COVID-19 May Damage Vision

Summary: Researchers discovered that SARS-CoV-2 can penetrate the blood-retinal barrier, potentially causing long-term eye damage. The study found that the virus induces a hyperinflammatory response and cell death in the retina.

This breakthrough emphasizes the importance of monitoring eye health in COVID-19 patients. The findings could lead to new therapies for preventing and treating COVID-19-related eye complications.

Key Facts:

  1. Barrier Breach: SARS-CoV-2 can penetrate the blood-retinal barrier, infecting the eyes.
  2. Inflammatory Response: The virus causes hyperinflammation and cell death in the retina.
  3. Health Monitoring: COVID-19 patients should have their eyes checked for potential damage.

Source: University of Missouri-Columbia

The blood-retinal barrier is designed to protect our vision from infections by preventing microbial pathogens from reaching the retina where they could trigger an inflammatory response with potential vision loss.

But researchers at the University of Missouri School of Medicine have discovered the virus that causes COVID-19 can breach this protective retinal barrier with potential long-term consequences in the eye. 

Pawan Kumar Singh, PhD, an assistant professor of ophthalmology, leads a team researching new ways to prevent and treat ocular infectious diseases.

This shows COVID and an eye.
Singh also discovered that extended presence of SARS-CoV-2 spike antigen can cause retinal microaneurysm, retinal artery and vein occlusion, and vascular leakage. Credit: Neuroscience News

Using a humanized ACE2 mice model, the team found that SARS-CoV-2, the virus that causes COVID-19, can infect the inside of the eyes even when the virus doesn’t enter the body through the surface of the eyes.

Instead, they found that when viruses enter the body through inhalation, it not only infects organs like lungs, but also reaches highly protected organs like eyes through the blood-retinal barrier by infecting the cells lining this barrier.  

 “This finding is important as we increase our understanding of the long-term effects of SARS-CoV-2 infection,” said Singh.

“Earlier, researchers were primarily focused on the ocular surface exposure of the virus. However, our findings reveal that SARS-CoV-2 not only reaches the eye during systemic infection but induces a hyperinflammatory response in the retina and causes cell death in the blood-retinal barrier.

” The longer viral remnants remain in the eye, the risk of damage to the retina and visual function increases.” 

Singh also discovered that extended presence of SARS-CoV-2 spike antigen can cause retinal microaneurysm, retinal artery and vein occlusion, and vascular leakage.   

“For those who have been diagnosed with COVID-19, we recommend you ask your ophthalmologist to check for signs of pathological changes to the retina,” Singh said.

“Even those who were asymptomatic could suffer from damage in the eyes over time because of COVID-19 associated complications.” 

While viruses and bacteria have been found to breach the blood-retinal-barrier in immunocompromised people, this research is the first to suggest that the virus that causes COVID-19 could breach the barrier even in otherwise healthy individuals, leading to an infection that manifests inside the eye itself. 

Immunocompromised patients or those with hypertension or diabetes may experience worse outcomes if they remain undiagnosed for COVID-19 associated ocular symptoms. 

“Now that we know the risk of COVID-19 to the retina, our goal is to better understand the cellular and molecular mechanisms of how this virus breaches the blood-retinal barrier and associated pathological consequences in hopes of informing development of therapies to prevent and treat COVID-19 induced eye complications before a patient’s vision is compromised,” Singh said. 

In addition to Singh, the research team from the University of Missouri School of Medicine included Vaishnavi Balendiran, MD, vitreoretinal surgery fellow; Monu Monu and Faraz Ahmad, post-doctoral fellows in the Department of Ophthalmology; and Rachel M. Olson, PhD, Chief Scientific Officer, Laboratory for Infectious Disease Research at the College of Veterinary Medicine. 

Funding: This research was supported through fundings from the University of Missouri and the National Institutes of Health (NIH)/National Eye Institute (NEI) grant R01EY032495. 

About this COVID-19 and visual neuroscience research news

Author: Rochita Ghosh
Source: University of Missouri-Columbia
Contact: Rochita Ghosh – University of Missouri-Columbia
Image: The image is credited to Neuroscience News

Original Research: Open access.
SARS-CoV-2 infects cells lining the blood-retinal barrier and induces a hyperinflammatory immune response in the retina via systemic exposure” by Pawan Kumar Singh et al. PLOS Pathogens


SARS-CoV-2 infects cells lining the blood-retinal barrier and induces a hyperinflammatory immune response in the retina via systemic exposure

SARS-CoV-2 has been shown to cause wide-ranging ocular abnormalities and vision impairment in COVID-19 patients. However, there is limited understanding of SARS-CoV-2 in ocular transmission, tropism, and associated pathologies.

The presence of viral RNA in corneal/conjunctival tissue and tears, along with the evidence of viral entry receptors on the ocular surface, has led to speculation that the eye may serve as a potential route of SARS-CoV-2 transmission.

Here, we investigated the interaction of SARS-CoV-2 with cells lining the blood-retinal barrier (BRB) and the role of the eye in its transmission and tropism.

The results from our study suggest that SARS-CoV-2 ocular exposure does not cause lung infection and moribund illness in K18-hACE2 mice despite the extended presence of viral remnants in various ocular tissues.

In contrast, intranasal exposure not only resulted in SARS-CoV-2 spike (S) protein presence in different ocular tissues but also induces a hyperinflammatory immune response in the retina.

Additionally, the long-term exposure to viral S-protein caused microaneurysm, retinal pigmented epithelium (RPE) mottling, retinal atrophy, and vein occlusion in mouse eyes.

Notably, cells lining the BRB, the outer barrier, RPE, and the inner barrier, retinal vascular endothelium, were highly permissive to SARS-CoV-2 replication.

Unexpectedly, primary human corneal epithelial cells were comparatively resistant to SARS-CoV-2 infection. The cells lining the BRB showed induced expression of viral entry receptors and increased susceptibility towards SARS-CoV-2-induced cell death.

Furthermore, hyperglycemic conditions enhanced the viral entry receptor expression, infectivity, and susceptibility of SARS-CoV-2-induced cell death in the BRB cells, confirming the reported heightened pathological manifestations in comorbid populations.

Collectively, our study provides the first evidence of SARS-CoV-2 ocular tropism via cells lining the BRB and that the virus can infect the retina via systemic permeation and induce retinal inflammation.

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