Can COVID Cause Cataracts? A Look at Potential Eye Risks
Explore the potential connection between COVID-19 and cataract development, including how inflammation and viral mechanisms may impact eye health.
Explore the potential connection between COVID-19 and cataract development, including how inflammation and viral mechanisms may impact eye health.
COVID-19 is known for its respiratory effects, but research suggests it may also impact eye health. Some patients have reported vision changes following infection, raising questions about potential long-term consequences such as cataract formation. While cataracts typically develop with age or due to other risk factors, scientists are exploring whether the virus could contribute to their onset.
Understanding how SARS-CoV-2 might affect the eyes requires examining inflammation, viral mechanisms, and clinical observations.
SARS-CoV-2, the virus responsible for COVID-19, has demonstrated an ability to infect ocular tissues. The eye contains several entry points for viral invasion, including the conjunctiva, cornea, and tear film, all of which express angiotensin-converting enzyme 2 (ACE2) receptors—the primary binding site for the virus. Studies have confirmed the presence of viral RNA in ocular secretions, suggesting the eye may serve as both a route of infection and a site of viral replication.
Once inside the eye, SARS-CoV-2 may exploit ACE2 receptors found in corneal epithelium, conjunctival cells, and retinal tissues. A study in The Lancet Global Health identified viral particles in post-mortem retinal samples, indicating the virus can reach deeper ocular structures. This suggests that SARS-CoV-2 may disrupt normal cellular function, leading to oxidative stress and metabolic imbalances. Given that the lens relies on a delicate balance of proteins and antioxidants to maintain transparency, any disruption to these processes could affect lens health.
Beyond direct viral invasion, the eye’s vascular system may also contribute to viral spread. The retina and choroid are highly vascularized, and endothelial cells lining these blood vessels express ACE2 receptors. A study in JAMA Ophthalmology reported retinal microvascular changes in COVID-19 patients, including cotton wool spots and microhemorrhages, suggesting viral-induced endothelial dysfunction could contribute to ocular pathology. If similar vascular disturbances occur in the lens or its supporting structures, they could interfere with nutrient delivery and waste removal, potentially accelerating degenerative changes.
Inflammation plays a significant role in ocular homeostasis, but when dysregulated, it can contribute to tissue damage. The lens is an avascular structure that relies on the aqueous humor for nutrient exchange and waste removal. Any disruption to this environment, particularly through inflammatory mediators, can lead to oxidative stress and protein aggregation—both linked to cataract formation. COVID-19 has been associated with a systemic inflammatory response, marked by elevated cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), which have been implicated in ocular pathologies. If these molecules reach the intraocular space, they could disturb the protein equilibrium within the lens, increasing the risk of opacification.
Cytokine-induced oxidative stress is particularly concerning for lens transparency. The lens depends on antioxidants, including glutathione, to prevent protein misfolding and aggregation. Studies have shown that inflammatory conditions can deplete glutathione levels, leaving lens proteins vulnerable to oxidation. A 2022 study in Experimental Eye Research found that systemic inflammation can alter the redox balance in ocular tissues, accelerating lens protein cross-linking—a hallmark of cataract development. Additionally, oxidative stress can activate matrix metalloproteinases (MMPs), enzymes that degrade structural proteins, potentially weakening the lens capsule.
Chronic inflammation may also affect lens epithelial cells, which play a role in maintaining lens homeostasis by regulating ion transport, protein synthesis, and cellular repair. A study in Investigative Ophthalmology & Visual Science reported that sustained exposure to inflammatory cytokines led to increased epithelial cell death in lens cultures, suggesting prolonged systemic inflammation—such as that seen in severe COVID-19 cases—could have lasting consequences for lens integrity.
The possibility that COVID-19 could contribute to cataract formation has drawn interest due to reports of post-infection vision disturbances. While cataracts are traditionally associated with aging, metabolic disorders, and ultraviolet exposure, emerging evidence suggests systemic disruptions caused by SARS-CoV-2 may influence lens physiology in ways that accelerate opacification.
One area of concern is metabolic stress following COVID-19 infection. The lens depends on glucose metabolism for energy production, primarily through anaerobic glycolysis, as it lacks direct vascular support. Any systemic condition that alters glucose homeostasis, such as the insulin resistance observed in some post-COVID cases, could impact the lens’s ability to maintain transparency. A study in Diabetes & Metabolism highlighted that COVID-19 has been associated with transient hyperglycemia, even in individuals without a history of diabetes. Given that elevated glucose levels are a known risk factor for cataract development due to increased lens protein glycation, prolonged metabolic disturbances following infection could contribute to early cataract formation.
Oxidative damage has also been proposed as a potential link between COVID-19 and cataract risk. The lens is particularly vulnerable to oxidative stress due to its high concentration of crystallin proteins, which must remain structurally intact to prevent light scattering. Research in Redox Biology has shown that SARS-CoV-2 infection can trigger mitochondrial dysfunction, increasing the production of reactive oxygen species (ROS). Excess ROS can cause irreversible modifications to lens proteins, hastening the development of lens opacities.
Clinicians have reported various ocular abnormalities in patients recovering from COVID-19, prompting interest in whether the virus could have lasting effects on lens health. Ophthalmologists have documented unexplained visual disturbances, including increased lens opacities, in individuals who previously had clear lenses or only mild age-related changes. Some specialists have noted an unusual acceleration of lens clouding in post-COVID patients, particularly in those who experienced prolonged hospitalization or systemic complications.
Reports from eye clinics have also highlighted cases where patients exhibited decreased contrast sensitivity and glare intolerance following COVID-19 infection—symptoms commonly associated with early cataract progression. Some ophthalmologists have observed an increased need for earlier-than-expected cataract surgery in recovered COVID-19 patients, suggesting a potential shift in disease progression timelines. While large-scale epidemiological data are still being gathered, these clinical observations underscore the need for further research into whether COVID-19 may act as a novel risk factor for cataract development.