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Zika virus (ZIKV) is an emerging flavivirus that causes congenital abnormalities and Guillain-Barré syndrome. ZIKV infection also results in severe eye disease characterized by optic neuritis, chorioretinal atrophy, and blindness in newborns and conjunctivitis and uveitis in adults. We evaluated ZIKV infection of the eye by using recently developed mouse models of pathogenesis. ZIKV-inoculated mice developed conjunctivitis, panuveitis, and infection of the cornea, iris, optic nerve, and ganglion and bipolar cells in the retina. This phenotype was independent of the entry receptors Axl or Mertk, given that Axl−/−, Mertk−/−, and Axl−/−Mertk−/− double knockout mice sustained levels of infection similar to those of control animals. We also detected abundant viral RNA in tears, suggesting that virus might be secreted from lacrimal glands or shed from the cornea. This model provides a foundation for studying ZIKV-induced ocular disease, defining mechanisms of viral persistence, and developing therapeutic approaches for viral infections of the eye.
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•ZIKV infects several different regions of the eye, including the retina•ZIKV RNA can be detected in tear fluid•Eye and brain infection in adult mice by ZIKV occurs independently of the AXL receptor•ZIKV infection results in apoptosis of neurons of the visual processing pathway
Miner et al. now describe how ZIKV infection in the eye results in inflammation and injury. ZIKV infected the iris, cornea, retina, and optic nerve and caused conjunctivitis, panuveitis, and neuroretinitis in mice. This manuscript establishes a model for evaluating treatments for ZIKV infections in the eye.