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?:abstract
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Introduction In December 2019, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic broke out. The virus rapidly spread globally, resulting in a major world public-health crisis. The major disease manifestation occurs in the respiratory tract. However further studies documented other systemic involvement. This study investigate histopathologic eye changes in post-mortem material of Coronavirus Disease 2019 (COVID-19) patients. Methods Sections of formalin-fixed, paraffin-embedded eyes from 5 patients (10 eyes) who died of COVID-19 at the University Hospital in Basel were included. Gross examination and histological evaluation were performed by three independent ophthalmopathologists. Immunohistochemical staining was performed using antibodies against fibrin, cleaved caspase 3 and ACE-2. Five enucleated eyes of patients not infected with SARS-CoV-2 served as control group. All cases have been studied for presence of SARS-CoV-2 RNA by means of RT-PCR and RNA in situ hybridization. The choroidal vessels of one case were analyzed with electron microscope. Results Ophthalmopathologically, eight eyes from four patients displayed swollen endothelial cells in congested choroidal vessels. No further evidence of specific eye involvement of SARS-CoV-2 was found in any of the patients. In the eight eyes with evidence of changes due to SARS-CoV-2, immunohistochemical staining demonstrated fibrin microthrombi, apoptotic changes of endothelial and inflammatory cells. In control eyes, ACE-2 was detectable in the conjunctiva, cornea, retina and in the choroidea, and displayed significantly lower amounts of stained cells as in COVID-19 eyes. SARS-CoV-2 RNA was detectable in both bulbi of 2/5 patients, yet in situ hybridization failed to visualize viruses. Electron microscopy showed no significant results due to the artifacts. Discussion/Conclusion As already described in other organs of COVID-19 patients, the ophthalmological examination revealed-microthrombi, i.e. hypercoagulation and vasculopathy most probably due to endothelial damage. A possible viral spread to the endothelial cells via ACE-2 provides one pathophysiological explanation. The expression of ACE-2 receptors in the conjunctiva hints towards its susceptibility to infection. To what extend eyes function are disrupted by SARS-CoV-2 is subject to further studies, especially in the clinic.
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