ArticleThe ocular surface2019
Interferon-stimulated gene 15 (ISG15) restricts Zika virus replication in primary human corneal epithelial cells.
Article in The ocular surface, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 63 citations in OpenAlex.
- Article
- Short-chain fatty acids butyrate and acetate limit Zika virus replication and associated ocular manifestations via the G-protein coupled receptor 43/FFAR2.Journal of virology · 2026Article
- IFN-λ4 Exhibits Differential Induction and Antiviral Activity in RSV and HMPV Infections.Viruses · 2026Article
- Review
- Comparison of human cerebral organoids infected with wild-type Zika versus attenuated DN-2 virus strains uncovers differences in host immune responses.Cell communication and signaling : CCS · 2025Article
- Influenza a(H1N1) virus infection impairs syncytiotrophoblast functions by promoting ferroptosis through the TNF-α/ISG15/EGR1 axis.Virology journal · 2025Article
- Interferon-induced protein ISG15 in the central nervous system, quo vadis?FEBS letters · 2025Review
- Identification of AMOTL2 as an antiviral factor that enhances the human type I interferon response against Zika virus.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Toll-like receptor response to Zika virus infection: progress toward infection control.Npj viruses · 2025Review
- Multiorgan proteomic analysis of infected animal models predict potential host factors for chikungunya virus.MedComm · 2025Article
- An Overview of Zika Virus and Zika Virus Induced Neuropathies.International journal of molecular sciences · 2024Review
- Interferon Epsilon-Mediated Antiviral Activity Against Human Metapneumovirus and Respiratory Syncytial Virus.Vaccines · 2024Article
- Exploring Zika Virus Impact on Endothelial Permeability: Insights into Transcytosis Mechanisms and Vascular Leakage.Viruses · 2024Review
- SARS-CoV-2 infects cells lining the blood-retinal barrier and induces a hyperinflammatory immune response in the retina via systemic exposure.PLoS pathogens · 2024Article
- ISG15: its roles in SARS-CoV-2 and other viral infections.Trends in microbiology · 2023Review
- RIPK3 promotes brain region-specific interferon signaling and restriction of tick-borne flavivirus infection.PLoS pathogens · 2023Article
- ZIKV infection differentially affects the transcriptional profiles in HTR8 and U251 cells.Virus research · 2023Article
- Constitutive expression and distinct properties of IFN-epsilon protect the female reproductive tract from Zika virus infection.PLoS pathogens · 2023Article
- Coronaviral PLpro proteases and the immunomodulatory roles of conjugated versus free Interferon Stimulated Gene product-15 (ISG15).Seminars in cell & developmental biology · 2022Review
- The Innate Defense in the Zika-Infected Placenta.Pathogens (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
purposeZika virus (ZIKV) has emerged as an important human pathogen causing ocular complications. There have been reports of the shedding of ZIKV in human as well as animal tears. In this study, we investigated the infectivity of ZIKV in corneal epithelial cells and their antiviral immune response.
methodsPrimary human corneal epithelial cells (Pr. HCECs) and an immortalized cell line (HUCL) were infected with two different strains of ZIKV (PRVABC59 & BeH823339) or dengue virus (DENV, serotypes 1-4). Viral infectivity was assessed by immunostaining of viral antigen and plaque assay. qRT-PCR and immunoblot analyses were used to assess the expression of innate inflammatory and antiviral genes. Supplementation of recombinant ISG15 (rISG15) and gene silencing approaches were used to elucidate the role of ISG15 in corneal antiviral defense.
resultsPr. HCECs, but not the HUCL cells, were permissive to both ZIKV strains and specifically to DENV3 infection. ZIKV induced the expression of viral recognition receptors (TLR3, RIG-I, &MDA5), and genes involved in inflammatory (CXCL10 & CCL5) and antiviral (IFNs, MX1, OAS2, ISG15) responses in Pr. HCECs. Furthermore, ZIKV infection caused Pr. HCECs cell death, as evidenced by TUNEL staining. Silencing of ISG15 increased ZIKV infectivity while supplementation with rISG15 reduced ZIKV infection by direct inactivation of ZIKV and inhibiting its entry.
conclusionsOur study demonstrates for the first time, that ZIKV can readily infect and replicate in Pr. HCECs. Therefore, ZIKV may persist in the cornea and pose the potential risk of transmission via corneal transplantation.
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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.