ArticlePLoS pathogens2020
S100A4+ macrophages facilitate zika virus invasion and persistence in the seminiferous tubules via interferon-gamma mediation.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Powassan Virus Infects Mouse Testes and Reveals a Protective Role for Phagocytic Cells.Viruses · 2026Article
- A mouse model of Zika virus sexual transmission reveals a limited transmission window shorter than viral RNA persistence in semen.PLoS pathogens · 2026Article
- Breaking barriers and beyond: Mechanisms and pathological implications of Zika virus traversal across blood-tissue interfaces.Virologica Sinica · 2026Review
- Macrophage transition to a myofibroblast state drives fibrotic disease in uropathogenic E. coli-induced epididymo-orchitis.The Journal of clinical investigation · 2025Article
- Review
- Host S100A6 inhibits ZIKV replication by degrading NS3 through lysosomal pathway.Frontiers in cellular and infection microbiology · 2025Article
- Immunocompetent mouse models revealed that S100A4Emerging microbes & infections · 2024Article
- CD8Npj viruses · 2024Article
- Identification of novel anti-ZIKV drugs from viral-infection temporal gene expression profiles.Emerging microbes & infections · 2023Article
- Article
- Regulation of PKR-dependent RNA translation inhibition by TRIM21 upon virus infection or other stress.PLoS pathogens · 2023Article
- Single-cell RNA sequencing reveals the fragility of male spermatogenic cells to Zika virus-induced complement activation.Nature communications · 2023Article
- Mice 3D testicular organoid system as a novel tool to study Zika virus pathogenesis.Virologica Sinica · 2023Article
- A novel IFNbeta-induced long non-coding RNA ZAP-IT1 interrupts Zika virus replication in A549 cells.Virologica Sinica · 2022Article
- Article
- Sertoli Cell Immune Regulation: A Double-Edged Sword.Frontiers in immunology · 2022Review
- Human Neutrophils Present Mild Activation by Zika Virus But Reduce the Infection of Susceptible Cells.Frontiers in immunology · 2022Article
- Mechanism of Inflammatory Associated Impairment of Sperm Function, Spermatogenesis and Steroidogenesis.Frontiers in endocrinology · 2022Review
- RETRACTED: Androgen receptor transactivates KSHV noncoding RNA PAN to promote lytic replication-mediated oncogenesis: A mechanism of sex disparity in KS.PLoS pathogens · 2021Article
- Neuroinvasiveness of the MR766 strain of Zika virus in IFNAR-/- mice maps to prM residues conserved amongst African genotype viruses.PLoS pathogens · 2021Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Testicular invasion and persistence are features of Zika virus (ZIKV), but their mechanisms are still unknown. Here, we showed that S100A4+ macrophages, a myeloid macrophage subpopulation with susceptibility to ZIKV infection, facilitated ZIKV invasion and persistence in the seminiferous tubules. In ZIKV-infected mice, S100A4+ macrophages were specifically recruited into the interstitial space of testes and differentiated into interferon-γ-expressing M1 macrophages. With interferon-γ mediation, S100A4+ macrophages down-regulated Claudin-1 expression and induced its redistribution from the cytosol to nucleus, thus increasing the permeability of the blood-testis barrier which facilitated S100A4+ macrophages invasion into the seminiferous tubules. Intraluminal S100A4+ macrophages were segregated from CD8+ T cells and consequently helped ZIKV evade cellular immunity. As a result, ZIKV continued to replicate in intraluminal S100A4+ macrophages even when the spermatogenic cells disappeared. Deficiencies in S100A4 or interferon-γ signaling both reduced ZIKV infection in the seminiferous tubules. These results demonstrated crucial roles of S100A4+ macrophages in ZIKV infection in testes.
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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.