| First Author | Yang W | Year | 2020 |
| Journal | PLoS Pathog | Volume | 16 |
| Issue | 12 | Pages | e1009019 |
| PubMed ID | 33315931 | Mgi Jnum | J:301677 |
| Mgi Id | MGI:6504966 | Doi | 10.1371/journal.ppat.1009019 |
| Citation | Yang W, et al. (2020) S100A4+ macrophages facilitate zika virus invasion and persistence in the seminiferous tubules via interferon-gamma mediation. PLoS Pathog 16(12):e1009019 |
| abstractText | 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-gamma-expressing M1 macrophages. With interferon-gamma 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-gamma signaling both reduced ZIKV infection in the seminiferous tubules. These results demonstrated crucial roles of S100A4+ macrophages in ZIKV infection in testes. |
