The high infection rate of SARS-CoV-2 is pushing researchers to identify—as quickly as possible—the molecular mechanisms that encourage viral entry and propagation. Findings of recent studies have been somewhat contradictory, given the rapidly evolving body of literature on the novel coronavirus, but the work in question argues that the ocular surface epithelium could serve as a point of entry for SARS-CoV-2.
Researchers point to two cell-surface receptors, angiotensin converting enzyme 2 (ACE2) and transmembrane protease serine type 2 (TMPRSS2), both of which are upregulated during inflammatory processes. The study evaluated these as potential entry factors that might enhance infection.
Researchers investigated SARS-CoV-2 movement in the embryonic, fetal and adult ocular surface. While the team detected the co-expression of ACE2 and TMPRSS2 in the adult cells, they did not find them in the embryonic or fetal ocular surface up to 21 weeks post-conception.
The authors also observed the co-expression of ACE2 and TMPRSS2 in the superficial limbal, corneal and conjunctival epithelium, and argue that this implicates them as target entry cells for SARS-CoV-2 in the ocular surface.
The investigators also identified various pro-inflammatory signals in the superficial conjunctival epithelium, and they suggest SARS-CoV-2 may capitalize on inflammatory-driven upregulation of ACE2 and TMPRSS2 expression as a route of infection.
“These findings suggest early but prolonged detection of SARS-CoV-2 in the ocular swabs and the possibility that ocular mucosa may be not only a site of virus entry but also a source of infection,” the study authors wrote in their paper.
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Collin J, Queen R, Zerti D, et al. Co-expression of SARS-CoV-2 entry genes in the superficial adult human conjunctival, limbal and corneal epithelium suggests an additional route of entry via the ocular surface. Ocul Surf. June 3, 2020. [Epub ahead of print].