus infections: mechanisms and therapeutic insights.Redox report : communications in free radical research · 2026Review
- Emerging and Re-Emerging Viral Pathogens in Oncolytic Virotherapy: A Comprehensive Review.Reviews in medical virology · 2026Review
- Zika virus impairs non-homologous end joining and exacerbates DNA damage in neural progenitors derived from Huntington's disease iPSCs via mutant huntingtin-elicited Ku70/Ku80 complex disruption.Stem cell research & therapy · 2025Article
- The human neural cell atlas of Zika virus infection in developing brain tissue.Cell reports. Medicine · 2025Article
- Genetic variants underlying congenital Zika syndrome and severe microcephaly: a systematic review and meta-analysis.Virusdisease · 2025Article
- A human-specific, concerted repression of microcephaly genes contributes to radiation-induced growth defects in cortical organoids.iScience · 2025Article
- Dual EMCV-IRES-integrated dengue virus can express an exogenous gene and cellular Mdm2 integration suppresses the dengue viral replication.Frontiers in microbiology · 2025Article
- The mechanisms of Zika virus-induced neuropathogenesis.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2024Review
- Erp57 facilitates ZIKV-induced DNA damage via NS2B/NS3 complex formation.Emerging microbes & infections · 2024Article
- Zika Virus Neuropathogenesis-Research and Understanding.Pathogens (Basel, Switzerland) · 2024Review
- Molecular and Cellular Mechanisms Underlying Neurologic Manifestations of Mosquito-Borne Flavivirus Infections.Viruses · 2023Review
- The Wheel of p53 Helps to Drive the Immune System.International journal of molecular sciences · 2023Review
- A neural stem cell paradigm of pediatric hydrocephalus.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- An entosis-like process induces mitotic disruption in Pals1 microcephaly pathogenesis.Nature communications · 2023Article
- P53 independent pathogenic mechanisms contribute to BubR1 microcephaly.Frontiers in cell and developmental biology · 2023Article
- DNA damage and repair: underlying mechanisms leading to microcephaly.Frontiers in cell and developmental biology · 2023Review
- Zika Virus Infection Downregulates Connexin 43, Disrupts the Cardiomyocyte Gap Junctions and Induces Heart Diseases in A129 Mice.Journal of virology · 2022Article
- Zika Virus Induces Mitotic Catastrophe in Human Neural Progenitors by Triggering Unscheduled Mitotic Entry in the Presence of DNA Damage While Functionally Depleting Nuclear PNKP.Journal of virology · 2022Article
- Apoptosis during ZIKA Virus Infection: Too Soon or Too Late?International journal of molecular sciences · 2022Review
- Zika Virus Neuropathogenesis: The Different Brain Cells, Host Factors and Mechanisms Involved.Frontiers in immunology · 2022Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
18 authors at 9 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidemiological evidence from the current outbreak of Zika virus (ZIKV) and recent studies in animal models indicate a strong causal link between ZIKV and microcephaly. ZIKV infection induces cell-cycle arrest and apoptosis in proliferating neural progenitors. However, the mechanisms leading to these phenotypes are still largely obscure. In this report, we explored the possible similarities between transcriptional responses induced by ZIKV in human neural progenitors and those elicited by three different genetic mutations leading to severe forms of microcephaly in mice. We found that the strongest similarity between all these conditions is the activation of common P53 downstream genes. In agreement with these observations, we report that ZIKV infection increases total P53 levels and nuclear accumulation, as well as P53 Ser15 phosphorylation, correlated with genotoxic stress and apoptosis induction. Interestingly, increased P53 activation and apoptosis are induced not only in cells expressing high levels of viral antigens but also in cells showing low or undetectable levels of the same proteins. These results indicate that P53 activation is an early and specific event in ZIKV-infected cells, which could result from cell-autonomous and/or non-cell-autonomous mechanisms. Moreover, we highlight a small group of P53 effector proteins that could act as critical mediators, not only in ZIKV-induced microcephaly but also in many genetic microcephaly syndromes.
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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.