SARS-CoV-2 and the Eyes: A Review of the Literature on Transmission, Detection, and Ocular Manifestations

Abstract

During the coronavirus disease 2019 (COVID-19) pandemic, numerous reports of ocular anomalies occurring in patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have emerged. The most frequently reported pathology is conjunctivitis, which may be the first or only clinical manifestation of the disease. Involvement of SARS-CoV-2 in development of alterations in other ocular structures was suggested, including the cornea, the retina, and blood vessels. Possible mechanisms include direct activity of the viral agent, as well as systemic inflammatory response with accompanying thromboembolic complications. Genetic material of SARS-CoV-2 was detected in ocular secretions of infected individuals, including asymptomatic patients. Moreover, angiotensin-converting enzyme 2 (ACE2), a receptor protein used by the virus to enter the cell, has been found on the surface of various structures of the eye, which indicates a risk of transmission through ocular tissues. Therefore, it is crucial to use eye protection by medical professionals having contact with potentially infected patients. This paper is a review of the literature regarding ocular manifestations of SARS-CoV-2 infection and a summary of the current state of knowledge about possibility of transmission from an ophthalmology point of view. For data collection, a thorough PubMed search was performed, using the key words: “COVID ocular”, “COVID eye”, “SARS-CoV-2 ocular”, and “SARS-CoV-2 eye”. Conclusions: SARS-CoV-2 infection may manifest itself in various ocular conditions. Eye protection should not be neglected, as recent studies suggest the eye as a potential route of transmission. Further search for adequate safety measures in ophthalmology practice is required.

Aerosol decontamination and spatial separation using a free-space LED-based UV-C light curtain

“…by mounting it between solid walls, aerosol viral load reductions higher than those observed with FFP2 masks are achievable as we have demonstrated. Besides, there are indications for aerosol transmissible viruses such as SARS-CoV-2, that they can also be taken up by impaction of infectious droplets on the conjunctiva [31,32] . To protect against this route of infection, masks are insufficient and specialised goggles would be additionally required.…”

Eye and SARS-CoV-2 in 2022

“…The published conjunctival smear rates in patients with SARS-Cov-2 have ranged from 0% to 16.7% and are probably even lower in patients without ocular symptoms, suggesting limited viral titers in the eye. Patients with confirmed SARS-Cov-2 infection usually did not show excretion of virus particles in tear secretions [5]. Certain conjunctival enzymes, including ADAR-1 and APOBEC3A, are thought to provide natural antiviral protection, reducing virus titers in the conjunctiva and minimizing the risk of their further transmission [6].…”

“…Certain conjunctival enzymes, including ADAR-1 and APOBEC3A, are thought to provide natural antiviral protection, reducing virus titers in the conjunctiva and minimizing the risk of their further transmission [6]. it is currently recommended that goggles or face shields be worn by healthcare workers with a high potential risk of transmission to the eye, as well as slit lamp shields [5,[7][8][9].…”

“…Swelling of the eyelids was found in 0.9% of COviD-19 patients, their irritation in 4.9% of individuals, most often in combination with conjunctival congestion [11,[18][19][20]. Retinal lesions were mainly observed in hospitalized COviD-19 patients with moderate to severe disease [5]. The pathomechanism of retinal damage is still not understood, but it may result from direct cytotoxic effects of the virus or, in the case of microangiopathy and vasculitis, from endothelial cell damage [1,5].…”

“…Retinal lesions were mainly observed in hospitalized COviD-19 patients with moderate to severe disease [5]. The pathomechanism of retinal damage is still not understood, but it may result from direct cytotoxic effects of the virus or, in the case of microangiopathy and vasculitis, from endothelial cell damage [1,5].…”