New insights on Zika-induced retinal damage

Scientists at the Kresge Eye Institute have shown how the Zika virus replicates and survives within retinal cells, causing severe tissue damage and in some cases, blindness.

In a study published last week in JCI Insight, Ashok Kumar, PhD, and colleagues showed in vitro that the Zika virus infects cells lining the blood-retinal barrier, the retinal endothelium and retinal pigment epithelium (RPE).  

In addition, Kumar and his team showed that the virus causes chorioretinal atrophy in mouse eyes, with RPE mottling, a common ocular manifestation of congenital Zika infection in humans. The team linked this response with induced expression of multiple inflammatory and antiviral response genes in the infected mouse retina.

“We believe we have a unique model to study molecular mechanisms of ocular Zika infection, and perhaps to test drugs or new anti-viral molecules to treat this blinding eye disease,” Kumar said.

The team also found increased virus replication and more severe retinal lesions in mice without the ubiquitin-like interferon (IFN)-stimulated gene 15 (ISG15), suggesting that the gene plays an essential role in providing retinal defense against Zika infection.

Kumar is optimistic that the mouse model can also be used to assess the long-term impact of ocular abnormalities in infants born with congenital Zika infection.

“Will they have a normal vision?  What kind of vision rehab might they need? What about the social and economic impact in raising these children with a vision disability, if any?” said Kumar, considering the possible long-term consequences that require investigation.

Researchers are currently looking into how the virus changes a cell, where they have already identified key targets but are working to validate them.