ArticleVirologica Sinica2021
Rearrangement of Actin Cytoskeleton by Zika Virus Infection Facilitates Blood-Testis Barrier Hyperpermeability.
Article in Virologica Sinica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Discovery of actinators, actin-derived bioactive peptides that modulate cytoskeleton and actin-related cellular activities.Science advances · 2026Article
- Breaking barriers and beyond: Mechanisms and pathological implications of Zika virus traversal across blood-tissue interfaces.Virologica Sinica · 2026Review
- Ultrastructural Features, Immune Response, and Junctional Proteins in the Seminiferous Epithelium of SARS-CoV-2-Infected Mice.International journal of molecular sciences · 2026Article
- Pathogenic breaches: how viruses compromise blood-tissue barriers.Tissue barriers · 2026Review
- HSV-1 infection induces brain cofilin hyperphosphorylation in the 5×FAD Alzheimer's Disease mouse model.bioRxiv : the preprint server for biology · 2025Article
- Zika virus disrupts steroidogenesis and impairs spermatogenesis by stalling the translation of CYP17A1 mRNA.Nature communications · 2025Article
- Aglycone Polyether Ionophores Affecting Actin Filaments as Broad-Spectrum Antiviral Agents.ACS pharmacology & translational science · 2025Article
- Review
- Rho-GTPases subfamily: cellular defectors orchestrating viral infection.Cellular & molecular biology letters · 2025Review
- Article
- Zika and dengue viruses differentially modulate host mRNA processing factors defining its virulence.NAR molecular medicine · 2025Article
- Zika virus NS1 drives tunneling nanotube formation for mitochondrial transfer and stealth transmission in trophoblasts.Nature communications · 2025Article
- Zika virus tropism and pathogenesis: understanding clinical impacts and transmission dynamics.Virology journal · 2024Review
- Interaction of Receptor-Binding Domain of the SARS-CoV-2 Omicron Variant with hACE2 and Actin.Cells · 2024Article
- Article
- Nuclear membrane protein SUN2 promotes replication of flaviviruses through modulating cytoskeleton reorganization mediated by NS1.Nature communications · 2024Article
- Zika Virus NS1 Drives Tunneling Nanotube Formation for Mitochondrial Transfer, Enhanced Survival, Interferon Evasion, and Stealth Transmission in Trophoblasts.Research square · 2023Article
- RhoA suppresses pseudorabies virus replication in vitro.Virology journal · 2023Article
- Severe acute respiratory syndrome coronavirus 2 infection leads to Tau pathological signature in neurons.PNAS nexus · 2023Article
- In vitro and in vivo efficacy of Molnupiravir against Zika virus infections.Virologica Sinica · 2023Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In recent years, various serious diseases caused by Zika virus (ZIKV) have made it impossible to be ignored. Confirmed existence of ZIKV in semen and sexually transmission of ZIKV suggested that it can break the blood-testis barrier (BTB), or Sertoli cell barrier (SCB). However, little is known about the underlying mechanism. In this study, interaction between actin, an important component of the SCB, and ZIKV envelope (E) protein domain III (EDIII) was inferred from co-immunoprecipitation (Co-IP) liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis. Confocal microscopy confirmed the role of actin filaments (F-actin) in ZIKV infection, during which part of the stress fibers, the bundles that constituted by paralleled actin filaments, were disrupted and presented in the cell periphery. Colocalization of E and reorganized actin filaments in the cell periphery of transfected Sertoli cells suggests a participation of ZIKV E protein in ZIKV-induced F-actin rearrangement. Perturbation of F-actin by cytochalasin D (CytoD) or Jasplakinolide (Jas) enhanced the infection of ZIKV. More importantly, the transepithelial electrical resistance (TEER) of an in vitro mouse SCB (mSCB) model declined with the progression of ZIKV infection or overexpression of E protein. Co-IP and confocal microscopy analyses revealed that the interaction between F-actin and tight junction protein ZO-1 was reduced after ZIKV infection or E protein overexpression, highlighting the role of E protein in ZIKV-induced disruption of the BTB. We conclude that the interaction between ZIKV E and F-actin leads to the reorganization of F-actin network, thereby compromising BTB integrity.
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