COVID Dry Eyes and Their Impact on Eye Health

Many people recovering from COVID-19 have reported experiencing dry, irritated eyes. While dry eye syndrome has various causes, emerging evidence suggests that COVID-19 may contribute to its onset or worsening through multiple mechanisms.

Understanding how the virus affects tear production and eye hydration can help in managing symptoms effectively.

Viral Mechanisms That May Impact Tear Secretion

SARS-CoV-2, the virus responsible for COVID-19, has been detected in ocular tissues, raising concerns about its effects on tear production. It enters cells through the angiotensin-converting enzyme 2 (ACE2) receptor, which is present in the conjunctiva, cornea, and lacrimal glands. A study in The Ocular Surface (2021) found that ACE2 expression in the lacrimal gland suggests a direct pathway for viral invasion, potentially disrupting tear secretion. Once inside these tissues, the virus may cause cellular damage or alter tear-producing structures, reducing tear volume and increasing dryness.

Beyond direct infection, SARS-CoV-2 has neurotropic effects, meaning it can impact the nervous system, including the autonomic pathways that regulate tear production. The lacrimal gland relies on parasympathetic and sympathetic nervous system input to control tear secretion. A study in JAMA Ophthalmology (2022) suggested that post-viral autonomic dysfunction could impair these signals, leading to persistent dryness even after recovery.

Another possible mechanism involves the virus’s impact on mucin production, a key component of the tear film. Mucins help stabilize tears and prevent rapid evaporation. Research in Investigative Ophthalmology & Visual Science (2023) indicated that SARS-CoV-2 may alter goblet cell function in the conjunctiva, reducing mucin secretion and compromising tear film stability. Patients with preexisting conditions such as meibomian gland dysfunction or ocular rosacea may be particularly vulnerable, as their tear film is already impaired.

Relationship Between Systemic Inflammation And Ocular Surface

COVID-19 triggers widespread inflammation, which can extend beyond the respiratory system and affect the eyes. Systemic inflammation can alter tear composition, disrupt epithelial integrity, and exacerbate existing ocular conditions. A key driver is the cytokine storm—an excessive immune response involving elevated levels of pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α). These molecules increase tear film osmolarity, promote corneal nerve hypersensitivity, and degrade the protective mucin layer.

Inflammatory cytokines can also infiltrate the lacrimal gland, reducing tear secretion. A 2022 study in The American Journal of Ophthalmology found that post-COVID patients had higher levels of inflammatory markers in their tear fluid, correlating with dryness, irritation, and foreign body sensation. Systemic inflammation not only affects tear production but also alters tear composition, making them less effective in maintaining hydration.

Beyond tear production, inflammation disrupts the corneal and conjunctival epithelium. Prolonged exposure to inflammatory mediators weakens tight junction proteins that maintain the epithelial barrier, making the ocular surface more susceptible to environmental stressors and microbial pathogens. Research in Ocular Surface (2023) found that post-COVID patients exhibited increased corneal fluorescein staining, an indicator of epithelial damage and tear film instability. This disruption contributes to prolonged irritation and a higher risk of chronic dry eye symptoms.

Environmental Changes During Quarantine And Eye Hydration

Prolonged indoor confinement during quarantine altered daily routines, affecting screen exposure, air quality, and humidity levels—factors that influence eye hydration. Many people shifted to remote work, online learning, and digital entertainment, leading to extended screen time. Research in Ophthalmology (2022) found that digital device use reduces blink frequency by up to 60%, impairing tear distribution and accelerating evaporation. Inadequate blinking also contributes to meibomian gland dysfunction, which disrupts the tear film’s lipid layer and worsens dryness.

Indoor air quality further exacerbated eye dryness. HVAC systems, particularly forced-air heating and cooling, lower indoor humidity, accelerating tear evaporation. A study in Building and Environment (2021) found that humidity levels below 40% increase tear break-up times, making individuals more prone to discomfort. Many people spent quarantine in low-humidity environments, particularly in winter months when heating systems further reduced moisture.

Artificial lighting also played a role. Fluorescent and LED lighting, common in home offices, emit high levels of blue light, which has been linked to oxidative stress on the ocular surface. A 2023 review in Experimental Eye Research suggested that prolonged exposure to artificial lighting may contribute to inflammation and discomfort, particularly when combined with reduced blinking and dry indoor air. The lack of natural light exposure during quarantine also disrupted circadian rhythms, which regulate melatonin production. Emerging evidence suggests melatonin influences tear secretion, meaning altered sleep-wake cycles may have indirectly affected eye hydration.

Mask Wear And Airflow Patterns Around The Eyes

Face masks played a crucial role in reducing viral transmission but also affected airflow dynamics around the eyes. Poorly fitted masks redirect exhaled air upward, increasing tear evaporation and exacerbating dryness. A study in Translational Vision Science & Technology (2021) used Schlieren imaging to measure airflow patterns and found that ill-fitting masks significantly increased the velocity of exhaled air reaching the ocular surface, intensifying tear film instability.

Continuous exposure to warm, dry air from exhalation disrupts the tear film’s lipid layer, which slows evaporation. This effect is particularly pronounced in individuals with meibomian gland dysfunction, as their tear film is already compromised. Contact lens wearers may experience heightened discomfort, as accelerated evaporation reduces the lens’s hydrating effect, increasing friction between the lens and the cornea. Some ophthalmologists have termed this phenomenon “mask-associated dry eye” (MADE), highlighting its prevalence among healthcare workers and individuals wearing masks for extended periods.

Symptom Patterns Distinguishing This Condition From Other Dry Eye States

Dry eye symptoms associated with COVID-19 often follow a distinct pattern. Unlike traditional dry eye syndrome, which is commonly linked to aging, autoimmune conditions, or prolonged screen use, post-COVID dry eye involves a broader range of sensory disturbances. Many individuals report not only dryness and irritation but also a persistent grittiness or burning sensation that fluctuates unpredictably. Unlike meibomian gland dysfunction, where symptoms worsen progressively throughout the day, post-viral dry eye may present with episodic flare-ups, even in individuals with no prior history of ocular surface disease.

Another distinguishing factor is neuropathic pain symptoms, which are less common in conventional dry eye cases. Some post-COVID patients describe stinging or hypersensitivity to wind and light, despite normal tear production levels in clinical tests. This suggests that SARS-CoV-2 may affect corneal nerves, leading to altered pain perception independent of tear film quality. A study in Cornea (2023) found that post-COVID individuals with dry eye symptoms exhibited increased corneal nerve fiber loss and dendritic cell activation, indicating a potential neuroinflammatory component. This sensory dysfunction may explain why standard dry eye treatments, such as artificial tears, provide incomplete relief, necessitating a more tailored approach that addresses both tear film stability and nerve-related discomfort.